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Neuro Anatomy Exam

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University at Buffalo
Exercise Science
ES 342

Neuroscience Exam 2: Neuromuscular Junction: -Site where the spinal motor nerve terminal meets a muscle fiber -Where the efferent nerve terminal evokes a muscle contraction -Contraction accomplished through the production of an excitatory synaptic potential called an END-PLATE POTENTIAL (EPP)…an EPSP but called an EPP -Normal skeletal muscle fiber, the EPP always reaches threshold for the production of anAP which then propagates along the muscle fiber and triggers muscle contraction. Basic Features of NMJ: End-Plate potential Spinal Motor Unit -Ach will bind to nicotinic receptors -1:4 (innervates 4 muscle fibers) -Cause opening of Na/K channels -All will contract near simultaneously -Na+ floods in -1:5(better control, Oculomotor muscles and visual tracking)-1:2000 (remain upright posture, antigravity, large bulky muscles) Post-Synaptic Potentials on NMJ: (Changes on Resting membrane/muscle membrane—what’s happening on the muscle) EPP: END PLATE POTENTIAL -Associated with a muscle contraction -DEPOLARIZATION that occurs on muscle membrane with arrival of anAP in terminal area of spinal motor nerve -Release of 150-300Q ofAch(2000 molecules) binding to nAch -nAch opens--↑Na/↑K=DEPOLARIZATION (Na floods in and changes permeability on muscle membrane) MEPP: MINIATURE END PLATE POTENTIAL -Did NOT lead to muscle contraction -Are random events of one vesicle unrelated toAP and doesn’t lead to threshold -one vesicle released, 2000 molecules released- muscle NEVER reaches threshold but has a miniature DEPOLARIZATION -Few receptors open and are unrelated to Ca+ entry CLINICAL CORRELATIONS: Denervation Hypersensitivity: -muscle fiber(spinal motor nerve) is injured and loses its neuro input -Sensitive toAch, muscles will contract & whole fiber becomes receptive toAch (Ach can only contract at NMJ whereAch receptors are) -Migration of receptors -Establishment of a new NMJ will make all other fibers disappear -Fibers will begin to discharge & twitch approx 2 weeks after losing their innervations. Twitching of single muscle fiber randomly contracting called FIBRILLATION (not visible through skin) Neuromuscular transmission can be affected by pharmacologic agents: (Any disease affecting NMJ=muscle weakness!) Curare and Alpha-Bungarotoxin: (plant poison and snake venom) -Act at NMJ by competitive inhibition -poison binds to recognition portion of nAch, Channel does not open/recognize it -No place forAch to bind cause receptor portion is occupied=No muscle contraction cause can’t open channel -Paralyzes person -Disease that affects POST-synaptic membrane -Is reversible -↓EPP & ↓MEPP Botulism: (toxin in food) -Attacks electrically gated Ca+ channels -Channels at NMJ- prevents entry of Ca+ at PRE-synaptic elementless release ofAchless binding on post-synaptic membraneDEPOLARIZATION -PRE-synaptic event -Botox-Paralyzes muscle, wrinkles caused from muscle spasms -↓EPP - MEPP=NORMAL Anticholinesterases: (used in drugs) -breaks down Ach -Prevents breakdown ofAch-Ach prolonged effect on nAch receptors (enhances neuromuscular transmission) -Person cannot turn off muscle contraction -Becomes in a period of spasm -In synaptic cleft (NOT pre/post synaptic membrane) -Paralyzes muscle in a contracted state Bear Box 5.5 -Bacteria Clostridium, black widow spiders, cobras and black widow spiders have in common= produce toxins that attack the chemical synaptic transmission that occurs at NMJ -Botulism produced by C. Botulinum in improperly canned foods. Toxins are very potent blockers of NM transmission. Destroys SNARE proteins in presynaptic terminals critical for transmitter release -Black widow spiders venom deadly effects. Venom increases then eliminatesAch release at NMJ. Axon terminals are swollen and synaptic vessels are missing. Venom binds with proteins on outside of presynaptic membrane forming a membrane pore that depolarizes the terminal and allows Ca+ to enter and trigger rapid & total depletion of transmitter -Taiwanese Cobra bite results in blockade of NM transmission in its victim by Peptide molecule, α-bungarotoxin that binds so tightly to the postsynaptic nACh receptors that it takes days to be removed. No time for removal because cobra toxin prevents activation of nACh receptors byAch which paralyzes the respiratory muscles of the victims. -Humans synthesized chemical that poisons synaptic transmission at NMJ called organophosphates. They are irreversible inhibitors ofAChE and by preventing the degradation of Ach, they probably kill their victims causing a desensitization ofAch receptors. These are used today as insecticides Clinical Disorders of the NMJ: (both associated with muscle weakness) Myasthenia Gravis: -Related to cancer of the thymus gland -Autoimmune disorder. -↓nACh receptors and widening of synaptic cleft -fewer receptors=less depolarization of post-synaptic membrane -Wider synaptic cleft=enzymes have longer time to degradeAch so fewer molecules reach membrane because they are being broken down -Receptors= POST-synaptic event / disorder because of reduction ofAch receptors -released Ach is far less effective and neuromuscular transmission often fails -characterized by weakness and fatigability of voluntary muscles including muscles of facial expression and can be fatal if respiration is compromised. Not a common disease only striking one in 10,000 people of all ages and ethnic groups -unusual feature is that severity of muscle weakness fluctuates even over the course of a single day -Treatment= drugs that inhibit enzyme acetylcholinesterase (AChE) which breaksdownAch in the synaptic cleft. In low doeses,AChE inhibitors can strengthen NM transmission by prolonging the life of releasedAch, however, too muchAch in the cleft leads to desensitization of the receptors and a block of neuromuscular transmission -Treatment= suppression of the immune system, either with drugs or removal of thymus gland. -BOTH MEPP and EPP are small Lambert-Eaton Myasthenic Syndrome (LEMS): -Autoimmune disorder associated with lung cancer -Attacks electrically gated Ca+ channels on pre-synaptic element -Less entry of Ca+  fewer vesicles of Ach released  less depolarization of muscle membrane -PRE-synaptic event -Patients get stronger as day progresses because of high level use of Ca+ will increase due to post-tetanic (Ca+ becomes leakier with high levels of activity) -MEPP are normal, EPP are small because of a decrease in the number of quanta released during anAP **Electrical Nerve Stimulation studies are useful for demonstrating the characteristic electrical phenomena of both above disorders. Low rates of stimulationamplitude of the muscleAP in rd th myasthenia gravis declines by at least 12% by the 3 or 4 stimulation with some mild recovery. MYASTHENIAGRAVIS LAMBERT-EATON “MYASTHENIC” SYNDROME PATHOLOGY -Post-SynapticAbnormalities -Pre-Synaptic abnormalities- Ca++ channels -Decrease of nACh receptors -Decreased Release ofAch at NMJ ETIOLOGY -Autoimmune -Autoimmune -Antibodies to nACh receptor-Antibodies to pre-synaptic Ca++ channels at terminal region of motor neuron ASSOCIATED TUMOR Thymoma (15%) Oat-cell carcinoma of lung (70%) SPEED OF ONSET Chronic SIZE OF EPP Less (fewer receptors) Less (fewerAch released, fewerAch migrate to connect with nACh receptors) SIZE OF MEPP Reduced Normal (unchanged) bc post- synaptic element is normal Consciousness Normal Normal C.L.M Normal Normal Sensory Normal Normal Autonomic Normal Abnormal (dry mouth) Motor Weakness that progressively Weakness- muscle strength worsens with muscle use improves with activity Cranial Nerves Normal cranial nerves. Normal Muscles innervated by cranial nerves (bulbar muscle) show -Proximal and Distal limb muscles appear to be affected weakness more than bulbar muscles -Ptosis (drooping of upper eyelid) -Voluntary muscles innervated by CN -Diplopia (double vision) -In brain stem- haven’t reached spinal cord yet -Dysphagia (difficulty swallowing) -Dysarthria (difficulty speaking) Region affected Peripheral Peripheral Demographics Affects all age groups (mean Affects older people (mean age of 20) age 55) Male/Female ratio (1:2) Male/Female ratio (10:1) Response to YES Minimal Anticholinesterases VASCULAR SYSTEM and STROKE The blood vessels to an organ provide it with a relatively constant supply of oxygen and other nutrients and a means for removal of metabolic wastes. (provide O2 to brain removal of CO2) Failure to meet these vital requirements results in disease in that organ. CEREBRALBLOOD FLOW: (for normal neural function, adequate blood flow and oxygenation must be maintained) -Cortical Gray Mater (cell bodies=metabolic center) Blood Flow is 4x6 times higher than cortical white mater (Axon=conducting element) -Brain supplied by 2 arterial systems (both connected through the circle of willis- interconnected): Carotid System: Vertebro-Basilar System: -Cerebral cortex perfused -provide blood to midbrain,cerebellum,brainstem -2 x 350 cc/min (left and right) -Also provides to part of occipital cortex -100-200cc/min Normal Cerebral Blood Flow: 750-1000cc/min 50cc/gm tissue Brain: 2% of body weight15% of Cardiac Output (resting state)20% of resting oxygen consumption (VO2) -↓Activation of neurons=↓Blood Flow -↑BrainActivity=↑Blood Flow to that area **In a hemodynamic system: blood flow is directly proportional to the perfusion pressure and inversely proportional to the total resistance of the system For the brain, this can be expressed by the equation: CBF=MeanArterial Pressure – Central Venous Pressure Cerebrovascular resistance *MAP is the most important factor on CBF* ↑MAP=↑CBF ↑CVP=↓CBF ↑CVR=↓CBF Factors that Modify Cerebral Blood Flow: 1.) Extracerebral Factors: Factors outside the cranial cavity that modify or regulate the CBF are primarily related to the Cardiovascular system. These include: 1.)Systemic Blood Pressure PvenousLOW Parterial most important factor 2.)Efficiency of Cardiac Output 3.)Viscosity of Blood (Thickness) ↑Viscosity, ↑Resistance, ↓Blood Flow Anemia= CBF ↑ 30% Polycythemia= CBF ↓ 50% through the resistance factor! 2.) Intracerebral Factors: The state of the Cerebral Vasculature also can influence CBF 1.)IntracranialArterial Disease (Atherosclerosis-Plaque)- ↑Resistance, ↓CBF 2.)↑Intracranial Pressure- ↑Pvenous, ↓CBF Normal pressure: 5-15 mmHg -If increases above 15, ↓CBF (Block in foramen, squeezes Blood vessels) Regulation of Cerebral Blood Flow: 1.) Neurogenic Control: Least important factor -SympatheticActivation (exercise/stress) produces vasoconstriction of blood vessels through norepinephrine BP increases so it is a protective mechanism against high BP and constricts blood vessel from expanding -ParasympatheticActiva
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