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by: Ndidiamaka Okorozo


Marketplace > University at Buffalo > Physiology > PGY 451LEC > PHYSIO FINAL EXAM STUDY GUIDE
Ndidiamaka Okorozo
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Human Physiology I
Baizer, J S
Study Guide
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This 120 page Study Guide was uploaded by Ndidiamaka Okorozo on Wednesday December 9, 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 176 views. For similar materials see Human Physiology I in Physiology at University at Buffalo.




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Date Created: 12/09/15
NEUROSCIENCE NERVOUS SYSTEM Neuron: a cell; building block of the nervous system.  Soma (neuron cell body)  Nucleus  Processes:  fibers emerging from the cell body  Dendrites:  Axons: could be myelinated or not.  Tracts: group of axons connecting different parts of the brain  When tracts cross from one side of the brain to another, they are said decussate  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  Neurons differ in: o Size & shape of soma o Destination of axon o Myelination of axon o Numbers and branching patterns of its dendrites  Communication is done electrically within each cell (action potential) and chemically  between cells (transmitters).  Synapse: an area of communication between two neurons Process of Communication o Axon from the presynaptic neuron travel to the postsynaptic neuron.  Axon terminals create synapses on the synaptic cleft between the two neurons  Neurotransmitters are released and they bind on receptors on the post synaptic neuron. Types of communication  Axodendritic: between an axon of a neuron and the dendrite of the other  Axosomatic: between an axon of a neuron and the soma of the other  Axoaxonic: between two axons of two neurons Ventral: stomach side                                                                Dorsal: refers to back side Cerebral hemispheres: cerebral cortex & subcortical structures Cortex: has four lobes: frontal, parietal, occipital and temporal  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.  Hippocampus: memory  Basal ganglia: deals with movement, cognition  Diencephalon (Thalamus & Hypothalamus)  Midbrain (5)  Cerebellum (4)  Pons (3)  Medulla (2)            5,4,3 and 2 are in the brain stem Cranial nerves deals with   all the sensory information that emerge from the head; hearing vision, olfaction, taste  and touch  motor signals to muscles of the head 12 pairs; olfactory, optic, oculomotor, trochlear, trigeminal, abducens, facial, auditory/vestibular, glossopharyngeal, vagus, spinal accessory, hypoglossal Spinal cord:  Motor – control of muscles  Sensory input from the body encased in bone protection Has four divisions:  Cervical (C1­ C7)  Thoracic (T1 – T12)  Lumbar (L1 – L5)  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 flexibility of lens lost with age; difficulty in focusing on close objects  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.  Corrected by surgical removal and replacing opaque lens with artificial ones (Intraocular lens) Iris: contracts and relaxes to control amount of light entering the eye. *Iris 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.  If infected or becomes inflamed, it is referred to as conjunctivitis or pink eye because eye looks pink.  Conjunctivitis: Blood vessels are inflamed  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 fluid filled to maintain intraocular pressure and shape. Anterior chamber is filled with aqueous humor Posterior chamber is filled 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 fixation point (center) 40° up. 60° down, 90° right and 90° left. Binocular visual field: can be seen by both eyes In humans: it’s out to about 60°. Monocular visual field: 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 fields 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 fields of both eye have a higher tendency to bisect. Maps of the CNS. Retina: has 2 halves: nasal retina and temporal retina *Images are UPSIDE DOWN and BACKWARDS! (Explanation of the Arrow Image) Remember that both eyes view out to about 60 degrees (binocular visual field). 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 field but each part of the brain gets information from ONLY ONE half of the eye and that is the contralateral/opposite 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 field 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 field closer to the temple in both eyes. And even though temporal retina is closer to the temple, it carries information about visual field closer to the nasal.  The right visual field 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 field closer to the nose) joins with the nasal axon (which is carrying information from the visual field 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 field. And all travelling to the right lateral geniculate nuclei have information about the left visual field. These rearranged fibers from the optic tracts. Therefore, at the level of the brain, each part of the brain gets information about the opposite/ contralateral visual field. Left Lateral geniculate nuclei (of the visual cortex): Right visual field Right Lateral geniculate nuclei (of the visual cortex): Left visual field Visual Cortex: Primary Visual cortex: Area 17 (according to Brodmann’s number) Area 18: additional visual cortex for more processing Retina: 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.  They convert light energy specifically 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.  There are two types: Rods: relatively require low levels of light to be activated  low acuity/clarity  no color vision  used at night (scotopic) Cones:  High acuity/clarity,  Color vision: 400 – 700 nm wavelength of light, 3 types of cones for different wavelengths; Short (Blue). Middle (Green), Long (Red)  day (photopic) Color Blindness: pigment missing/ abnormal, X-linked, 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.  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 field that a neuron receives stimulus from. 2 Types of ganglion receptive field  On center, off surround: responds better to a small spot of light illumination of the retina  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 field. Some are directionally sensitive: respond better to stimulus from above than beneath. AUDTION SYSTEM Ototoxic: damaging to receptive cells Otoscope: modified flashlight Frequency – pitch (20-20,000 cps)  We are sensitive to all frequencies but not equally.  At 5000Hz, sound need to be louder for us to hear it.  With age, frequency decrease because of noise induced damage on receptor hair cells. Amplitude – loudness  At 130dB is painful sound Tinnitus: perception of “phantom sound,” ringing or buzzing noise. Common in males and military veteran. Its frequency increases with age. Outer Ear: also known as pinna  External auditory canal – air filled passage.  Tympanic membrane (ear drum) is the boundary between outer and middle ear. Middle ear: air filled.  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 fluid.  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.  Low frequency sounds sometimes get in the bones in skull, which is the reason your voice sounds different when it’s recorded. Otitis Media: fluid ends up in middle ear and bacteria grows, happens a lot in children. Cn be treated by surgical insertion of tubes to drain out fluids if antibiotics don’t work. Eustachian tube: connection of the middle ear and back of the throat. Inner 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.  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 th concentration change that generates a signal to the auditory nerve (8 cranial nerve) so you hear the sound.  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 Its source is identified 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.  Cutaneous (skin) modalities: Touch, Pain, Warm and Cool  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 fibers: There are four of them: Nociceptors (pain), mechanoreceptor (touch) and thermoreceptors (warm and cool). Innervation & Transduction No receptor cells; first order fiber axons innervate the body. These cell bodies are in the Dorsal Root Ganglion. There different fibers for each modality, the proteins/channels on each ending of the primary afferent fibers are different. The different fibers are intermingled in skin giving the mosaic model of skin.  Sensation at each point is determined by the type of fiber innervating that point. Anatomical classification of Fibers 1. Aβ (beta) fibers: 6-12µm diameter, 30 – 70m/sec conduction velocity. Myelinated. Mechanoreceptors. For Touch (for cutaneous), Pain and Pressure (for deep). Have encapsulated endings: Ruffini ending, Markel disc, Pacinian corpuscles and Kraus end bulbs. 2. Aδ (Delta) fibers: 1-5µm diameter. 12-30m/sec. Myelinated. Nociceptors (Pain), Thermoreceptors (warm, cool). Have free nerve endings and not encapsulated. 3. C fibers: 0.4-1.2µm, 0.5-2 m/sec Conduction velocity. Nociceptors, thermoreceptors. Free nerve endings. Innervation Density: nerve endings per unit of skin. Can be measure in two ways:  Localization: the ability to identify area of stimulus  2 point threshold: the distance between two stimuli before they are recognized as one. Receptive field: region of the skin where stimulus affects an axon High innervation density  small receptive field  better 2 point threshold and localization Low innervation density  large receptive field – worse 2 point discrimination and location 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 Aβ 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 first synapse occurs. Cells here project their axons past the mid line in a fiber bundle called Medial Lemniscus which synapse on the thalamus and it relays the info to the somatosensory cortex in the Parietal Lobe (AREAS 3,1 &2)  For level of spinal cord: Ipsilateral 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 Aδ and C fibers. Expanded representation in cortex  smaller receptive field  high innervation density Smaller representation in cortex  larger receptive field  low innervation density *Receptive fields as shown in cortex are larger than that of primary afferent fibers 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 finger 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.  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 fibers). The transmitter release by the fibers is called Substance P. A branch with substance P divides into 3: one sent to the blood vessel to increase blood flow 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 (Aδ 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 fibers 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  reticular formation of pons  thalamus (mid brain)  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 modifies pain input. 1. Transmitter and receptors:  Opiates and receptors are at key sites along pain pathways  Spinal cord dorsal horn  Brainstem reticular formation  Frontal lobes  Opiate receptors: δ(delta), µ(mu), κ (kappa)  Endogenous Opioid Peptide: Transmitter Receptor Enkephalins µ, δ Dynorphins κ Beta-endorphin µ, δ  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  activate dorsal horn interneurons (by releasing inhibitory enkephalins)  synapse on incoming pain fibers to decrease their synapse strength.  This is done at the level of spinal cord at first 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  motor cortex at top and muscles at the bottom. However, all structures work together in movement. Function: Coordination, Posture  In coordination, there are changes in joint angle and muscle length. Flexion  Decrease in joint angle  Contraction/shortening of flexor  Stretching/lengthening of extensor. Extension Increase in joint angle  Contraction/shortening of extensor  Stretching/ lengthening of flexor 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  carried out by extensors (antigravity muscles)  Antagonist: flexors.  Position fixation: 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 finger and eyeball movements Force, resistance and speed result from the muscle’s structure while fineness 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 fibers or change muscle fiber with training  fixed composition. Each muscle has different % of fiber types. But composition of a particular muscle may vary among individuals, may correlate with athletic ability. Motor innervation  Alpha (α) motor neuron (lower motor neuron): axons have large diameter, myelinated, Aα fibers, 12- 20 µm, 70 – 120m/s. Each innervate muscle fibers, 2-1000’s, depends on size. Muscle fiber receives innervation from one and only one motoneuron. Range of size of motoneurons:  Larger MN’s  larger Cell body  larger diameter  Axons with more branches  higher number of muscle fibers.  Larger MN’s  larger Cell body  larger diameter  Axons with more branches  higher number of muscle fibers. 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 death/atrophy. 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 fibers 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 fiber in a motor unit.  Average Motor unit size differs among muscles  Fine control: Smaller  Force, speed: Larger Size Principle: Motor units are recruited in order of increasing size; smallest first and largest last. Drop out happens in reverse order. S fibers 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 2-12 specialized muscle fibers called intrafusal fibers. Ordinary muscle fibers are extrafusal fibers. a) Maintained length b) Rate of change of length. 2. Muscle force: receptor is the Golgi Tendon Organ (GTO).  Receptors for gamma, attached in series with muscle, sensory innervation for Ib fiber (12- 20µm diameter and 70-120m/sec conduction velocity). Ib fibers crunch on axons of gamma motor neurons, depolarize them creating action potentials. Intrafusal fibers have contractile poles and noncontractile centers. a) Nuclear bag (dynamic) b) Nuclear chain (static) Types of sensory fibers: Group IA, 12-20µm, 70-120 m/sec. innervate all intrafusal fibers, has primary/annulospiral endings. Carry info about maintained muscle length (static) and rate of change of muscle length. Group II, 5-12µm, 30-70 m/sec. Innervate only nuclear chain fibers, has secondary/flower spray endings. Carry info about maintained muscle length (static). Transduction in the spindle Muscle Stretched  Endings become polarized  action potentials generated Motor innervation of spindle: Gamma MN’s, “fusimotor” neurons, 5 – 12µm diameter, 30-70m/sec conduction velocity. Cell bodies are in ventral horn of spinal cord. Ensure steady action potential. Problem: Muscle shortens  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 & DESCENDING CONTROL OF REFLEXES Reflex: unlearned motor response to a sensory stimulus.  Components: muscles, motor neurons. Sensory input from body, spinal interneurons. Abnormal Reflex: reflection of dysfunction of some component of the motor system.  Circuit for a reflex could be present at the level of spinal cord/brain stem but descending pathway modulates the reflex strength  stronger, weaker or totally suppressed. Spinal Transection: cause loss of sensation and voluntary movement below the cut but spinal reflexes remain. Muscle Tone: resistance to passive stretch (an involuntary movement being imposed from the outside). Reflexes 1. Stretch Reflex: IA fibers (afferent), α MN’s (efferent) Stretch of muscle (stimulus)  activated IA fibers  excitatory synapse on α MN’s  same muscle contracts (response). o Underlies Muscle Tone by producing resistance  Short latency reflex: occurs fast  Monosynaptic reflex: only one in a circuit. Coordination: built into stretch reflex. Agonist contracts while antagonist relaxes.  Reciprocal Innervation: IA fiber branch synapses on inhibitory interneuron  interneuron inhibits MN’s innervating antagonist muscle. 2. Flexion Reflex: noxious stimulus that damages the tissue activates Aδ and C pain fibers which causes the contraction of flexors and relaxation of extensors at every joint of the limb.  Flexion occurs with great pain even after spinal transection and leads to posture disturbance. This is resolved by flexion crossed- extension reflex. Flexion crossed- extension reflex: Double Reciprocal innervation Stimulus excites flexors and inhibits extensors in one limb and excites extensors and inhibits flexors in the other. 3. Tonic Neck Reflex: position of head through a reflex determines position of the limbs. Example: fencer’s pose Descending Control of Reflexes ALL Reflexes are under the control of higher motor system a) Flexion Reflex Modulation: suppressing flexion reflex circulation by higher motor system. b) Tonic neck reflex disappearance: develops as soon as myelination occurs. Limb position aren’t determined by position of head. c) Spinal shock: complete absence of reflexes following spinal transection. Reflexes gradually return but is slower for organisms with complex central nervous system. Amy result in hyperreflexia (reflexes 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 Reflex and Muscle Tone  Low Muscle Tone: flaccidity, hypotonia and decrease in stretch reflex. Down syndrome.  High Muscle Tone: Rigidity, Hypertonia, increase in stretch reflex. 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 fibers for stretch were gone. Decorticate Rigidity: increased muscle tone in flexors of arms and extensors of legs opposite to the position of the stroke. There is contraction for a single stretch.  Clonus: more than contraction for a single stretch. Spasticity: increased muscle tone, rigidity, hyperactive stretch reflexes, clasp knife reflex and Babinski sign. Clasp Knife reflex: arm is extended, increase in resistance but melts away because pain fibers that inhibited the reflexes. Rigidity in Cerebral Palsy: developmental disability, third quarter of 1 million U.S. population. From damage in component of motor system; motor system, PT, basal ganglia, etc. CP causes spasticity/rigidity 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: Inhibit stretch reflex.  Surgical: selective dorsal rhizotomy: cut SOME dorsal roots to remove some IA fiber and decrease the spinal reflexes.  Medical: injections of baclofen into spinal cord to inhibit stretch reflex. BLOCK 2 MEMBRANE POTENTIAL [X]i Nernst equation = x = ( RTln X o ) + (ZxFVm) [ ] where the first group accounts for chemical component ΔC  concentration and the second for electrical component ΔE  charge. Inside Outside ΔC ΔE concentratio concentratio n n Glucose 2mM 5mM In None, no charge Sodium 12mM 145mM In In Potassium 120mM 4mM Out In Chloride 30mM 105mM In Out *cell is at -60mV When there is no net movement, the Nernst equation is equal to 0, the chemical and electrical components equal. 61.5 [X]o At 37ºC, Ex= Zx log [ ]i For Na+ = 66.6mV, K+ = -90.8mV, Cl- = -33.5mV Hyperkalemia: high concentration of K+ in the cell because of kidney malfunction. Increases likelihood of heart firing action potential (AP). Leads to cardiac arrhythmias and cardiac arrest. Hypokalemia: frequent urination by individuals on diuretics causes loss of K+ ions, decreases likelihood of firing AP, causes cardiac arrhythmias and cardiac arrest. Resting Membrane Potential : the Vm (membrane potential) where the net current is 0. measured from the inside relative to the outside.  -70mV for a neuron and -90mV for a skeletal muscle cell.  Depends on:  Ion concentration across membrane  Relative conductance of the membrane of different ions  Primarily determined by K+ because it is the most permeable to it  Ii = (Vm – Ei) x gi (where Ii is the current, Ei and gi are Nernst potential and conductance for that ion respectively. GNa GK GCl  Vm = E Na+ + E k+ + ECl- where ΣG is sum of all ΣG ΣG ΣG conductance, which = 100pS in a normal neuron. So, GNa+ = 15% = (10/100) = 0.15  Thus, Vm = 0.15 x 66.6mV + 0.8 x (-90.8mV) + 0.05 x (-33.5mV) = -64.325mV Most cells have the highest conductance to K+ because its Vm is the closest at the RMP, so it has 80% of the ΣG while Na is 15% and Cl- is 5%. Vm for Na+ is very high  +65mV and for K+ is too low  -90mV so Vm is always in between these two values. Only a tiny percentage of K+ needs to diffuse out of the cell to maintain RMP. ATP-dependent Na+, K+ Pump: pumps out 3K+ while pumping in 2 Na+ ACTION POTENTIAL ATP-dependent pump in an axon pumps out 3 Na+ ions while pumping in 2 K+ ions to maintain ion concentration across the membrane. This pumps contributes about 5mV to the RMP. Types of ion channel: 1. Voltage-gated ion channels: open or close in response to membrane potential. 2. Ligand-gated ion channels: open or close when a neurotransmitter (ligand) binds to the ion channel. Na channels: voltage gated, 1 pseudo tetramer α subunit, has 6 intra membrane cylinders repeated four times and ions bind on α surface. Intracellular loop between III and IV block Na+ from entering after depolarization. + K channels: voltage gated, tetramer, has four subunits with 6 transmembrane regions and allows only potassium passage. β subunit only helps with selectivity and regulation. Graded potential: increase in stimulus strength which produces in amplitude of the depolarization. Local or Sub-threshold depolarization: conducted decrement and doesn’t generate action potential (AP). The depolarizing stimulus doesn’t reach the threshold and so is unable to fire an AP. They are graded and non- regenerative and decay over time and distance. All-Or-None Response: either produces a full sized AP or nothing at all. In this case, amplitude doesn’t correlate with stimulus strength because threshold was reached. Suprathreshold Response Firing an AP: A stimulus causes the Vm to rise to threshold and as it is reached, sodium channels open, allowing a massive influx of sodium into the cell. This causes a rapid up stroke of the AP which is referred to as depolarization because its moving the Vm closer to zero. However, the influx of Na+ is too rapid that the AP reaches up to +50mV. The area above 0mV is called overshoot. Meanwhile the potassium channels are increasingly opening because the Vm is being moved far away from their membrane potential (-90mV). At 50mV, the peak of the AP, sodium channels close and K+ channels start pushing out K+ which repolarizes the cell as it takes it back to the negative membrane potential. The force of pushing K+ is too fast (because of both electrical and chemical forces) that the AP falls below the RMP (-70mV), which is called afterhyperpolarization, before the K+ channels close and the membrane potential returns to rest. Total period of firing AP lasts for about 3-4 msec.  Rising phase of AP: opening of the voltage dependent NA+ channels and depolarizing action of Na+ current.  Falling phase of AP: reduction in g Naand increase in gK Positive feedback loop in Na : when threshold is reached, gNa (Na + + conductance) increases as massive entry in to the cell occurs  Na activation. So as Vm increases, more Na+ channels open and more Na+ ions enter and the Vm increases even more till at +50mV when the sodium channels close. Closing of Na+ channels starts repolarization while g helpK complete it. Right at the peak, of AP:  Na+: ΔE is going out and ΔC is going in, opposite.  K+: same, both ΔE and ΔC are going out, so K+ has a great driving force! Absolute Refractory Period: Na+ channels are inactivated and cannot be reopened till the membrane is repolarized. This consists of the rapid rising and falling phases. Parallel with Na+ activation and inactivation. About 1msec in an axon. Relative Refractory period: cell is able to fire a second AP in the later part of the first AP but a stronger than normal stimulus is required. Consists of the latest part of repolarization and afterhyperpolarization. Parallel with changes in gK+. About 3-4msec in an axon. Refractor period limits the frequency of AP, if RF period = 4msec, the max freq = 250Hz because max freq = 1000 spikes per second. ANESTHETICS: Cocaine: first anesthetic discovered, block Na+ channels from outside of the membrane to prevent Na+ from coming in when threshold is reached. Poisons: 1. Tetradotoxin (TTX): Block Na+ channels from outside, prevent generation of AP. 2. Saxitonin (STX): blocks Na+ channels from outside, prevent generation of AP.  They don’t work on the heart because it has an amino acid that prevents the blockage. Propagation of AP: AP is generated at the axon hillock where there is an abundance of Na+ which lowers the threshold and makes it easier to propagate an AP. Conduction of AP: back propagation doesn’t occur because the threshold there is high and the Na+ channels are inactivated after just receiving an AP (refractory period) so propagation moves forward to the activated Na+ channels waiting for propagation. Unidirectional. Length Constant: 37%, 1/e, how long AP can go without disappearing. λ (LC) correlates with radius of axon (larger longer LC & slower the decay) and membrane resistance (R m. aRm λ= √ 2Ri Ri = intracellular resistance. Unmyelinated axons: support conduction but AP has to be generated all the time to propagate so it uses a lot of energy and conduction velocity is slow (CV). Therefore, the freq of AP depends on how big the LC is.  Axon diameter  LC  Conduction Velocity of AP Myelinated axons: Schwann cells in Peripehral Nervous System and Oligodendrocytes in Central Nervous System. Increase membrane resistance greatly.  Increase insulation of axons  prevents leaking  increases Rm & LC  Don’t have refractory periods and hyperpolarizing after potential because there are no K+ channels at the nodes so less energy is used.  Nodes of Ranvier: no K+ channel, concentrated amount of Na+ channel. AP is generated without fail  higher CV. A much smaller myelinated axon is better than a big unmyelinated axon. Saltatory Conduction: AP appears to jump from node to node. Permits reflex. Internode (insulated areas) aren’t involved in propagation and generation of AP. Occurs only in myelinated axons. Myelination  lowers energy expenditure  generate AP fewer times  generate higher CV Multiple Sclerosis: demyelinating disorder, patches of demyelinated axons in the CNS. Loss of motor control because axons fail to fire AP because of demyelination which cause loss of current. NEUROMUSCULAR JUNCTION (NMJ) Junction between a the axon terminal of an alpha motor neuron and a skeletal muscle cell/fiber., One NMJ per muscle fiber and it’s located near the middle of the muscle fiber/cell. One α motor neuron  one axon  different axon collaterals innervating different muscle fibers. RMP of a muscle fiber = -90mV End Plate Potential (EPP): potential of the muscle fiber which increases in response to the presence of Ach.  Ach are synthesized and packaged in the synaptic vesicles which are aligned with the acetylcholine receptor (AchR) to generate the greatest response.  Depolarization is produced by increase of gNa+ and gK+ in the AchR on the end plate (EP).  Outside of the EP region, it is propagated by local current flow which decreases with distance. Ach Synthesis: Neurotransmitter (NT) vesicles are made in the cell body and transported to the terminal. Ach are synthesized and packages in these vesicles. Choline-acetyltransferase (ChAt) catalyzes the production of Ach from choline and acetyl-CoA. A proton pump pumps protons into the vesicle creating an acidic environment. Another pump pumps out the proton while pumping in Ach into the vesicle. Process: AP arrives at the presynaptic terminal and depolarizes it thus induces the inflow of Ca 2+into the nerve cell from the voltage-gated channels. Presence of calcium causes the fusion of the vesicle with the membrane and releases the contents of the vesicle – Ach. Ach, now in the synaptic cleft, bind to receptors on the postsynaptic cells which open up and lead to changes in the Vm of the cell by allowing the inflow of Na+, K+ and 2+ Ca . This produces EPP and it ALWAYS fires an AP. Ach is retaken up from the synaptic cleft by acetylcholine esterase (AchE) and recycled. Ach Receptor: non-selective cationic ligand gated channel, has 6 subunits and the two α ones allow for Ach to bind. Opens when two Ach are bound to it, allow for only cations to enter. Influx of positive ions brings the Vm closer to 0mV which depolarizes the motor end plate. Ina normal muscle cell:  Na+: ΔC and ΔE are pushing Na+ in.  K+: ΔC is pushing out and ΔE is pushing out. Curare: prevents Ach from binding to Ach receptors so no AP is produced.  But EPP always produces an AP, suprathreshold. 40mV is suprathreshold in a healthy person. Graded potential: the amplitude of the AP is dependent on the amount Ach released and amount of AchR it activated – not all-or-none principle. Myasthenia Gravis: severe muscle sickness. An autoimmune disease where antibodies bind to and destroy AchR. It decreases the amplitude of EPP to below threshold thereby preventing the generation of AP. Causes sickness and fatigue. Treatment: introducing physostigmine to the synaptic cleft inhibits acetylcholine esterase and prolongs the presence of Ach in the cleft. Also drugs that suppresses the immunes system to stop the production of the antibodies and lastly surgical removal of the thymus gland. Some agents at the NMJ 1. Skeletal Na+ channel blockers: tetradotoxin, saxitoxin and µ conotoxin. 2. K+ channel blocker: dendrotoxin 3. Ach release blockers: tetanus and botulinum toxins. 4. AchE blockers: physostigmine and DFP. 5. AchR blockers: d-tubocurarine, succinylcholine and alpha-bungarotoxin (binds to same α subunit as Ach). 6. Ca2+ channel blocker: in axon terminal  ω conotoxin. SYNAPTIC TRANSMISSION Types of Synapses: 1. Electrical Synapse: has gap junctions, low resistance pathway and allows exchange of small molecules in addition to ions (permeable to up to 1kDA). Occurs between glial cell and neurons. Fast and bidirectional, can be regulated. 2. Chemical Synapse: involves neurotransmitter and does majority of interactions between cells. Fast and unidirectional. Focused more on for this class. Chemical Synapses: 1. Anatomical categorization: axosomatic (inhibitory), axodendritic (excitatory), axoaxonal (regulates release), dendrodendritic and dendrosomatic (not common). 2. Functional categorization: a. Excitatory: postsynaptic density (PSD) b. Inhibitory: symmetric (no PSD) c. Modulatory: GPCR Neuron doctrine: neuron are the information processing units of the nervous system. Neurotransmitters: according to impact on AP firing 1. Excitatory: a. Glutamate: ligand-gated channels i. NMDA receptors ii. AMPA receptors iii. Kainate receptors b. Acetylcholine: nicotinic receptors 2. Inhibitory: ligand-gated channels a. GABA: GABA recAptors (also GABA ) C b. Glycine receptors 3. Modulatory (or metabotropic): GPCRs a. monoamines (dopamine, serotonin, etc) b. acetylcholine (muscarinic) c. glutamate: metabotropic glutamate receptors d. GABA: GABA B Fast NTs: act on ligand gated channels and mediate synaptic transmission. Slow NTs : modulate ligand gated or voltage gated channels. Modulate synaptic transmission. EPSP: receptor channels opened by glutamate, Na+ in and K+ out. At resting potential, EPSP is caused by Na+ influx. There is an increase in gNa+ and gK+ but because the Vm is further from E , tNare is a greater inward movement of Na+ than the outward movement of K+. Amplitude is dependent on holding potential. Increases probability of firing AP by bringing the Vm closer to threshold. IPSP: receptor channels opened by GABA, allows Cl- in. Increase in gCl- allows it to go in and hyperpolarizes the cell. Also, gK+ can also hyperpolarize cell in certain cases where there is increase in gK+ and K+ ions leave the cell. Decreases probability of firing AP by moving the VM farther from the threshold. *ONLY ionotropic ligand-gated ion channels result in EPSPs and IPSPs.  They are graded potentials and are conducted with decrement. Summations: a. Temporal summation: if synapses occur within a short amount of time, they are summed up and could produce AP. b. Spatial summation: synaptic potentials generated in soma and dendrites interact. *Different neurons can produce EPSPs and IPSPs at the same time, so their some is taken. Amplitude of an AP does NOT provide information about the strength of the stimulus because of all-or-none response, only the STRENGTH provides this information. Refractory period limits the max frequency of AP because if total refractory 1000msec period is 4msec, you can only generated 250AP/sec. ( 4msec ). But more large myelinated axons can do up to 100AP/sec. Clearance of NTs from Synaptic Cleft After NTs has been released by presynaptic neuron into the cleft, it has to be terminated to create the AP. This is done by: a. Reuptake: the NTs are taken up from the cleft by plasma membrane NT transporter wither on presynaptic or postsynaptic neurons. It is usually co-transported with Na+, Cl- and H+ ions. b. Degradation: by NT degrading enzymes like choline esterase for Ach and COMT for dopamine. c. By diffusion down the concentration. Synthesis: Glutamine is converted to glutamate by glutaminase  Glutamine is converted to GABA by glutamate decarboxylase  Tyrosine is converted to L-DOPA by tyrosine hydroxylase and L-DOPA is converted to Dopamine by AADC. Sequestration of the NTs into the vesicle is done by NT transporter and driven by proton gradient across the vesicle membrane. Neurotransmitters: 1. Small-molecule neurotransmitters: packaged in vesicle, released in cleft and terminated a. Acetylcholine b. Amino acids: i. Glutamate: major Excitatory NT in CNS. ii. GABA: in GABA-ergic Neurons. Major inhibitory NT iii. Glycine: modulate NMDA-mediated synaptic transmission. c. Biogenic Amines: i. Catecholamines: dopamine, epinephrine, norepinephrine ii. Serotonin: made from tryptophan iii. Histamine: made from histidine. d. Purines 2. Neuropeptides: a. synthesized as precursors in cell body (just like proteins). b. Carried from cell body to terminal via the axon. c. sequestered in large electron dense-core vesicles d. release can be non-synaptic and only with large freq of stimulation 3. Gaseous neurotransmitter: NO and CO a. highly permeable, diffuse everywhere and not in vesicles b. release upon synthesis, which is triggered by Ca2+ influx, no reuptake. Difference between nonpeptide and peptide NTs. Nonpeptide Peptide Synthesized & packaged in terminal. Synthesized & packaged, transported to terminal. Synthesized in active form. Active when fused with larger polypeptide In small and clear vesicles In large electron dense vesicles Released in the synaptic cleft and has Could be released a bit far from short latency and duration. postsynaptic cell, long latency and duration is seconds. Terminated by reuptake. Terminated by proteolysis or diffusing. Receptors for Classic Neurotransmitters 1. Acetylcholine: Nicotinic: pentameric nonselective cationic channels gated by Ach Muscarinic: five different GPCRs, two classes: M 1,3,5coupled to Gq); M 2,4coupled to Gi). 2. Amino acids: Glutamate: Ionotropic: tetrameric nonselective cationic channels gated by Glu. Cocentrated at postsynaptic densities (PSDs). NMDA Receptors: NR1 and NR2A,B,C,D  acts as “coincidence detector.” Mg 2+blocks NMDA at resting Vm, depolarization removes it. Involved in regulation mental and cognitive attributes. AMPA Receptors: GluR1-4  mediate fast synaptic transmission Kainate receptors: GluR5-7, KAR1,2 Metabotropic: 8 different GPCRs Group I: mGluR1,5 Group II: mGluR2,3 Group III: mGluR4,6,7,8 GABA: Ionotropic: GABA Aconcentrated at soma and proximal dendrites), GABA (peCtameric Cl- channel gated by GABA) Metabotropic: GABA (GPCR) B Glycine: ionotropic, pentameric Cl- channel gated by glycine 3. Biogenic Amines: Except 5-HT3, all GPCR. Many subtypes for each. dopamine, epinephrine, norepinephrine, serotonin, histamine 4. Purines: receptors for ATP Ionotropic: P2X, 7 subtypes, non-selective cationic channels, distinct form others. Metabotropic: P2Y, 10 subtypes. NT Receptors: 1. Ligand-gated channels (ionotropic) Receptors: act on EPSP or IPSP directly.  Two types generally: Cys loop family channels; Ach, GABA , A Glycine and Seratonin AND glutamate channels; NMDAR, AMPAR and KAR. 2. G-protein Coupled Receptors: modulate EPSP or IPSP indirectly. *PentoBarbital enhances IPSP’s.  Other agents that enhance IPSPs by binding to GABA R are:A  Benzodiazepines: increase the freq of Cl- channels opening.  Barbituates: increase the duration of Cl- channels opening.  Enhanced inhibition  sedation.  Have same effects but bind to different sites: progesterone & corticosterone. SENSORY TRANSDUCTION Vision (photons) Hearing (mechanical via air compression) Taste (chemical) Smell (chemical) Touch-pressure (mechanical) Proprioception (mechanical) Pain-temperature (mechanical, thermal) *All these are converted to generator potentials which produce AP’s. Coding of AP’s done by: frequency of firing, temporal patterns, periodicity and consistency. Process of sensory transduction: a single axon from the sensory organ transmits AP to the next neuron in the spinal cord. For example: stretch of muscle spindle generates AP which is sensed by mechanosensitive receptors and transmitted to the spinal cord and releases Glu. Glu elicits EPSP on the alpha neuron which releases Ach on the muscle and it contracts. (The stretch on the muscle spindle is interpreted by the sensory neurons into patterns of AP). Motor Unit: an alpha motor neuron and all the muscle fibers it innervates. The number of fibers innervated by a motor neuron is dependent on the fineness of control: higher # of fibers  less fine control while lower # of fibers  more fine control. Muscle Unit: all the muscle fibers innervated by one motor neuron. Always belong to the same type - slow or fast twitch. Dermatome: area innervated by a dorsal root ganglion neuron. Shingles: reactivation of herpes zoster virus, lies dormant in the DRG after chickenpox. Reflex: predictable, involuntary and stereotyped response to a stimulus. Reflex arc: basis circuit that mediated a reflex (has three components: afferent limb – carry info to brain, central component – synapses on interneurons in CNS and efferent limb – cause motor response). IA Fibers: carries AP to spinal cord and synapse on the motor neuron in the spinal cord. Stretch Reflex (tendon tap): Muscle spindle stretches which produces a generator potential (GP) and creates an AP on the IA sensory axon. Transient Receptor Potential (TRP) Channels are involved in temperature sensing.  Hair cells have mechanosensitive TRP channels. Types of Ion Channels: 1. Voltage-gated Na+ and K+ channels for AP in axons and skeletal muscles. 2. Voltage-gated Ca2+ channels in axon terminals (heart and smooth muscle). 3. Ligand-gated ionotropic Na+, K+ and Cl- channels (EPP, EPSP, IPSP). 4. Stretch-activated ion channels in sensory receptor sensitive to mechanical stimuli (GP). 5. G-protein activated metabotropic ion channels in special senses, smooth muscle, glands, etc. Mechanoreceptors in the skin: FA- fast-adapting to change in stimuli  senses change, SA-slow adapting  only tell when you’re touching something (pressure).  FA1 and SA1: shallow in skin, sense direct pressure and small receptive field.  FA2 and SA2: deep, sense broad contact and large receptive field. Homunculus: topographical correspondence between motor cortex and body parts. For better 2-point discrimination: small receptive fields, high density of touch-pressure receptors and large cortical representation. Vision Retinal neural processing: retina converts photons to AP sent to the brain for interpretation. GP produced by photoreceptors are processed to AP in optic nerves. Cones: day vision, color, less sensitive, concentrated in fovea, less numerous. Rods: night vision, detects luminescence, more sensitive and more numerous.  Amplifies signals, one photon causes membrane potential alteration by 1mV. Rhodopsin - GPCR Light enters  Rhodopsin (contained in disc) increases  PDE increases  cGMP decrease  cGMP-gated decreases  Vm decreases  Release decreases cGMP gates the channel and when it is destroyed, channel opens less and Na+ enters less, decreasing the Vm leading to less NT release. Taste Sweet (sucrose; energy), Salty (NaCl: minerals), Sour (HCl: bad), Bitter (quinine: bad), Umami (monosodium glutamate: meat).  Receptor cells are specialized epithelial cells (not neurons) that convert taste to NTs which are sensed by the cranial nerves then generate GP which might generate AP. To elicit GP, there are three different pathways: a. Na+ and H+ which are have high concentrations outside go in and changes Vm  depolarization  generate GP  Ca2+ influx  increase NT release b. Changes make channels open  goes in  increase Vm  NT release c. Bitter/Sweet/Umami – bind to GPCR  intracellular pathway  Ca2+ influx. Smell (Olfaction) Odor receptors (GPCRs): activate G olfG-Protein is activated)  increase cAMP activated cAMP-gated channels  Na+ and Ca2+ influx  Cl- outflow  depolarization  produce GP. Odorants receptor cells regenerate every 60 days. A single smell can activate may different receptor proteins and the convergence of their AP’s determine what you smell. AUTONOMIC NERVOUS SYSTEM a. Does NOT control skeletal muscles. b. Controls smooth muscles, cardiac muscles and glands of the internal organ (viscera). c. Helps in maintaining homeostasis d. Coordination of responses to external stimuli; fight or flight. 3 Major Divisions a. Sympathetic NS: Thoracolumbar (T1-L3) division of ANS, mobilization of body – “fight-or-flight” response. One preganglionic neuron innervates a few postganglionic neurons. Wide spread and greater divergence in effect. Sensory input on short preganglionic neuron  releases Ach on long postganglionic neuron  releases Ach on muscarinic receptor on organ. b. Parasympathetic NS: craniosacral division of ANS. Concerned with the “Resting” response. One preganglionic neuron innervates many postganglionic neurons. Discrete and short spread response which is localized. The postganglionic neuron is short and is very proximal to the organ. c. Enteric NS: oldest part of ANS, controls GI tract, pancreas gall bladder to help in digestion. Doesn’t require inputs from other parts on the nervous system. Sympathetic Parasympathetic Locations of preganglionic thoracic (T1-12) brainstem soma upper lumbar (L1-3) sacral (S2-4) Length of preganglionic fiber short Long Locations of postganglionic paravertebral close to target soma ganglia prevertebral organ ganglia Length of postganglionic fiber Long Short Ratio of pre/post fibers 1:10 1:3 (divergence) Functions Both systems act in coordinated manners to maintain homeostasis. Neurotransmitters: Ach Ach preganglionic Neurotransmitters: Norepinephrine Ach postganglionic Muscarinic receptors that the postganglionic Ach from parasympathetic neuron binds to” M1 class: couple with Gqto increase Ca2+ M2 class: with G1to inhibit PKA.  Atropine blocks all muscarinic receptors. Agonists: carbachol, muscarine, oxotremorine  help with Ach binding to receptors. Because all postganglionic parasympathetic neurons release Ach to act on muscarinic receptors on effector cells, the non-selective antagonist atropine blocks the action of parasympathetic neurons effectively. E.g. resuscitation with atropine injection in bradycardia (to inhibit the parasympathetic vagus nerve, which slows heart beat). GIT SECTION INTRO TO DIGESTIVE SYSTEM The GI tract is a hollow tube that brings the outside world inside. Inside the lumen of the esophagus is considered external (outside world) because it connects with the outside. Helps maintain homeostasis. Its primary function is to digest food and absorb nutrients, electrolytes and water into the body’s internal environment. Functions: Motility, Secretion, Digestion, Absorption, Excretion and Protection. Epithelium is a single layer of cells that protects the inside from the outside world. It is involved in regulation of materials across compartments. Layers of the stomach: a. Longitudinal muscle: increases volume b. Circular muscle: causes propulsion and mixing c. Oblique: causes stomach to twist because of contractions. *These three layers makes up muscularis externae and engage in motility. Invagination called gastric glands increase surface area in the stomach. Intestinal surface have invaginations called crypts. This is found in Small intestine (SI) and large intestine. However, SI also has villi that enable further increased absorption. GI Physiology Regulation: a. Endocrine: hormone is released and it circulates in blood before reaching target cells b. Neurocrine: a neuron innervates the target cell using neurotransmitter. c. Paracrine: cell releases hormone to neighboring cells. Enteric Nervous System: intrinsic network of the gut. Can function independently of the ANS. However, it is modulated by the parasympathetic (Ach) and sympathetic (NE) nervous systems. Parasympathetic is controlled by medulla oblongata and uses the vagus nerve. ENS network is imbedded in submucosal plexus and myenteric plexus. Its receptors are mechanoreceptors and chemical receptors. The ENS and two branches of ANS are all interconnected. GI MOTILITY Two functions: a) Movement of food from the mouth to the anus. b) Mechanically mixing food to break it into smaller particles and to mix with digestive juices. Muscle types: Striated (Skeletal): muscles of moth, pharynx, upper esophagus and external anal sphincter. These are innervated by the somatic motor neurons. Smooth muscles: rest of the GIT (GI Tract) and are innervated by autonomic motor neurons. They are involuntary and contract spontaneously. Smooth muscles are driven by pace makers, electrically connected by gap junctions and different regions exhibit different types of contractions: Tonic contractions: can contract and remain like that for long periods of time. Enables them to be used in sphincters. Phasic contraction: changes - contracts and relaxes. They also exhibit slow wave potential: RMP is not fixed but continuously wavering. Because of the gap junctions, information is passed easily and the cells contract or relax at the same time. *Not all slow waves reach threshold. GI Motility processes include ingestion, mastication, deglutition (swallowing food), peristalsis (rhythmic wavelike contractions that move food forward) and segmentation (mixing contractions in different segments) and defecation. Interstitial Cells of Cajal Pacemaker cells where slow waves are initiated. Have gap junctions. These slow waves affect the opening of Ca2+ channels and therefore can lead to contraction when threshold is reached. Amplitude and frequency are modulated by extrinsic and intrinsic nerves and hormones; Ach and substance P (excite) while VIP & NO (nitric oxide) will inhibit. Slow waves are: 3-5 per min in stomach, 12-20 per min in small intestine and 6-8 per min in colon. The force and duration of muscle contraction are directly related to the amplitude and frequency of the action potentials. Contraction of GI smooth muscle Threshold is reached  Ca2+ enters, associates with CAM  activates MLCK which uses ATP to activate inactive myosin  myosin and actin contract. This complex stay intact as long as myosin stays phosphorylated and when it stops being phosphorylated, myosin and actin relax. Exhibits the tonic contraction characteristic. Motor patterns of Small Intestine (SI) a) Peristalsis: wavelike movement from side to side which produces pressure that pushes the food forward. b) Segmentation: mixing the food in different segmen


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