Study Guide for Neuroscience Exam 1
Study Guide for Neuroscience Exam 1 PGY 451LEC
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This 16 page Study Guide was uploaded by Ndidiamaka Okorozo on Saturday September 19, 2015. The Study Guide belongs to PGY 451LEC at University at Buffalo taught by Baizer, J S in Fall 2015. Since its upload, it has received 404 views. For similar materials see Human Physiology I in Physiology at University at Buffalo.
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Date Created: 09/19/15
NERVOUS SYSTEM Neuron a cell building block of the nervous system 0 Soma neuron cell body 0 Nucleus 0 Processes fibers emerging from the cell body gt Dendrites gt Axons could be myelinated or not 0 Tracts group of axons connecting different parts of the brain gt When tracts cross from one side of the brain to another they are said decussate gt An axon from a presynaptic neuron the neuron that is transmitting a signal projects to the postsynaptic neuron Nuclei group of neurons Gray matter cells appear gray in dissection White matter axons appear white in dissection 0 Neurons differ in 0 Size amp shape of soma 0 Destination of axon O Myelination of axon 0 Numbers and branching patterns of its dendrites 0 Communication is done electrically within each cell action potential and chemically between cells transmitters gt Synapse an area of communication between two neurons Process of Communication 0 Axon from the presynaptic neuron travel to the postsynaptic neuron 0 Axon terminals create synapses on the synaptic cleft between the two neurons 0 Neurotransmitters are released and they bind on receptors on the post synaptic neuron Types of communication gt Axodendritic between an axon of a neuron and the dendrite of the other gt Axosomatic between an axon of a neuron and the soma of the other gt Axoaxonic between two axons of two neurons Ventral stomach side Dorsal refers to back side Cerebral hemispheres cerebral cortex amp subcortical structures Cortex has four lobes frontal parietal occipital and temporal 0 Different cortical region deals with different function motor sensory language etc Sulci infoldings on brain Gyri surface folds on brains Note that the patterns of sulci and gyri is similar but different in different parts of the brain Brodmann an anatomist that numbered different areas of the brain based on their functions gt Hippocampus memory gt Basal ganglia deals With movement cognition gt Diencephalon Thalamus amp Hypothalamus gt Midbrain 5 gt Cerebellum 4 gt Pons 3 gt Medulla 2 543 and 2 are in the brain stem Cranial nerves deals With gt all the sensory information that emerge from the head hearing vision olfaction taste and touch gt motor signals to muscles of the head 12 pairs olfactory optic oculomotor trochlear trigeminal abducens facial auditoryvestibular glossopharyngeal vagus spinal accessory hypoglossal Spinal cord gt Motor control of muscles gt Sensory input from the body encased in bone protection Has four divisions gt Cervical C1 C7 gt Thoracic T1 T12 gt Lumbar L1 L5 gt Sacral S1 S6 Afferent innervation by sensory signals to the brain Efferent innervation by motor signals from the brain to the body Sensory dorsal Motor ventral VISION SYSTEM Sclera white covering all over the eyes Cornea transparent covering only in the anterior part of the eye Choroid Layer innermost from sclera contains the blood vessels Lens elaborated in the anterior part of the choroid layer behind the iris Focuses light on the retina and changes its shape to adjust light so it can be focused on retina Loss of exibility of lens lost with age difficulty in focusing on close objects gt Around age 45 called presbyopia need for reading glasses Cataracts occurs with age Lens are opaque and cloudy instead of transparent Occurs around 60 age gt Corrected by surgical removal and replacing opaque lens with arti cial ones lntraocular lens lris contracts and relaxes to control amount of light entering the eye lris controls light that enters the lens by contraction and relaxation while lens focuses the light on the retina Retina Visual neurons and Optic nerves are axons leaving the retina Conjuctiva membrane covering the sclera lf infected or becomes in amed it is referred to as conjunctivitis or pink eye because eye looks pink Conjunctivitis Blood vessels are in amed gt Common in kids and very infectious among them Glaucoma Occurs when there is an increased intraocular pressure The interior eyeball is divided into two chambers which are uid lled to maintain intraocular pressure and shape Anterior chamber is lled with aqueous humor Posterior chamber is lled with vitreous humor When canal of Schlemm which is in the anterior chamber becomes plugged there is increased pressure because aqueous humor can t drain into the venous blood in the blood vessels resulting in glaucoma Can result in optic nerve damage and loss of vison Treated surgically Visual Field Visual Space area that our eyes see Visual Field is starting from the xation point center 40 up 60 down 90 right and 90 left Binocular visual eld can be seen by both eyes In humans it s out to about 60 Monocular visual eld seen by one eye In humans it s the outermost 30 60 90 Left monocular crescent site seen by only left eye in humans Right monocular crescent site seen by only right eye in humans Organisms with lateral eyes tend to have monocular visual elds since eye are towards the sides and see different things Example frog rabbit etc Organisms with eyes towards the frontal part of the face would have a more binocular vison since the visual elds of both eye have a higher tendency to bisect Maps of the CNS Retina has 2 halves nasal retina and temporal retina lmages are UPSIDE DOWN and BACKWARDS Explanation of the Arrow Image Remember that both eyes view out to about 60 degrees binocular visual eld Objects out to about 60 90 degrees to the left are only seen by the left eye and out to 60 90 degrees to the right are only seen by the right eye Each eye sees both halves of the visual eld but each part of the brain gets information from ONLY ONE half of the eye and that is the contralateralopposite side Nasal retina Part of retina closer to nose info from the visual field closer to the temple Temporal retina Part closer to the temple info from the visual eld closer to the nasal Because images are upside down and backwards Since image is upside down and backwards whatever is seen from the left falls on the nasal retina of the left eye and what is seen from the right falls on the nasal retina of the right eye Therefore even though nasal retina is closer to the nose it carries information about the visual eld closer to the temple in both eyes And even though temporal retina is closer to the temple it carries information about visual eld closer to the nasal gt The right visual eld that falls on the temporal for the left eye and falls on the nasal for the right eye Pathway Axons of the ganglion cells in the retina form the optic nerves while leaving the eye to travel to the brain As they travel they get to the optic chiasm junction where they join Right at that junction axons from the nasal retina of both eyes cross the midline while temporal axons of the retina of both eyes do not cross remain ipsilateral So temporal axons of the left eye which is carrying information about the visual eld closer to the nose joins with the nasal axon which is carrying information from the visual eld closer to the temple of the right eye Now all axons travelling in same path down to the left Lateral Geniculate nuclei visual cortex have information of the right visual eld And all travelling to the right lateral geniculate nuclei have information about the left visual eld These rearranged bers from the optic tracts Therefore at the level of the brain each part of the brain gets information about the opposite contralateral visual eld Left Lateral geniculate nuclei of the visual cortex Right visual eld Right Lateral geniculate nuclei of the visual cortex Left visual eld Visual Cortex Primary Visual cortex Area 17 according to Brodmann s number Area 18 additional visual cortex for more processing Re na The retina has 5 different interneurons Photoreceptors in the eye comes in contact with the light entering the retina They mediate phototransduction which is the conversion of light energy to energy used by the nervous system 0 They convert light energy speci cally to electrical signals called receptor potentials Process As light falls on photoreceptors it causes a conformational change in the photopigment of the photoreceptor and a series of biochemical events lead to a change in membrane potential and a change in transmitter release 0 There are two types Rods relatively require low levels of light to be activated gt low acuityclarity gt no color vision gt used at night scotopic Cones gt High acuityclarity gt Color vision 400 700 nm wavelength of light 3 types of cones for different wavelengths Short Blue Middle Green Long Red gt day photopic Color Blindness pigment missing abnormal Xlinked common in men Distribution of rod and cones The fovea is the central 4 degrees on the retina It has a relatively high number of cones with no rods As you move away from the fovea the number of cones decreases As you move away from the fovea the amount of rod increases out to about 15 degrees and then decreases dramatically Rods are more in the periphery gt To view an object better at night you have to look from the sides because rods are periphery and you want the image to fall on the side The blind spot is the optic disc where the optic nerve leaves eye Light entering the retina hyperpolarizes the rods and cones causing a decrease in the release of the inhibitory neurotransmitter on bipolar cells So as inhibitory neurotransmitter is reduced bipolar cells become depolarized causing an increase in another neurotransmitter that in turn depolarizes the ganglion cells Because ganglion cells can generate action potentials they do and their axons form optic nerves that leave the eye Transmitter is release as a function of membrane potential hyperpolarization inhibits release of transmitter and depolarization releases more neurotransmitter Receptive Field the part of a visual eld that a neuron receives stimulus from 2 Types of ganglion receptive eld gt On center off surround responds better to a small spot of light illumination of the retina gt Off center on surround responds better to dark spot on light background Some are orientation sensitive respond better to square stimulus inside a rectangular shaped receptive eld Some are directionally sensitive respond better to stimulus from above than beneath AUDTION SYSTEM Ototoxic damaging to receptive cells Otoscope modi ed ashlight Frequency pitch 2020000 cps gt We are sensitive to all frequencies but not equally gt At 5000Hz sound need to be louder for us to hear it 0 With age frequency decrease because of noise induced damage on receptor hair cells Amplitude loudness At 130dB is painful sound Tinnitus perception of quotphantom soundquot ringing or buzzing noise Common in males and military veteran lts frequency increases with age Outer Ear also known as pinna gt External auditory canal air lled passage Tympanic membrane ear drum is the boundary between outer and middle ear Middle ear air lled gt 3 bones fused together malleus incus and stapes These bones help with transmission of sound Mechanically prevent sound loss as the medium changes from air to uid gt 2 muscles control bones and provide protection to loud sounds less sensitivity to your own speech stapedius and tensor tympani When middle ear pressure is not equal to outside pressure like in airplanes Eustachian tube has to be opened to adjust pressure by yawning 0 Low frequency sounds sometimes get in the bones in skull which is the reason your voice sounds different when it s recorded Otitis Media uid ends up in middle ear and bacteria grows happens a lot in children Cn be treated by surgical insertion of tubes to drain out uids if antibiotics don t work Eustachian tube connection of the middle ear and back of the throat lnner Ear basilar membrane where hair receptor cells sit Low frequency sounds have their peak at the apex farthest from the middle ear while high frequency sounds have their peak at the base gt Cochlear which has three chambers scala vestibule scala tympani scala media Transduction Tympanic membrane ear drum vibrates as sounds enters the ear Bones in the middle ear mechanically transmit the sounds and the stapes which is closer to the inner ear pushes on the oval window This creates pressure on the cochlea causing the basilar membrane to vibrate up and down as the wave sounds travel up Hair cells on the membrane bend leading to ion concentration change that generates a signal to the auditory nerve 8th cranial nerve so you hear the sound 0 Hair cells do not generate ion action potentials The ion concentration change causes neurotransmitter release graded with membrane potential They synapse directly on the auditory nerve Hyperpolarization more transmitter release and depolarization causes transmitter release The sound comes back down and the round window opens to dissipate the energy Pathway Multiple brainstem nuclei and a lot of input is distributed bilaterally Information from ear travels through the dorsal and ventral cochlear nuclei in the medulla of the brain stem This is where the information cross the midline and travel to the inferior colliculus in the mid brain where they are sent to the medial geniculate nucleus to be relayed to the primary auditory cortex in the temporal lobe Sound analysis of frequency lts source is identi ed different for different sounds Brief sounds by time of arrival Ongoing sound intensity difference high frequency phase different and low frequency SOMATIC SENSATION There are two types and each has a separate neural system from periphery to the cortex gt Cutaneous skin modalities Touch Pain Warm and Cool gt Deep modalities Pressure Pain Position Any point on the skin gives rise to only one cutaneous sensation Touch Pain Warm or Cool Shingles Caused by varicella virus from chicken pox lies dormant in Dorsal Root ganglion DRG but activated by factors like aging cancer or certain drugs Causes painful blisters Treated with antiviral drugs Functional primary afferent bers There are four of them Nociceptors pain mechanoreceptor touch and thermoreceptors warm and cool Innervation amp Transduction No receptor cells rst order ber axons innervate the body These cell bodies are in the Dorsal Root Ganglion There different bers for each modality the proteinschannels on each ending of the primary afferent bers are different The different bers are intermingled in skin giving the mosaic model of skin gt Sensation at each point is determined by the type of ber innervating that point Anatomical classi cation of Fibers 1 AB beta fibers 612um diameter 30 70msec conduction velocity Myelinated Mechanoreceptors For Touch for cutaneous Pain and Pressure for deep Have encapsulated endings Ruf ni ending Markel disc Pacinian corpuscles and Kraus end bulbs 2 A6 Delta bers 15um diameter 1230msec Myelinated Nociceptors Pain Thermoreceptors warm cool Have free nerve endings and not encapsulated 3 C bers 0412um 052 msec Conduction velocity Nociceptors thermoreceptors Free nerve endings Innervation Density nerve endings per unit of skin Can be measure in two ways 0 Localization the ability to identify area of stimulus 2 point threshold the distance between two stimuli before they are recognized as one Receptive eld region of the skin where stimulus affects an axon High innervation density l small receptive eld better 2 point threshold andlocaHza on Low innervation density large receptive eld worse 2 point discrimination andloca on Pathway There are two different anatomical systems for both skin and deep tissue 1 Dorsal Column Medial Lemniscal System touch pressure position They receive input from AB fibers skin and deep tissue Cell body in DRG bifurcates and one end travels to the spinal cord and through the dorsal root all the way to the dorsal column at the medulla where the rst synapse occurs Cells here project their axons past the mid line in a ber bundle caed Medial Lemniscus which synapse on the thalamus and it relays the info to the somatosensory cortex in the Parietal Lobe AREAS 31 amp2 o For level of spinal cord psiatera half of body Level of thalamus and cortex contralateral half Axons from the dorsal column nuclei 2 Anterolateral System pain temperature crude touch not as effective as the first Receive input from A6 and C fibers Expanded representation in cortex smaller receptive eld high innervation density Smaller representation in cortex larger receptive eld low innervation dens y Receptive elds as shown in cortex are larger than that of primary afferent bers due to convergence in different levels of the system Plasticity ability of somatosensory cortex representation to change Can occur with certain events like amputation of nger or greater use of a part PAIN Pain is relatively different because it involves an emotional component it s a strong determinant of factor of behavior and the link between stimulus and response varies Strong stimulus can produce no pain because of excitement No stimulus can produce pain in cases of chronic pain syndrome 0 Example is Phantom Limb Pain where there is alteration of processing of the pain signals by emotional or cognitive state Transduction Stimulus of pain extreme temperatures result in tissue damage which causes release of chemical mediators that act on the endings of nociceptors pain bers The transmitter release by the bers is called Substance P A branch with substance P divides into 3 one sent to the blood vessel to increase blood ow in lesion site second goes to mast cell which activates the release of histamine and third goes to the lesion site where serotonin prostaglandin and bradykinin are present Histamine produced from mast cell goes to the lesion site too and helps with better activation of Substance P Pain fibers A6 and C fibers are chemoreceptors Chemical mediators serotonin bradykinin prostaglandin and histamine indirectly Hyperalgesia increases sensitivity to pain dues to tissue damage Ex sunburn Pathway Tracts of Lissauer ensures that information is distributed up and down the spinal cord Pain bers synapse on cells in dorsal horn of the spinal cord These cells send their axons across the midline to ascend in anterolateral tracts At the level of spinal cord Information about pain and temperature is of the contralateral side Anterolateral pathway leads to the reticular formation medulla l reticular formation of pons l thalamus mid brain l cingulate cortex and somatosensory cortex in Parietal Lobe Referred Pain tissue damage on internal organ is thought to be from surface of skin overlying that organ There is a convergence of pain signals coming from the skin and intestines to the second order dorsal neuron Endogenous Pain control mechanism of how brain modi es pain input 1 Transmitter and receptors Opiates and receptors are at key sites along pain pathways gt Spinal cord dorsal horn gt Brainstem reticular formation gt Frontal lobes Opiate receptors 6delta umu K kappa Endogenous Opioid Peptide Transmitter Receptor EnkephaHns u6 Dynorphins K Betaendorphin u 6 Feedback system with pain as input releases these opiates 2 Descending control of pain 2 brainstem nuclei a Nucleus raphe Magnus Serotonin Nucleus in NRM send their axons back to the dorsal horn l activate dorsal horn interneurons by releasing inhibitory enkephalins l synapse on incoming pain bers to decrease their synapse strength gt This is done at the level of spinal cord at rst synapse b Second pathway locus ceruleus norepinephrine From the brain to the dorsal hon almost same pathway as the above MOTOR SYSTEM Motor control not intuitive Motor system motor hierarchy l motor cortex at top and muscles at the bottom However all structures work together in movement Function Coordination Posture o In coordination there are changes in joint angle and muscle length Flexion l Decrease in joint angle l Contractionshortening of exor l Stretchinglengthening of extensor Extension Increase in joint angle l Contractionshortening of extensor l Stretching lengthening of exor Agonist muscle doing the movement Antagonist muscle with opposite action at the joint Synergist all muscle doing the same action at a joint Posture resisting forces of gravity l carried out by extensors antigravity muscles gt Antagonist exors 0 Position xation elimination of unwanted movement at a joint in order to achieve desired movement Muscles vary in properties 1 Force amount generated by each muscle 2 Resistance to fatigues 3 Speed of contraction how fast they respond to stimuli 4 Fineness of control important for nger and eyeball movements Force resistance and speed result from the muscle s structure while neness of control is as a result of structure and pattern of innervation Muscle Fiber Types 1 Fast Twitch a FF fast fatigable large force fast contraction time fatigue readily Biochemical differences white muscle b FR fast resistant Large force fast contraction time more resistant to fatigue Biochemical differences white muscle 2 Slow Twitch a S slow Least force slowest contraction time most resistant to fatigue Red muscle Cannot increase the number of muscle bers or change muscle ber with training xed composition Each muscle has different of ber types But composition of a particular muscle may vary among individuals may correlate with athletic ability Motor innervation 0 Alpha on motor neuron lower motor neuron axons have large diameter myelinated Ad fibers 12 20 um 70 120ms Each innervate muscle bers 21000 s depends on size Muscle ber receives innervation from one and only one motoneuron Range of size of motoneurons 0 Larger MN s D larger Cell body larger diameter l Axons with more branches l higher number of muscle bers 0 Larger MN s larger Cell body larger diameter l Axons with more branches l higher number of muscle bers ALS MN s release chemical called trophic factors The absence of these trophic factors which are essentials for the health of muscles leads to ALS Because the death of motoneuron leads to muscle deathatrophy Motoneuron Pool MN s innervation particular muscle are divided in segments which are called pools Composed of different range of sizes The Motor Unit A single motoneuron and all its muscle bers innervated by it Its size depends on the size of the motoneurons Large MN s Larger Muscle Fibers large motor unit Same type of muscle ber in a motor unit 0 Average Motor unit size differs among muscles gt Fine control Smaller gt Force speed Larger Size Principle Motor units are recruited in order of increasing size smallest rst and largest last Drop out happens in reverse order S bers in use more of the time Feedback Info from muscle 1 Muscle length receptor is the muscle spindle Muscle Spindle is a connective tissue sheath containing 212 specialized muscle bers called intrafusal bers Ordinary muscle bers are extrafusal bers a Maintained length b Rate of change of length 2 Muscle force receptor is the Golgi Tendon Organ GTO gt Receptors for gamma attached in series with muscle sensory innervation for lb ber 12 20pm diameter and 70120msec conduction velocity lb bers crunch on axons of gamma motor neurons depolarize them creating action potentials lntrafusal bers have contractile poles and noncontractile centers a Nuclear bag dynamic b Nuclear chain static Types of sensory bers Group IA 1220um 70120 msec innervate all intrafusal bers has primaryannulospiral endings Carry info about maintained muscle length static and rate of change of muscle length Group II 512um 3070 msec Innervate only nuclear chain bers has secondary ower spray endings Carry info about maintained muscle length static Transduction in the spindle Muscle Stretched l Endings become polarized l action potentials generated Motor innervation of spindle Gamma MN s quotfusimotorquot neurons 5 12pm diameter 3070msec conduction velocity Cell bodies are in ventral horn of spinal cord Ensure steady action potential Problem Muscle shortens l Spindle goes slack No stretch on spindles No sensory input Solution with gamma MN s innervating the contractile poles of spindle it facilitates the contraction of spindle while muscle shortens REFLEXES amp DESCENDING CONTROL OF REFLEXES Re ex unlearned motor response to a sensory stimulus gt Components muscles motor neurons Sensory input from body spinal interneurons Abnormal Re ex re ection of dysfunction of some component of the motor system gt Circuit for a re ex could be present at the level of spinal cordbrain stem but descending pathway modulates the re ex strength l stronger weaker or totally suppressed Spinal Transection cause loss of sensation and voluntary movement below the cut but spinal re exes remain Muscle Tone resistance to passive stretch an involuntary movement being imposed from the outside Re exes 1 Stretch Reflex IA fibers afferent d MN s efferent Stretch of muscle stimulus l activated IA bers l excitatory synapse on d MN s l same muscle contracts response 0 Underlies Muscle Tone by producing resistance 0 Short latency re ex occurs fast Monosynaptic re ex only one in a circuit Coordination built into stretch re ex Agonist contracts while antagonist relaxes o Reciprocal Innervation IA ber branch synapses on inhibitory interneuron l interneuron inhibits MN s innervating antagonist muscle 2 Flexion Reflex noxious stimulus that damages the tissue activates A6 and C pain bers which causes the contraction of exors and relaxation of extensors at every joint of the limb o Flexion occurs with great pain even after spinal transection and leads to posture disturbance This is resolved by exion crossed extension re ex Flexion crossed extension re ex Double Reciprocal innervation Stimulus excites exors and inhibits extensors in one limb and excites extensors and inhibits exors in the other 3 Tonic Neck Re ex position of head through a re ex determines position of the limbs Example fencer s pose Descending Control of Re exes ALL Re exes are under the control of higher motor system a Flexion Re ex Modulation suppressing exion re ex circulation by higher motor system b Tonic neck re ex disappearance develops as soon as myelination occurs Limb position aren t determined by position of head c Spinal shock complete absence of re exes following spinal transection Re exes gradually return but is slower for organisms with complex central nervous system Amy result in hyperre exia re exes become stronger when they return d Babinski Sign response to stimulus shows damage to motor cortex Normal in newborns whose descending axons are not myelinated yet Descending control of Stretch Re ex and Muscle Tone Low Muscle Tone accidity hypotonia and decrease in stretch re ex Down syndrome 0 High Muscle Tone Rigidity Hypertonia increase in stretch re ex Cerebral palsy Decerebrate Rigidity midbrain lesion that cuts intercollicular transection increase muscle tone in extensors of all four limbs neck and tail When dorsa roots were cut rigidity disappeared because IA bers for stretch were gone Decorticate Rigidity increased muscle tone in exors of arms and extensors of legs opposite to the position of the stroke There is contraction for a single stretch gt Clonus more than contraction for a single stretch Spasticity increased muscle tone rigidity hyperactive stretch re exes clasp knife re ex and Babinski sign Clasp Knife re ex arm is extended increase in resistance but melts away because pain bers that inhibited the re exes Rigidity in Cerebral Palsy developmental disability third quarter of 1 million US population From damage in component of motor system motor system PT basal ganglia etc CP causes spasticityrigidity which affects appearance posture and ability to move Contractures lead to problems in joint like arthritis Causes no signal cause most causes resulting from pregnancy problem in developing baby like head trauma intracranial hemorrhage prematurity etc Treatment lnhibit stretch re ex gt Surgical selective dorsal rhizotomy cut SOME dorsal roots to remove some IA ber and decrease the spinal re exes gt Medical injections of baclofen into spinal cord to inhibit stretch re ex
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