Student Neurology Microanatomy Physiology PDF
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Uploaded by DistinctivePromethium
AHS 2202
Dr. Jacqueline Mobley
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Summary
These notes cover neurology microanatomy and physiology, including neurons, synapses, and neurotransmitters. The document also covers related topics like depolarization, repolarization, and the sodium-potassium pump. It's suitable for undergraduate-level study.
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NEUROLOGY MICROANATOMY & PHYSIOLOGY Dr. Jacqueline Mobley AHS 2202 Neurons are the functional unit of the nervous system High O2 requirements NEURONS Neurons cannot reproduce via mitosis Neurons can regenerate cell processes...
NEUROLOGY MICROANATOMY & PHYSIOLOGY Dr. Jacqueline Mobley AHS 2202 Neurons are the functional unit of the nervous system High O2 requirements NEURONS Neurons cannot reproduce via mitosis Neurons can regenerate cell processes if the cell body is intact Neurons receive & transmit impulses BASIC NEURON STRU CTURE Cell body: Soma or perikaryon Dendrites: receive signals from the body Axons: transmit signals to the body Dendrites are referred to as afferent processes Numerous and branching Axons are referred to as efferent processes Singular extension from each neuron A single nerve is a bundle of many axons NEURONS CONTINU ED Axons are covered in a fatty sheath called myelin The white appearance of myelin gives “white matter” its name This Phot o by Unknown Author is licensed under CC BY-NC-ND NEU RONAL S UPPORTING C EL LS Neuroglia AKA “glial cells” Outnumber neurons 10:1 Helps neurons to function Oligodendrocytes Specialized glial cells in the brain and spinal cord Produce myelin Schwann cells Specialized glial cells in the peripheral nerves Produce myelin MYELIN SHEATH Oligodendrocytes and myelin cells Form a tight wrap around the axon Line the axon end to end Node of Ranvier The small gap between each Schwann cell or oligodendrocyte The myelin and the gaps function to increase the speed of conduction of nerve impulses Myelinated is faster than unmyelinated nerve sheaths AFFERENT IMPULSES Afferent nerve fibers Conduct the impulse from the periphery to the CNS Typically sensory in nature Efferent nerve fibers Conduct the impulse from the CNS to the periphery Typically motor in nature This Phot o by Unknown Author is licensed under CC BY-SA The actual physical nerve is a bundle of afferent & efferent axons Sensory nerves only have sensory nerve fibers Motor nerves only have motor nerve fibers Mixed nerves have a mixture of sensory & motor nerves Somatic nervous system Conscious Involves both motor and sensory nerves Motor nerves sense impulses to skeletal muscle Autonomic nervous system Unconscious Involves both motor and sensory nerves AUTONOMIC VS. Motor nerves send impulses to smooth muscle, cardiac muscle & glands SOMATIC This Phot o by Unknown Author is licensed under CC BY-NC-ND DEPOLARIZATION & REPOLARIZATION When a nerve is returning to its A nerve “firing” is a resting state is depolarization undergoing repolarization SODIUM POTASS IU M ATPASE PU MP At rest the neuron is polarized The sodium-potassium ATPase pump maintains the state of polarization 2 K ions are pumped from outside the membrane to inside the cell 3 Na ions are pumped from inside the membrane to outside the cell The membrane is “polarized” because one side is more positively charged (outside) and one side is more negatively charged (inside) RESTING MEMBRANE POTENTIAL Resting membrane potential The difference of electrical charge across the neuron cell membrane The net charge of the resting membrane is -70 mV This Phot o by Unknown Author is licensed under CC BY-SA DEPOLARIZATION 1) A nerve is stimulated by another nerve impulse or sensation (touch, heat, etc) 2) Sodium channel on the membrane OPENS 3) Sodium flows into the cell via diffusion and to establish electrical neutrality Depolarization The opening of sodium channels and the sudden influx of many sodium ions into the cell (“Action Potential”) The inside of the cell goes from -70mV to positive charge The change of electrical charge from negative to positive REPOLARIZATION Almost immediately after Na channels open, they close K channels open at the same time K ions passively diffuse out of the cell through the channels Flow via the concentration gradient and to away from the positive charge within the cell The positive charge in the cell returns to a negative charge as K leaves K channels nearly immediately close Repolarization The change of the cell’s charge back toward the net negative resting membrane potential Both states have a positive outside and negative inside Resting membrane potential K inside, Na outside REPOLARIZATION VS. THE RESTING Repolarization STATE K outside, Na inside How to go from repolarization to resting membrane potential? Na-K ATPase pump restores order D E P O LA RI Z AT I O N TH RE S H OL D , N E RV E I M P U L SE , C O N D U C TI ON A N D A L L - O R- NO TH ING P RIN CIPL E Does every stimulus result in depolarization? No. Stimulus threshold must be met to cause depolarization Threshold stimulus A threshold of intensity of the stimulus to This Phot o by Unknown Author is licensed under CC BY-SA generate a depolarization If a weak stimulus occurs, Na channels open, but not many, depolarization does not occur WAVE OF DEPOLARIZATION What happens when a stimulus is successful at opening sufficient Na ion channels? Adjacent ion channels open, too Channels adjacent to those channels open A wave of depolarization occurs This can also be called conduction of the action potential In practical terms, this is known as a “nerve impulse” When a stimulus reaches its threshold, the impulse will be generated along the axon THE ALL- OR- with uniform strength NOTHING A strong stimulus and a weak PRINCIPLE impulse will generate the same impulse so long as threshold is met REFRACTORY PERIOD The refractory period is the time in which the nerve is incapable of making another impulse The refractor period is when the Na or K channels are open The cell must finish the depolarization-repolarization cycle Relative refractory period The cell is refractory to normal intensity stimuli, but a very strong stimuli may cause a depolarization This can only occur toward the tail end of repolarization If depolarization occurred from one end of the neuron to the other, it would take a long time Myelin coating prevents Na from flowing across the neuron except at thegaps of the myelin sheet (Nodes of Ranvier) Saltatory Conduction Instead of ion channels opening slowly, they occur only at the Nodes of Ranvier SALTATORY This has the effect of conduction jumping from one node to the next CONDUCTION MULTIPLE S CLEROSIS Autoimmune disease in humans Schwann cells are damaged Destruction of the myelin sheaths Decreased ability to conduct impulse quickly down the axon Sensory and motors deficits occur This Phot o by Unknown Author is licensed under CC BY HOW NEU RONS COMMUNIC ATE: THE SYNAPSE The synapse is the junction between 2 neurons or a target cell The junction is a gap (synaptic cleft) where there is no physical contact between the 2 cells Telodendron A branched structure at the end of the presynaptic neuron Each branch has a terminal bouton, synaptic end bulb or synaptic knob Mitochondria powers activity here Vesicles containing neurotransmitters live in the knob This Phot o by Unknown Author is licensed under CC BY SYNAPTIC TRANSMISSION 1. Depolarization reaches the synaptic knob 2. Calcium channels open 3. Extracellular calcium enters the synaptic knob 4. Vesicles fuse with the knob’s cellular membrane 5. Vesicles release neurotransmitters into the synaptic cleft 6. Neurotransmitters diffuse across the synaptic cleft Neurotransmitters bind to receptors on the postsynaptic membrane PO ST SY NA PTI C M EM BR AN E Binding of neurotransmitters results in the action of the target cell or generation of a new action potential EX CITATORY & INHIBITORY NEUROTRANSMITTERS Two types of neurotransmitters Excitatory Usually cause an influx of sodium to move postsynaptic membrane to threshold Inhibitory Usually hyperpolarize the postsynaptic membrane Open Cl & K channels to allow Cl- in and K+ out Inside of cell becomes more negatively charged This Phot o by Unknown Author is licensed under CC BY-SA Makes it harder for another impulse to occur NEUROTRANSMITTERS Some neurotransmitters are inhibitory or excitatory depending on the cell Acetylcholine (ACh) is both Excitatory at the neuromuscular junction Inhibitory at the parasympathetic nerves of the heart (slows heart rate) Catecholamines Norepinephrine Dopamine Epinephrine Norepinephrine Fight-or-flight of the nervous system Epinephrine Released from adrenal medulla C ATECHOLAMINES Fight or flight Dopamine Brain Autonomic functions & muscle control Parkinson’s → deficiency in dopamine Inhibitory neurotransmitters Gamma-aminobutyric acid (GABA) Found in the brain GABA & Some drugs (valium, gabapentin) GLYCINE increase GABA in the brain Increasing GABA inhibits brain activity Glycine Primarily in the spinal cord Slug bait toxicity “Shake & bake” Pathophysiology – reduces inhibitory neurotransmitter GABA, lowers seizure threshold C LI NI C AL by affecting other neurotransmitters C A SE : Clinical signs: Severe muscle tremors, M ETAL DE HYD E hyperesthesia, tachycardia, hyperthermia TOX IC IT Y Treatment: Gastric lavage, activated charcoal (if safe to do so), diazepam, supportive care, intralipid Prognosis: Most fully recover in 2-3 days, assuming prompt treatment and no progression to DIC (disseminated intravascular coagulopathy) CLINIC AL C ASE: OTHER NEUROTOXINS Pesticides Strychnine → inhibits glycine in the spinal cord Permethrins → affect sodium channels Cats especially sensitive Bromethalin → demyelination and cerebral edema Rat bait No antidote This Phot o by Unknown Author is licensed under CC BY-SA Ivermectin → increased inhibitory effect of neurotransmitters CL INIC AL C ASE : G ABAPENTIN Extremely fractious cats Fear not! Gabapentin 100 mg sprinkled onto food the night before, 100 mg the morning of appt Some cats need 150-200 mg per dose Increases effect of gaba in the brain, which is inhibitory Sedation More relaxed and compliant This Phot o by Unknown Author is licensed under CC BY-NC-ND STOPPING AND RECYCLING THE NEUROTRANSMITTER Neurotransmitters should not stay in the synaptic cleft indefinitely How is breakdown/removal of neurotransmitter accomplished? Enzymes! Acetylcholine → acetylcholinesterase Synaptic knob reabsorbs breakdown products & repackages them in vesicles Organophosphates (common pesticides) inactivate acetylcholinesterase Overstimulation of acetylcholine receptors occurs RECYCL ING NEU ROTRANS MITTERS Norepi Monoamine oxidase (MAO) breaks down norepi in the synaptic knob Catechol-O-methyl transferase (COMT) breaks down norepi in the synaptic cleft Some human antidepressants work to inhibit MAO & COMT CLINIC AL C ASE: MYASTHENIA GRAVIS MG is a disease resulting in muscle weakness Pathophysiology: Autoimmune destruction of the acetylcholine receptors on the postsynaptic membrane Congenital deficiency in ACh receptors Clinical signs: Megaesophagus, progressive exercise weakness Diagnosis: ACh antibody test, Tensilon test (temporarily decreases breakdown of ACh) Treatment: Pyridostigmine bromide prolongs ACh in the synaptic cleft. Steroids if https://vetneuromuscular.ucsd.edu/cases/2010/July.html autoimmune. THE END