Fundamentals of Neurobio Lectures
Fundamentals of Neurobio Lectures 146:245
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Lecture 6 ~LGN ~individual neurons in lateral geniculate nucleus are monocular, receive input from only one eye ~LGN has 6 layers ~two ventral layers (1, 2)—called magnocellular because big cells ~four dorsal layers (3, 4, 5, 6)—called parvocellular because small cells ~the ganglions that project to M layer vs. P layer are also accordingly large/small cells ~M ganglion cells project to layers 1, 2 of LGN ~P ganglion cells project to layers 3, 4, 5, 6 of LGN ~retinogeniculate pathway has parallel magnocellular and parvocellular streams going to cortex ~M ganglion cells have larger receptive fields, faster conductance on axons ~M ganglion cells respond to a visual stimulus momentarily, P ganglion cells have a sustained response ~P ganglion cells can give info on color, M ganglion cells can’t ~nasal side of retina projects to layers 1, 4, 6 -goes to contralateral side of LGN w.r. to eye ~temporal side of retina projects to layers 2, 3, 5 -goes to ipsilateral side of LGN w.r. to eye ~the LGN it goes to is the same as the optic tract side, and same as optic radiation and cortex side ~on the occipital cortex: ~fovea projects to the most posterior part of cortex ~away from fovea, towards temporal/nasal edges of retina, projects to more anterior parts of cortex ~upper visual field is mapped below calacrine sulcus ~lower visual field is mapped above calacrine sulcus ~macula is the area around fovea, including fovea ~there is more cortex devoted to macula ~cortex has 6 layers ~LGN axons go to layer IV (4) ~layer IV has 3 sublayers—A, B, C ~LGN projects to layer IVC (4C) ~layer IVC has tiers alpha and beta ~magnocellular LGN projects to IVC alpha ~parvocellular LGN projects to IVC beta ~remember: M = layers 1, 2 of LGN P = layers 3, 4, 5, 6 of LGN nasal retina = layers 1, 4, 6 of LGN temporal retina = layers 2, 3, 5 of LGN M = IVC alpha P = IVC beta -nasal retina = contralateral LGN -temporal retina = ipsilateral LGN Lecture 1 ~eye has three layers around it -innermost is retina -middle is uveal tract -outermost is sclera ~innermost layer is retina, has neurons sensitive to light ~next layer is uveal tract, uveal tract has a bunch of stuff in it -has choroid in the posterior—rich capillary bed and a lot of melanin -anterior part of uveal tract is ciliary body (ring of muscle around lens and iris -ciliary muscles adjust refractive power of lens -iris adjusts size of pupil ~outermost layer is sclera, tough and opaque ~BUT at the front of the eye, sclera turns into cornea, transparent ~conjunctiva attaches sclera to eyelid ~6 extraocular muscles hold the eyeball in place in the orbit of the skull ~vitreous humor is between lens and retina, gives most of the eye volume, gives spherical shape of eye ~to get to retina, light goes from: -corneaaqueous humor in anterior chamberlensvitreous humor ~cornea and lens refract light to focus it on retina ~cornea does most of the refraction, lens does some ~lens is normally round, need to use ciliary muscles to pull it out flat ~the actual ciliary muscle is connected to lens by the anterior zonule fibers ~accommodation—changing refractive power of lens by contracting/relaxing ciliary muscle -to see distant objects, need less refractive power, lens becomes flatter, relax ciliary muscles so that anterior zonule fibers are pulled and they pull on lens -to see near objects, need more refractive power, lens becomes more curved, contract ciliary muscles so that anterior zonule fibers are loose and allow lens to become curved ~using iris to reduce size of pupil reduces spherical and chromatic aberration and allows more depth ~but reducing pupil size also limits amount of light that can reach retina ~retina—cells in retina transduce light into neural activity, retina is part of CNS ~five cell types in retina: -photoreceptors -horizontal cells -bipolar cells -amacrine cells -ganglion cells ~the cells are stacked in layers ~main route of information flow is photoreceptorbipolarganglion ~BUT the cells are actually stacked up in reverse -ganglion layer is closer to center of eye, photoreceptor layer is farther from center of eye -photoreceptor layer = outer nuclear layer -bipolar cell layer = inner nuclear layer ~horizontal and amacrine cells have cell bodies in inner nuclear layer ~horizontal cells do lateral stuff in outer plexiform layer, project from photoreceptors to bipolar cells ~amacrine cells do lateral stuff in inner plexiform layer, project from bipolar cells to ganglion cells ~photoreceptors are either rods or cones -only photoreceptors are light-sensitive -both have an outer segment (the actual rod/cone shaped part) with membranous lamellae, called outer because it’s farther away from center of eye than the inner segment with the cell body ~axons of ganglion cells form the optic nerve, fire action potentials to carry visual info to CNS ~note: pigmented epithelium at the back of the eye absorbs light not absorbed by photoreceptors -pigmented epithelium is even more distal than outer segment of photoreceptors ~before light reaches photoreceptor outer segments, it passes through ganglion and bipolar cells Lecture 2 ~phototransduction ~photoreceptors and bipolar cells have graded potentials, NOT action potentials ~graded potentials means the rate of NT released is increased/reduced, not an all-or-none event ~photopigments are in the lamellae of photoreceptors ~a photopigment is made of retinal (lipid) + some kind of opsin ~opsins are specialized for certain wavelengths of light ~the most studied photopigment is rhodopsin ~rhodopsin is the photopigment in rods ~retinal absorbs a photon, which causes activation of transducin (intracellular messenger), which activates enzymes that hydrolyze cGMP (turn it into GMP) ~light actually hyperpolarizes photoreceptors ~in the dark,2+hotoreceptors are depolarized to -40 mV -more Ca channels open -a lot of cyclic GMP in outer segment, keeps Na and Ca 2+channels open + -movement of Na to inside the cell is called dark current ~max light causes hyperpolarization to -65 mV -G-protein is activated, which activates enzymes that decrease amount of cGMP (2 ndmessenger) + 2+ -less cyclic GMP (bc converted to GMP), keeps Na and Ca channels closed -fewer Ca 2+channels open means less NT released ~there is a lot of signal amplification in this cascade ~the physics stuf ~distant objectslight rays run parallel ~light rays bend as they refract, and go slower in denser mediums (cornea and humor) ~focal distance is where the image forms for distant objects -distance between cornea and retina -depends on curvature of cornea -around 2.4 cm ~9 meters or closer—light rays are not parallel ~refractive power changes by changing lens shape ~accommodation alters light rays that would normally be parallel ~making the pupil smaller—you can see more depth but not very well focused ~field of view is 150o o -90otemporal -60 nasal ~types of sightedness ~emmetropia is normal vision, don’t need accommodation for parallel rays ~hyperopia is farsightedness, eyeball is too short, image focused behind retina -lens cannot accommodate for near objects, near point is v. far -correct with convex lens to increase refractive power ~myopia is nearsightedness, eyeball is too long, image focused in front of retina -lens cannot accommodate for far objects, far point is v. close -correct with concave lens Lecture 4 ~cones ~three types of cones, named by their wavelengths -blue (short) -green (medium) -red (long) ~all identifiable colors are made by mixing proper ratios of blue, green, red ~white color = activation of all three ~each ganglion cell has a specific receptive field on the retina (collection of the photoreceptors that converge to that ganglion cell) ~the receptive field is circular, has a center and a surround (periphery) ~two types of ganglion cells ON cells—fire more action potentials when light is shined on their receptive field center -get a brief burst of excitation when light is turned on -they are inhibited (fire less) when light is on receptive field surround OFF cells—inhibited when light is shined on receptive field center -get a brief burst of excitation when the light is turned of -they are activated when light falls on receptive field surround -basically the opposite of ON ~they are also called on-center and of-center ~basically ON cells fire when there is light, OFF cells fire when there is dark ~there are equal amounts of ON and OFF cells, have overlapping receptive fields ~thus any change in light intensity causes firing of action potentials -brighter lighting causes firing of ON cells -darker lighting causes firing of OFF cells ~ganglion cells are sensitive to luminance contract—amount of light falling on receptive center vs. receptive surround fields, center-surround antagonism ~when there is not much luminance contrast, the ganglion cells return to resting firing rate ~in light adaptation—consider a spot of bright light -the intensity of the light is related to response rate -BUT you have to take into account the background level of illumination -a bright spot of light in an already bright background will not cause a lot of firing -thus there is an adaptation—if background is illuminated, an adaptive shift requires more stimulus to achieve same response firing rate ~bipolar cells ~ON ganglion cells synapse with ON bipolar cells ~OFF ganglion cells synapse with OFF bipolar cells ~unlike ganglion cells, bipolar cells have graded potentials ~more glutamate released by bipolar cells = more firing of ganglion cells ~on-center bipolar cells have metabotropic receptors, GPCR, hyperpolarize in response to glutamate release from photoreceptors ~of-center bipolar cells have ionotropic receptors, depolarize in response to glutamate release from photoreceptors ~remember that photoreceptors release more glutamate in the dark ~more light = on-center bipolar cells depolarize, of-center hyperpolarize ~more dark = of-center bipolar cells depolarize, on-center hyperpolarize ~horizontal cells ~two way synapse between photoreceptors and horizontal cells ~horizontal cells show the amount of illumination over a broad area of retina ~glutamate from photoreceptors is depolarizing for horizontal cells ~GABA from horizontal cells is hyperpolarizing for bipolar cells Lecture 3 ~light adaptation—when lighting is dim, photoreceptors are most sensitive to light ~as illumination increases, they become less sensitivecan absorb more light without getting saturated ~with adaptation, rhodopsin is broken down and regenerated ~changes associated with adaptation—pupil diameter increases ~rod vs. cone ~distinguished by shape of outer segment (rod and cone) ~rods have more disks in lamellae, cones have fewer ~rod has low spatial resolution but high sensitivity to light ~cone has high spatial resolution but low sensitivity to light ~rods always have only rhodopsin pigment, higher pigment concentration ~cones have three different kinds of pigments, sensitive to different wavelengths of light ~in scotopic (dark) conditions, only rods are activated ~in photopic (more light) conditions, you begin to use more of the cone system ~in photopic conditions, rod system dies out because rods become saturated, have all channels closed -saturated = bleached, no more Na+ channels can close because they’re all already closed ~in mesopic (a little light) conditions, you use rods and cones -this would at like twilight ~most of your everyday vision is from the cone system ~because rods are more sensitive, it only takes one photon to activate a rod, but takes ~100 for cone ~cones get saturated less easily ~for most of the retina, a ganglion cell receives input from both rods and cones but early on in this pathway to ganglion cells, the rod and cone inputs are v. distinct ~rods first synapse with rod bipolar cellsrod bipolar cells synapse with amacrine cells instead of going straight to ganglion cell -a bunch of rod cells converge on a single rod bipolar cells, and a bunch of rod bipolar cells converge on a single amacrine cell -so there is a lot of convergence ~with cones, the cone bipolar cell synapses directly with ganglion cell -a single cone synapses on a single cone bipolar cell which synapses with a single ganglion cell -so each ganglion cell only receives input from one cone cell -much less convergence in cones ~the 1:1 convergence of cone:ganglion cell gives cones high acuity ~distribution of rods and cones ~there’s way more rods in the retina than there are cones ~in most of the retina, density of rods is greater than density of cones ~BUT in the fovea, cone density increases dramatically and rod density decreases dramatically ~in the fovea, the cone outer segment is actually flattened so that more can be packed in ~at the very center of the fovea (foveola) there are no rods at all, only cones ~farther from the fovea, visual acuity rapidly drops off ~in the periphery of retina, there are only rods ~outside central vision, you can more easily detect a light stimulus -see stars by looking to the side so that the light falls on the rod-rich periphery ~in the fovea and especially foveola, there are no layers of ganglion and bipolar cellsmore acuity -that is why the fovea is a pit ~optic disk is the entrance for the optic nerve ~blood vessels also originate in optic disk ~optic disk is a blind spot ~has no photoreceptors Lecture 5 ~primary visual pathway—from retina to dorsal laterate geniculate nucleus to primary visual cortex ~there’s also parallel processing that projects to a bunch of different areas of cortex ~optic disk—where the axons of ganglion cells exit and go deep into the brain ~optic disk is on nasal side of eye ~all the ganglion axons bundles together = optic nerve ~optic disk has no photoreceptors, so it’s a blind spot ~optic disk is also where arteries enter and veins leave ~axons in optic nerve go straight to optic chiasm ~decussation—60% of axons cross lateral sides in chiasm, 40% stay on their lateral side ~optic chiasm is at base of diencephalon ~after passing chiasm, the ganglion axons form the optic tracts, one on each side ~the optic tract has the fibers that ran straight and the ones that crossed over to that lateral side ~through optic tract, they go on to the diencephalon and midbrain -major target in diencephalon is dorsal lateral geniculate nucleus in thalamus ~from thalamus they go through optic radiation, to primary visual cortex, aka striate cortex -primary visual cortex is along calacrine fissure in occipital lobe ~apart from LGN in thalamus, another target is the pretectum -pretectum coordinates pupillary light reflex -pupillary light reflex—in bright light, pupil becomes smaller by muscles in iris constricting -both eyes exhibit pupillary light reflex even when only one of them is stimulated ~another target is the suprachiasmatic nucleus (SCN) in hypothalamus -changes in light levels affect visceral functions related to circadian rhythm ~another target is the superior colliculus in the tectum in the midbrain -10% of info goes to superior colliculus -coordinates head and eye movements directed at visual targets ~info from left visual field ends up in right brain ~info from right visual field ends up in left brain ~each eye has a nasal and temporal visual field ~the point of fixation forms image on fovea ~image on retina is inverted vertically and horizontally -objects on temporal side of the eye are seen by nasal side of retina -upper part of object is seen by lower part of retina ~the center of the fovea divides the retina into nasal and temporal ~temporal retina is larger than nasal ~the visual fields from both eyes overlaps a lot -the overlap is called the binocular field of view -left half of the binocular field is seen by left nasal retina and right temporal retina -right half of the binocular field is seen by right nasal retina and left temporal retina ~basically remember that vision entering the eye at an angle hits the retina at the same angle ~the very far left field is only seen by left eye (monocular), at the edge of the nasal retina ~the very far right field is only seen by right eye (monocular), at the edge of the nasal retina ~information from the visual fields ultimately has to end up in the contralateral part of the brain -note that it says visual field, NOT eyes -each eye sees stuff from left and right visual fields ~ganglions in nasal side of retina have axons that cross in chiasm, since the nasal side of retina only sees things in the same lateral side as that eye, and information ultimately has to cross -this includes the edge of the nasal for monocular fields of vision ~ganglions in temporal side of retina have axons that do not cross in chiasm, since they already only see stuff from the contralateral visual field Lecture 7 ~audition ~sound is pressurized air waves ~is a longitudinal wave, has rarefactions and compressions of air molecules ~has the qualities of a wave—waveform, frequency, amplitude, phase ~amplitude is intensity, loudness ~frequency is pitch ~waveform is plot of amplitude vs. time ~we can hear between 20 to 20k Hz ~overview of sound processing ~outer and middle ears collect sound and amplify their pressure ~in the inner ear, the sensory hair cells do biochemical processes to transduce sound ~auditory nerve fibers transmit info ~at the cochlear nucleus, the info diverges into a bunch of parallel pathways ~cochlear output has a bunch of different targets in the brain ~three divisions of ear -outer ear—pinna, concha, auditory canal -middle ear—tympanic membrane, ossicles, Eustachian tube -inner ear—cochlea, vestibular apparatus ~outer ear ~has pinna—the cartilage/skin outgrowth most people call ear ~concha is the conch shaped part of the cartilage, more proximal than pinna ~auditory canal is a canal leading from outside environment up to surface of tympanic membrane ~pinna, concha, and auditory canal gather sound energy and focus it on the eardrum ~middle ear ~because the inner ear (where sound is transduced) is liquid, the middle ear has to accommodate for transition from air to liquid medium ~normally a sound traveling from low n (air) to high n (liquid) would mostly get reflected ~tympanic membrane prevents reflection by boosting pressure of sound 200x ~two processes happen in middle ear to boost pressure: -first, the force incident on the relatively large tympanic membrane is concentrated on the much tinier oval window -oval window is where the middle ear bones meet the inner ear -second, the three ossicles (malleus, incus, stapes) do lever action ~lever action of ossicles: -movement of tympanic membrane makes malleus move like a lever, with the top moving towards the outer ear -malleus pulls on top of incus, top of incus is pulled outward, bottom is pushed towards inner ear -incus pushes stapes against oval window -oval window gets compressed ~two muscles in middle ear—tensor tympani and stapedius—can stiffen to limit amount of sound transmitted to cochlea ~eustachian tube connects middle ear to mouth, has a valve Lecture 8 ~inner ear ~the main thing is the cochlea, is where movement of oval window is transduced into neural activity ~cochlea amplifies sound, transduces it, breaks down complex waves into smaller elements ~cochlea is like a rolled up tube ~the tube is bisected by the cochlear partition almost all the way through ~cochlear partition has the tectorial membrane and basilar membrane ~there’s actually two walls in the cochlea, divides it into three sections of the tube: -scala vestibuli -scala tympani -scala media ~fluid is continuous between scala vestibuli and scala tympani ~inward movement of oval window displaces fluid of cochlea, causes round window to bulge ~this conserves the wave properties of sound since the wave is carried in fluid ~the key is that basilar membrane is flexible, vibrates in response to sound ~outer + inner hair cells = sensory cells of ear ~hair cells are in organ of corti, in the scala media, on top of the basilar membrane ~waves from the oval window bend the hair part (stereocilia) of the hair cells on the basilar membrane ~bending of stereocilia causes voltage change in hair cell membrane ~cochlea has bipolar spiral ganglion cells ~bipolar ganglion cell has peripheral and central processes -peripheral process synapses with an inner hair cell -central processes make up auditory nerve, goes to cochlear nucleus in brain ~structure of basilar membrane ~wider at apex than at base ~apex is very flexible, base is less flexible ~low frequency sounds are low energy, can only displace apical (flexible) end ~high frequency sound has higher energy, can displace basal (stiffer) end ~base responds to high frequency, apex responds to low frequency ~basilar membrane moves in response to stapes, the whole complex moves either towards or away from tectorial membrane ~hair cell ~hair cell is an epithelial cell ~hair cells extend above reticular membrane, come in contact with tectorial membrane ~has hair-like processes extending from apical end of cochlea into scala media ~there’s a bunch of stereocilia, and one longer kinocilium ~only the kinocilium is a true cilia ~lateral motion of reticular membrane bends stereocilia ~the stereocilia are lined up in height order ~bending towards the longest stereocilium causes depolarization ~bending towards shortest stereocilium causes hyperpolarization ~displacement perpendicular to the line of stereocilia does not cause any membrane potential change ~they use mechanically gated transduction channels for rapid communication of sound info ~have graded receptor potentials ~there’s filaments connecting the t+ps of the ste+eocilia ~stretching the filaments opens K channels, K flows into celldepolarization -going towards taller one -potassium channels opening causes Ca 2+channels to open, influx of calcium causes NT release + ~pushing the tips together closes K channels, stops flow of K hyperpolarization -going towards shorter one ~at resting potential of hair cell membrane, only a few K+ channels are open ~when depolarization happens, NT is released onto auditory nerve endings ~because it is a graded potential, a sinusoidal stimulus can generate a sinusoidal pattern of depolarization and hyperpolarization, which preserves the wave nature of the sound ~the original sound can be preserved up to 3000 Hz frequency sound Lecture 9 ~there’s one row of inner hair cells and three rows of outer hair cells ~the inner hair cells are the real sensory receptors ~95% of axons in auditory nerve are from inner hair cells ~outer hair cells mostly get efferent info from some other place (?) ~outer hair cells can change stiffness of tectorial membrane, helps the cochlea sharpen the frequency ~info going from cochlea to brain stem ~parallel organization ~auditory nerve is the major part of cranial nerve VIII (8) ~there are two cochlear nuclei in brainstem, one for each ear ~action potential happens in spiral ganglion cells ~multiple outer hair cells synapse with a single ganglion cell ~each ganglion only synapses with one inner hair cell ~remember the spiral ganglion cells have their central processes going towards cochlear nucleus in brain ~when the auditory nerve fibers reach cochlear nucleus, they branch into ascending and descending -ascending branch goes to anteroventral cochlear nucleus (ACN) -descending branch goes to posteroventral cochlear nucleus (PCN) & dorsal cochlear nucleus (DCN) ACN is important for detection time different of a sound between the two ears PCN and DCN send efferent projections to contralateral inferior colliculus -this is via nucleus of lateral lemniscus ~neurons in cochlear nuclei project to a bunch of different pathways ~one function is sound localization ~two different strategies to locate horizontal position of a sound source, depending on frequency -for frequency below 3000 Hz—interaural time difference is used to locate sound -for frequency above 3000 Hz—interaural intensity difference is used to locate sound ~we can detect interaural time difference as small as 10 microseconds for frequency below 3000 Hz—through the medial superior olive ~medial superior olive (MSO) gets input from left and right anteroventral cochlear nuclei -has bipolar cells with lateral and medial dendrites -lateral dendrites get input from ipsilateral ACN -medial dendrites get input from contralateral ACN -both lateral and medial connections are excitatory -MSO cells are coincidence detectors—responds when both excitatory signals coincide ~different MSO neurons are sensitive to different time delays ~axons coming from ACN vary in length systematically to make delay lines to account for time difference from the two ears and cause the signal to arrive at the same time from both ears ~each MSO cell is sensitive to sound coming from a specific place, so whichever cells receive excitatory input indicates location of source ~so length of axons determine which MSO cell is activated ~MSO system is for sounds below 3000 Hz because phase-locked info is only available below 3000 Hz Lecture 10 for frequency above 3000 Hz—sound localization by interaural intensity ~the head diameter is 20 cm ~in high frequency sound, the head is an obstacle and the sound waves have too short wavelength to bend around head ~there is an acoustical shadow on the farther ear ~so here, the location of sound is determined by sound intensity, (for <3000 Hz it was time difference) ~circuit involves lateral superior olive (LSO) and medial nucleus of the trapezoid body (MNTB) ~you know that there are axons going from ACN to MSO there are also excitatory axons going from ACN to LSO (from ipsilateral ACN) -this is direct projection from ACN ~LSO also gets inhibitory neurons from the contralateral ear, via inhibitory neuron in MNTB -this is indirect projection ~ipsilateral excitation and contralateral inhibition results in net excitation of LSO, ipsilateral to the sound o ~when a sound is directly to your right/left (lets call it 180 ) -maximum firing from ipsilateral ACN, and more firing for more intense sound -minimal inhibition from contralateral MNTo ~when a sound is closer to your middle (90 ) -lower firing from ipsilateral ACN -more inhibition from contralateral MNTB ~when a sound is at the midline, or at the other side of the LSO you’re looking at -maximum inhibition from MNTBcompletely silences LSO activity ~basically interaural intensity differences are processed in LSO ~this is for greater than 3000 Hz ~pathways from MSO and LSO converge at midbrain auditory centers (inferior colliculus) ~there are other cochlear outputs there are pathways that terminate in nuclei of lateral lemniscus, on contralateral side of brain stem -monaural because they respond to sound at one ear only -some signal the onset of a sound, some signal duration of a sound, etc. -these pathways also converge at midbrain auditory center (inferior colliculus) ~there are also monaural pathways from DCN and PCN nuclei ~in the inferior colliculus: ~space is not mapped in the auditory receptorsperception of auditory space must happen elsewhere ~in the inferior colliculus, there is a topographical auditory space map ~think of it like a circular (x,y) coordinate systemneurons in the space map are specific to sounds originating at a certain elevation and azimuth (horizontal position) ~inferior colliculus also has neurons specific to frequency, duration, etc. Lecture 12 ~two-point discrimination test—to determine tactile sensitivity of different areas of body ~shows density of receptors and receptive fields in a region of skin ~high density and small receptive field = better discrimination in two-point test ~proprioceptors ~they are mechanoreceptors specialized for mechanical forces coming from the body -etymology = proper receptors, receptors for yourself ~give information about position of body parts in space, also direction and speed ~proprioceptors is a class of receptors—includes muscle spindles, Golgi tendon organs, joint receptors ~information on position of head is v. important, has proprioceptors integrated with vestibular system ~muscles spindles—type of proprioceptor, most studied ~they are encapsulated ~muscle spindles found in almost all muscles, except for a few skeletal muscles ~muscle spindle made of some intrafusal muscle fibers surrounded by capsule of connective tissue ~a single intrafusal fiber is a collection of cells ~intrafusal fibers are specialized ~intrafusal fibers are distributed among normal (extrafusal) fibers in parallel in skeletal muscle tissue ~nuclear bag fibers -in the spindle there are one or two large intrafusal fibers that have the nuclei of the cells gathered in a bulged region -hence “bag” ~nuclear chain fibers -in the other intrafusal fibers that make up the spindle, the nuclei are arranged in a line -hence “chain” ~the intrafusal fibers contract in response to motor axons ~muscle spindles provide information about muscle length, i.e. the level of stretching in the muscle ~large muscles in limbs are for coarse movement, don’t have a lot of muscle spindles ~extraocular muscles, muscles in hand and neck are for fine movement, have a lot of muscle spindles ~Golgi tendon organs—type of proprioceptor ~found in the collagen fibers of tendons ~low-threshold proprioceptors ~provide information on muscle tension ~joint receptors—type of proprioceptor ~rapidly adapting ~found in and around joints Lecture 11 ~four types of mechanoreceptors, all encapsulated: -Meissner’s corpuscle -Pacinian corpuscle -Merkel’s disc -Ruffini’s corpuscle these are all low threshold, high sensitivity—make action potentials with even light stimulation ~low threshold receptors have large myelinated axons ~they all have a specific range of frequencies that they respond to ~Meissner’s corpuscles—between dermal papillae (fingerprint ridges) -most common type of mechanoreceptor in glabrous skin (hairless places i.e. palms, soles of feet) -encapsulated, capsule made of lamellae layers of Schwann cells -center of capsule has afferent nerve fibers -the fibers make up 40% of sensory innervation of hand -the nerve fibers make rapidly adapting action potentials -respond strongly to even light skin depression -transduce low-frequency vibration—30-50 Hz -responding to texture moving across skin basically ~Pacinian corpuscles—in subcutaneous tissue -also found deep in interosseous membranes (joints) and mesenteries in gut -has onion-like capsule -has inner core of lamellae and outer lamellae -inner and outer lamellae separated by a fluid-filled layer -center of core has rapidly adapting afferent axons -transduce high-frequency vibration—250-350 Hz -so they can discriminate fine texture, moving stimuli that make high- frequency vibration -make up 10-15% of receptors in subcutaneous part of hand ~Merkel’s disks—cutaneous, in epidermis, aligned with papillae under dermal ridges -terminal end of the nerve fiber has a wide disk shape that is closely applied to another cell that releases vesicles of peptides -sensitive to light pressure -slowly adapting, detect static properties, unlike Pacinian and Meissner’s -good for static tactile discrimination of shapes, edges, rough texture -make up 25% of mechanoreceptors in hand -high density in fingertips, lips, outer genitals ~Ruffini’s corpuscles—has spindle-shaped capsule deep in skin -also deep in ligaments and tendons -sensitive to cutaneous stretching produced by limb movement -make up 20% of receptors in hand -no response to electrical stimulation -don’t know much about them, they probably respond to internal stimuli ~mechanoreceptors in general are differentiated by stimulus frequency, pressure, receptive field Lecture 14 ~nociceptors ~nociceptors are free nerve endings (not encapsulated), not very specialized -remember free means they don’t have myelin ~found in most tissues of the body, but not in brain ~they transduce stuff into receptor potentials, which trigger afferent action potentials ~the cell body is in dorsal root ganglia, with one axon to periphery and one to spinal cord ~they have little to no myelination and thus have slow conductance ~the nerve endings are all pretty general, so they are categorized by their axons -some axons conduct faster than others, so there are fast and slow pain pathways ~two categories of pain perception: -first pain is sharp -second pain is more diffuse, longlasting ~stimulus for a nociceptor can be mechanical, thermal, or chemical -thermal is activated at dangerous temperatures, not the same as thermoreceptors -chemical stimulus could be external or internal secretions of body o ~they are sensitive to heat (above 45 C) and capsaicin ~pain pathways ~like other receptors, they have cell bodies in dorsal root ganglion with central axon going to spinal cord ~so 1 order is in dorsal root ganglion ~2 ndorder cells are in Rexed’s laminae in spinal cord nd ~axons of 2 order cells cross to contralateral side -decussation happens in spinal cord ~then the 2 ndorder axons ascend up to contralateral brainstem/thalamus this is the ST (spinothalamic) tract -ST tract is the main ascending pathway for pain and temperature info ~the target of the info is in the ventral posterior nucleus in thalamus, just like for mechanoceptors ~from the VP in the thalamus, they project to primary and secondary somatosensory cortex ~nociceptors have small receptive fields ~in the cortex they can discriminate location, intensity, quality of pain ~information for pathways for pain and temperature remain separate, segregated all the way to cortex Lecture 10 ~there are parallel auditory pathways for midbrain (colliculus) and hindbrain (brain stem) BUT for any ascending auditory info to get to cortex (forebrain), it needs to pass through thalamus specifically, needs to relay through medial geniculate nucleus (MGN) in thalamus ~goes from midbrain/hindbrain to thalamus to cortex ~most input to MGN is from inferior colliculus, some from lower brainstem ~MGN has neurons selective for different combinations of frequencies and time spacing of sounds ~ultimate target for afferent auditory info is cortex at temporal lobe ~in the cortex, there is primary area and belt (periphery) area ~primary auditory cortex = A1 ~A1 has a precise tonotopic map because it gets point-to-point input from ventral MGC ~A1 has a topographic map of cochlea ~belt areas have less precise map ~in the tonotopic map is a striped arrangement of binaural strips -one strip has neurons excited by both earscalled EE -other strip has neurons excited by one ear and inhibited by other earcalled EI -EE and EI strips alternate ~there are isofrequency bands in A1, neurons in each band respond specifically to their frequency range ~intensity of sound coded by higher firing rate of individual hair cells and more hair cells firing ~more amplitude wave = more hair cells activated ~somatic sensory system ~two subsystems -one is mechanosensory system—for mechanical stimuli—touch, vibration, pressure, tension -one for detecting painful stimuli and temperature ~there are receptors in cutaneous and subcutaneous layers of body surface -for external stimuli ~there are proprioceptors in muscles, joints, deep structures -for internal stimuli ~there are a bunch of parallel pathways ~main target is primary somatosensory cortex in parietal lobe ~primary somatosensory cortex then projects to association cortex and other areas of brain ~there’s like four senses -temperature -pain -body position -touch ~all together they can gauge place, pressure, sharpness, texture, duration of a stimulus ~within the class of receptors for cutaneous/subcutaneous, there’s specialized receptors: -mechanoreceptors -nociceptors -thermoceptors ~they can also be divided by morphology -free nerve endings—nociceptors and thermoceptors, their axons have non-encapsulated terminal branches, unmyelinated, highly branched into dermis and epidermis -encapsulated—mechanoreceptors, have branched axons in a capsule of connective tissue ~they do sensory transduction in the same basic way: -a stimulus on the skin deforms or changes the nerve ending -this affects ionic permeability of cell membrane -makes a depolarizing currentmakes a generator potential (aka receptor potential) -this triggers action potentials -and voila, energy of stimulus is transduced into electrical signal in the receptor ~strength of a stimulus = firing rate of action potentials ~another way of classifying receptors—by adaptability -phasic is rapidly adapting, have high initial response but it’s shortlived, fire at the onset of stimulus and then become quiescent, good for detecting changing stimuli -tonic is slowly adapting, have sustained response, will keep firing for as long as stimulus is there Lecture 13 ~the action potentials made by tactile stimuli are transmitted to spinal cord by afferent axons in peripheral nerves ~the cell bodies for these axons are in dorsal root (sensory) ganglia -remember dorsal root ganglia are associated with each spinal nerve -these cells are called first-order neurons ~ganglion cell has a peripheral axon and central axon -peripheral is towards PNS -central is towards CNS ~the ganglion cells have long peripheral axons that have the receptor specializations at the end -the ganglion cells ARE the receptor cells ~central axon is shorter, goes to dorsolateral part of spinal cord via dorsal roots, for each spinal segment ~mechanoreceptors are low-threshold, large and myelinated axonassociated with large ganglion cells ~nociceptors and thermoceptors are high-thresholdassociated with small ganglion cells ~there are distinct somatic sensory pathways in CNS for mechano vs. noci/thermos ~dorsal column-medial lemniscus pathway (DCML) carries info from mechano and proprioceptors ~spinothalamic pathway carries info from noci/thermo, for pain and temperature ~DCML pathway—for tactile and proprioception ~the first order axons bifurcate into ascending and descending branches ~the ascending branch goes up ipsilaterally through dorsal columns of spinal cord, up to medulla in brain st nd ~1 order axon terminates there in medullasynapses with 2 order neurons in dorsal column nuclei -dorsal column nuclei = gracile + cuneate nuclei ~axons in dorsal column are topographically organized -fibers for info from lower limbs are medial, in gracile tract -fibers for info from upper body are lateral, in cuneate tract ~dorsal column lesion (injury): -affects ability to detect direction and speed of stimuli -affects ability to detect spatial location of limbs ~so the 2 ndorder neurons in dorsal column nuclei send axons to somatic sensory part of thalamus ~on the way to thamalus, they decussate (cross over to become contralateral) ~after decussation the tract is called medial lemniscus ~medial lemniscus goes to ventrdl posterior lateral (VPL) nucleus in thalamus ~the cells in thalamus are 3 order in the DCML pathways ~aside on spinal anatomy ~each spinal nerve bifurcates into dorsal and ventral roots that go into spinal cord ~the area on the body innervated by a spinal nerve (the dorsal root) is a dermatome ~dermatomes overlap, so damaging one doesn’t mean you’ll lose all sensation in that region ~four segments of the spinal cord, and four segments of dermatomes: think of as a quadruped animal -cervical dermatomes—originate from C1-C8spans all regions above sternum, including back of head, BUT not face -thoracic dermatomes—originate from T1-T12spans sternum down to waist -lumbar dermatomes—originate from L1-L5spans front of legs and front belly area -sacral dermatomes—originate from S1-S5back of legs and genitals ~info from face is transmitted to CNS via trigeminal somatic sensory system ~these ascending pathways converge mainly on ventral posterior complex in thalamus ventral posterior complex has a lateral nucleus and a medial nucleus -VPL (ventral posterior lateral)—gets info from medial lemniscus ~axons from neurons in VPL of thalamus project to layer IV in somatosensory cortex ~somatosensory cortex is in/around post-central gyrus in parietal lobe, does the complex processing ~there are four sections of the somatosensory cortex, and each one has a somatotopic map ~the map is not continuous, not scaled to human body ~there is more cortex devoted to areas of the body with more sensory input -large amount of cortex for face, hands, lips ~from primary somatosensory cortex, info is projected to higher-order association cortex ~primary somatosensory cortex only gets simple segregated info ~integration of info happens in posterior parietal cortex Lecture 17 ~α motor neurons innervate extrafusal muscle fibers ~a single muscle has many muscle fibers ~thus a single axon branches a lot so that it can innervate each fiber ~motor unit—a single motor neuron and the muscle fibers it innervates ~small α motor neurons have small motor units, less force generated ~large α motor neurons have large motor units, more force generated ~three types of motor units: based on speed of contraction, max tension, how much they fatigue -slow (S) motor units—small unit and small neuron, contract slowly, have small force, but sustained -fast fatigable (FF) motor units—large unit and large neuron, contract quickly, generate large force, but fatigue easily, for brief muscle exertions -fast fatigue-resistant (FR) motor units—intermediate size unit and neuron, intermediate speed, 2x as fast as S, intermediate force generated, more resistant to fatigue than FF ~slow (S) motor units are tonic, have low threshold and sustained response ~fast fatigue (FF) motor units are phasic, have high threshold for activation ~depending on function, different types of muscles will have different amounts of S/FF/FR ~clinical implication ~damage to α motor neurons (LMN) -causes flaccid paralysis, muscle weakness (paresis), loss of reflexes (aflexia), loss of muscle tone -can also cause twitching in single fibers or motor units ~damage to upper motor neurons -causes rigid paralysis Lecture 16 ~upper motor neurons—descend onto circuits of LMN and modulate activity ~upper motor neuron cell bodies are in cortex or brainstem nuclei ~there are interneurons in the spinal cord/brainstem ~so upper motor neurons do not directly synapse with LMN ~the interneurons also get sensory input, important for reflexes ~four subsystems for the control of movement LMN and interneurons -any command for movement, whether voluntary or reflexive, goes through LMN -in brain stem and spinal cord upper motor neurons in cortex/brainstem -their descending axons synapse with interneurons, and (rarely) directly with LMN -important for voluntary and coordinated movement -separate pathways for brainstem and cortex -brainstem pathways important for navigation and posture -cortical pathways important for planning, initiating, directing voluntary movement cerebellum -on dorsal surface of pons -has efferent pathways modulating upper motor system -no direct contact with LMN -detects motor error—when the executed movement is different from intended -coordinates complex movement -might be involved in motor learning basal ganglia -in forebrain -suppress unwanted movement -prime upper motor neuron circuits for initiation of movement ~lower motor system ~each neuron innervates exactly one muscle ~but each muscle is innervated by several neurons ~all the neurons for a single muscle = its neuron pool ~the motor neurons are clustered in the spinal cord and run parallel to spinal cord -can span many spinal segments ~there is relationship between the location of the motor neuron pools and location of their muscles -this relationship is lengthwise and mediolateral in spinal cord -lengthwise—upwards on the spinal cord innervates upper body, and lower is lower body -mediolateral—medial part innervates axial muscles, lateral parts innervate distal muscles Lecture 18 ~spinal cord circuitry for reflexes ~simplest one—stretch reflex -sensory response to stretch in muscle -causes excitation of the LMN innervating that muscle ~stretch reflex: -sensory signal comes from muscle spindles (proprioception) -there are large Ia afferent fibers attached to spindle -the Ia fibers have rapid response because they’re large diameter fibers -Ia fiber is the peripheral branch of that cell, so when it’s activated, the central branch goes and makes monosynaptic excitatory synapse with spinal cord LMN for that muscle -the LMN are in ventral horn of spinal cord -this synapse al circuit interneurons and makes inhibitory synapses with antagonistic muscle’s LMN -this causes contraction of flexor (bicep) muscles and inhibits contraction in extensor -this reflex monitors muscle length, responds to passive stretching reciprocal inhibition—in stretch reflex -Ia fiber has a central fiber that synapses with α motor neurons in flexor to cause contraction -it also makes another synapse with interneuron that inhibits contraction in extensor muscle ~stretch reflex maintains steady level of muscle tone—normal stretching of muscles at rest ~another spinal cord reflex—involves Golgi tendon organ -Golgi tendon organ is encapsulated, afferent nerve endings -Golgi tendon organs connect muscle to tendon -each GTO is innervated by a single Ib afferent axon -active contraction of muscle causes tension in collagen fibers of GTO -the Ib axons synapse with interneurons in spinal cord -those interneurons are inhibitory, they synapse with the LMN that innervate that same muscle -interneuron inhibits α motor neurons and causes the muscle to relax -negative feedback loop for muscle strain, monitors muscle force to return to homeostasis ~GTO reflex opposes action of stretch reflex ~flexion reflex—reflex to remove body away from something hot or other harmful environment -polysynaptic connections -the nociceptor picks up on a dangerous stimulus -afferent fiber makes 4 synapses simultaneously—two on one limb and two on contralateral limb -called crossed extension reflex, maintains posture during withdrawal of limb -(1) excitation of ipsilateral flexor -(2) reciprocal inhibition of ipsilateral extensor -(3) inhibition of contralateral flexor -(4) excitation of contralateral extensor Lecture 15 ~hyperalgesia—after you get a painful stimulus that causes actual tissue damage, the pain-sensitivity of the damaged tissue is amplified -happens because nociceptors are made more sensitive because of stuff released by damaged tissue, like prostaglandins, histamines, etc. ~descending pathways from spinal cord can modulate transmission of pain info ~gate theory of pain—non painful stimulus (i.e. mechanical stimulus) near the site of prevents the flow of pain info and relieves pain -this is why you rub your toe when you stub it ~there are regions of the brain that can suppress pain -PAG (periaqueductal gray matter) projects to raphe (with serotonin NT), raphe sends axons to spinal cord -5-HT is inhibitory, blocks synapses ~endorphins—have opioid properties, can bind to opioid receptors in brain -opioid receptors found throughout body, but especially in brain -in brain, they are dense in areas that process and modulate nociceptive info (PA, raphe, spinal cord) ~thermoceptors o ~so the brain needs to be kept at a specific temperature—37 C -above or below this temperature is dangerous ~skin has receptors to pick up on temperature change of as little as 0.01 C o ~two types of thermoceptors—warm and cold o o o -warm starts firing at 30 C up to 45 C (after 45 C is painful) -cold fires below 35 C to 10 Co ~receptors are adaptive, pick up on temperature changes ~follows same pathway as nociceptors (ST pathway) ~movement—lower motor system ~lower motor neurons initiate all movement in skeletal muscle ~lower motor neurons are in spinal cord and brainstem ~lower motor neurons are controlled directly by local circuits (in brainstem and spinal cord) and controlled indirectly by upper motor neurons that regulate those circuits ~striated muscle contraction initiated by lower motor neurons ~cell bodies of lower neurons are in ventral horn of spinal cord (gray matter) and motor nuclei in cranial nerves (brainstem) ~lower motor neurons are also called α motor neurons ~LMN axons go straight to skeletal muscle -from spinal cord they go via ventral roots and spinal peripheral nerves -from brainstem they go via cranial nerves ~LMN are the final common pathway for motor behavior Lecture 19 ~central pattern generators—spinal cord circuits for rhythmic things like walking ~brain initiates movement, but individual movements are controlled in spinal cord ~oscillatory circuit that causes alternating flexion and extension ~upper motor neurons—their axons descend to interneurons which then affect LMN ~for voluntary and goal-directed behavior ~there are different centers of upper motor neurons in brainstem/cortex ~four main areas in brainstem -vestibular nucleus -reticular formation -red nucleus -superior colliculus ~vestibular nucleus and reticular formation (both in brainstem) affect body position and posture ~motor and premotor areas in frontal cortex are for planning precise movement ~upper motor neurons in cortex can also descend to upper motor neurons in brainstem ~finals targets for upper motor neurons are interneurons for LMN ~somatotopic organization of LMN in ventral horn of spinal cord -mediolateral axis is for axial-appendicular muscles ~the interneurons for spinal cord LMN are in intermediate zone between ventral and dorsal horns ~the more medial interneurons synapse with medial LMN, involved more in posture ~the more lateral interneurons synapse with lateral LMN ~medial and lateral interneurons also have different pathways and functions -medial interneurons have axons projecting to many segments of spinal cord, or even entire cord -medial interneurons also have some axons that stay ipsilateral and some that cross commissure (decussate) to innervate contralateral parts of the spinal cord, still medial though -lateral interneurons have short axons, cannot project to many spinal segments, restricted for finer control of distal muscles, like fingers -lateral interneurons have all axons innervate ipsilateral part of spinal cord ~projections from upper motor neurons onto medial interneurons come from: -vestibular nuclei and reticular formation in brainstemmakes sense because they control posture -superior colliculus in brainstemprojects to axial cervical part of spinal cord, controls neck muscles ~projections from upper motor neurons onto lateral interneurons come from: -motor cortexmakes sense because fine movement -red nucleusrubrospinal tract projects to lateral cervical part of spinal cord, controls arms -the red nucleus is actually huge, but most of it is involved in other circuits Lecture 23 ~parasympathetic division ~the parasympathetic ganglia are very close to the target organs, or even in the target organ -unlike sympathetic chain ganglia which are right next to the spinal cord ~the cells in parasympathetic ganglia have very little dendritic branching, innervated by only one or a few preganglionic axons ~the preganglionic cells are in brain stem and sacral segments of spinal cord brainstem nuclei include… -there is the Edinger-Westfall nucleus in the midbrain -(innervates ciliary ganglia to control pupil size) -superior and inferior salivary nuclei in pons/medulla -(innervate salivary and tear glands) -nucleus ambiguus in medulla -dorsal motor nucleus of vagus nerve in medulla -(innervates ganglia in thorax, abdomen, heart, lungs, gut) in the sacral part of spinal cord -specifically in lateral gray matter of spinal cord -these axons travel through splanchnic nerves ~parasympathetic functions are basically the opposite of sympathetic -rest and digest -doing metabolic processes, expending energy for normal functions -pupils constrict -heart rate slows -peristaltic motion in gut ~also because sympathetic system is inactive, blood vessels dilate and there is less outflow of catecholamines from adrenal medulla -note that there are some organs controlled ONLY by sympathetic system sweat glands, adrenal medulla, piloerector (skin hair) muscles, arterial blood vessels ~SKIPPING ENTERIC SYSTEM ~going straight from uzwiak’s notes now ~hypothalamus—in the diencephalon of forebrain ~inferior to thalamus rd ~is part of the wall of the 3 ventricle ~components of hypothalamus—5 things! -hypothalamic nuclei -optic chiasm -tuber cinereum -this is the floor of the 3 ventricle -median eminence is the vascular lower part of the tuber cinereum -infundibulum—tissue connecting hypothalamus to pituitary gland -mammillary bodies Lecture 22 ~visceral motor system—aka autonomic nervous system ~for involuntary functions ~control comes from hypothalamusmodulates circuits in reticular formation (brain stem) and spinal cord, which then affect neurons in autonomic ganglia ~controls smooth muscle, cardiac muscle, glands ~includes sympathetic and parasympathetic and enteric system (for gut) ~sympathetic is usually for mobilizing to deal with a challenge ~parasympathetic is for restoring energy, at rest ~autonomic ganglia have the cell bodies of primary visceral motor neurons ~primary visceral motor neurons are analogous to the lower motor neurons of motor system ~for sympathetic division, autonomic ganglia are close to spinal cord ~for parasympathetic division, autonomic ganglia are close to target organs ~visceral motor axons are highly branched, have varicosities (bulges along axon branch) -form synapses at varicosities -the NT released usually diffuses across a distance to reach target organ ~going over sympathetic nervous system first ~sympathetic nervous system—preparing for flight-or-flight ~for promoting survival in dangerous situations ~in high levels of sympathetic activity -pupils dilate and eyelids retract to allow more light to retina to see better -blood vessels constrict to redirect more blood to muscles -breathing and heart rate increase -bronchi dilate to increase oxygenation -vegetative functions are deactivated, such as digestion, sex, menstruation -adrenal medulla is stimulated to release norepinephrine and epinephrine -pancreas is stimulated to release glucagon and insulin ~the CNS neurons for sympathetic division are in spinal cord -in the lateral horn gray matter in spinal cord (aka intermediolateral column) -spans thoracic and lumbar segments of spine -these are the preganglionic neurons -the ones for head and thorax are in thoracic segments -the ones for abdominal and pelvic are in lower thoracic/upper lumbar -these preganglionic neurons are analogous to somatic motor interneurons ~the preganglionic neurons have short axons ~the sympathetic ganglions are arranged in a chain right next to the spinal cord -thus called paravertebral aka sympathetic chain ganglia -the neurons in the ganglia are analogous to lower motor neurons -the axons from the ganglia (postganglionic axons) directly innervate the target organs ~there’s another set of ganglia—prevertebral ganglia -the preganglionic axons from the spinal cord travel in the splanchnic nerves -the ganglions that they synapse with are called prevertebral ganglia -prevertebral ganglia found in cardiac plexus, celiac ganglion, mesenteric ganglia, pelvic plexus -the organs that these ganglia target include heart, lungs, gut, kidneys, pancreas, liver, etc. -some of these organs are also targeted by sympathetic chain ganglia ~preganglionic nerves going in splanchnic nerve ALSO innervate the adrenal medulla -adrenal medulla is like a modified ganglion, for the endocrine function of releasing catecholamines in response to stress ~there’s paravertebral chain ganglia and prevertebral ganglia ~cells in the sympathetic ganglia tend to have a lot of dendritic branching, and thus are innervated by multiple different preganglionic axons ~sympathetic system is running all the time, but becomes extra active in times of stress/agonism Lecture 21 ~indirect pathways from primary motor cortex to spinal cord ~go from motor cortex to red nucleus or reticular formation axons going from cortex to red nucleus -axons originate in cortex areas that project to lateral spinal cord -for movement of limbs axons going from cortex to reticular formation -axons originate in cortex areas that project to medial spinal cord -for movement of axial muscles ~premotor area = premotor cortex + supplemental motor cortex (dorsal) ~premotor cortex ~rostral to primary motor cortex ~premotor cortex also has upper motor neurons ~has reciprocal connections with primary motor cortex and direct axons through corticobulbar/corticospinal pathways ~involved in intention of movement and movement selection ~stimulation elicits movement but different from in primary motor cortex, this movement needs greater stimulation than primary motor cortex ~results in complex movements, engaging both sides of the body ~mental rehearsal involves only supplemental motor area ~basically ~primary motor cortex is for execution of movement ~premotor area is for planning and programming movement ~upper motor neuron syndrome—damage to any pathways of upper motor neurons ~common because so much of cortex has upper motor neurons and they have long axons ~damage to motor cortex or descending axons in internal capsule: -flaccid paralysis in contralateral muscles of body/face depending on topography -in limbs—if you elevate limb and drop it, it just drops passively, no reflex activity -but control of trunk muscles is preserved -there is initially hypotonia, called spinal shock—decreased activity in spinal circuits because they no longer have the input from motor cortex after some days, hypotonia somehow goes away and circuits become more active -Babinski’s sign, the reflex from infancy returns—in adults, stroking the foot normally causes flexion of toes (curling inwards) but in babies it causes extension and fanning, and after the period of hypotonia, the fanning returns -spasticity—increased muscle tone, hyperactive stretch reflexes, clonus in response to muscle stretch, and in severe cases there is rigidity of extensors in leg and flexors in arm -loss of ability to do fine movements -hypoflexia of superficial reflexes—less rigor in superficial reflexes like corneal and abdominal Lecture 20 ~upper motor neurons vestibular nuclei and reticular formation together control balance and posture ~vestibular nuclei receive axons from 8 cranial nerve -get info on position and acceleration of head ~the upper motor neurons in vestibular nuclei descend onto medial parts of spinal cord -some are also a little more lateral, to control proximal muscles for limbs so there are two separate tracts—medial and lateral vestibulospinal tracts ~reticular formation is network of circuits going through the core of the brainstem -complex, involved in a lot of functions including heart and respiratory control, sensory motor reflexes, sleep and arousal, etc. ~vestibular nucleus responds to signals from inner ear ~RF nuclei respond to other nuclei in cortex/brainstem ~motor cortex has direct and indirect pathways to spinal cord ~direct pathway is for the intended movement ~indirect pathway goes to RF/vestibular apparatus to stabilize posture during the desired movement ~upper motor neurons in cortex ~in frontal lobe cortex ~for planning and initiation of sequences of voluntary movement ~get input from basal ganglia and cerebellum, through relay from ventrolateral thalamus ~get some somatosensory input from parietal lobe ~primary motor cortex—in precentral gyrus ~premotor area is next to primary motor cortex ~primary motor cortex ~pyramidal cells in layer V of primary motor cortex are the upper motor neurons ~the axons descend to brainstem and spinal cord through corticobulbar and corticospinal tracts ~these tracts pass through internal capsule of forebrain, enter cerebral peduncle in midbrain ~then they go through base of pons, get scattered, then coalesce on ventral surface of medulla -note that along the way, the branches of the corticobulbar tract branch off where they have to—at cranial nerves, reticular formation, and red nucleus ~at this point they’re called pyramidal tracts, one for each lateral side -pyramidal tract actually has other fibers not involved with motor function -but who cares ~at the end of the medulla, when they’re about to enter spinal cord, most axons in the pyramidal tract decussate to enter lateral column of spinal cord -3/4 of the pyramidal tract fibers -they become lateral corticospinal tract -these axons originated in the motor cortex areas for limbs -lateral tract terminates in lateral spinal cord—(lateral part of ventral horn and intermediate zone) -direct pathway from primary motor cortex to spinal cord ~some axons don’t decussate, continue straight on into spinal cord -1/4 of the pyramidal tract fibers -they become the ventral corticospinal tract -these axons originate from areas in motor cortex for posture (neck, axial muscles, shoulders) -ventral tract terminates in medial spinal cord (medial part of ventral horn and intermediate zone) this corresponds to topographical organization in motor cortex ~lateral corticospinal tract is direct pathway from primary motor cortex to spinal cord Lecture 24 ~connection of hypothalamus with pituitary gland ~pituitary is below hypothalamus ~connected by the infundibulum, which is stalk-like -connects brain to endocrine system ~two lobes in pituitary -anterior lobe (adenohypophysis) is made of glandular tissue -posterior lobe (post. lobe + infundibulum = neurohypophysis) ~posterior pituitary ~is an outgrowth of the brain ~stays connected to the hypothalamus through hypothalamic-hypophyseal tract -aka supraopticoparaventriculohypophyseal tract -axons that form tract come from neurons in supraoptic nuclei (SON) & paraventricular nuclei (PVN) -the axon terminates in posterior pituitary ~neurons in SON and PVN release hormones upon electrical stimulation -hormone is secreted into interstitial space, picked up by capillary plexus in posterior pituitary ~oxytocin is mainly made by SON ~antidiuretic hormone is mainly made by PVN ~anterior pituitary ~anterior lobe is not an outgrowth of brain, comes from epithelial tissue ~not directly connected to hypothalamus there is a vascular connection between them -called the hypophyseal portal system -portal system connects median eminence to secretory cells in anterior pituitary ~hormones released by hypothalamus are carried to anterior pituitary via portal system -they regulate the secretory cells in the anterior pituitary Lecture 25 ~hypothalamic nuclei ~there’s a magnocellular and parvocellular system ~magnocellular neurosecretory system -includes SON and PVN in hypothalamus -SON makes vasopressin (antidiuretic hormone) -PVN makes oxytocin ~parvocellular neurosecretory system -in ventromedial nucleus of hypothalamus -axons of this nucleus converge towards pituitar
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