Study BIOL 472 Topic 3 Flash Cards
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Pile Management Card
BIOL 472 Topic 3
BIOL 472 Topic 3
| efferent neurons |
|
-somatic motor division (controls skeletal muscles) -autonomic motor division aka visceral (controls smooth and cardiac muscles, exocrine glands, some endocrine glands, adipose tissues) -PNS |
| LTP |
|
-hippocampus: memory pathways -glutamate stimulates (increases Ca into neurons to stimulate) -heavilty used neurons experience long term increase in effectiveness of operation -increased Ca uptake increase nuerotransmitter output -2nd messengers involved -activity at synapse induces sustained changes in quality/quantity of synaptic connections -glutamate important -NMDA channel -Ca+2 goes into cell -releases a paracrine that acts on presynaptic cell to release more neurotransmitter -postsynaptic cell also becomes more sensitive to glutamate (inserting more glutamate receptors in post synaptic membrane?) |
| presynaptic inhibition |
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-inhibition of Ca+2 channel openings, reduces amount of neurotransmitter released -decreases neurotransmitter released -changes synthesis of enzymes, membrane transporters, receptors |
| presynaptic facilitation |
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-stimulation of Ca+2 channel openings, more neurotransmitter released -increases neurotransmitter released |
| convergence |
|
-input from mult sources -summed input |
| NE deactivation |
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-Monamine oxidase (MAO) -from mitochrondria in nerve endings -many antidrpessants are MAO inhibitors Catechol-O-methyltransferase (COMT) -peripheral tissues (liver, kidney, etc.) -actively transported back to presynaptic terminal -either repackaged into vesicles or broken down by MAO |
| acetylecholinesterase |
|
degrades ACh choline transported back to axon terminal -in ECF -and in membrane of postsynaptic cell -choline actively transported back to presynaptic cell |
| neurotransmitter termination |
|
-diffuse away from synapse -inactivated by enzymes in the synatic cleft -transport into presynaptic cell or glial cells |
| alpha receptors for NE, E |
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-greater affinity for NE a1: stimulates constriction of smooth muscles, esp. in vessels a2: same and inhibition of preganglionic neurons (neurotransmitter inhibition) |
| Muscarinic |
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-smooth, cardiac muscles, glands -blocked by atropine (dilation of pupils) -CNS and autonomic parasympathetic division of PNS |
| nicotinic |
|
-neuron and skeletal muscles -nicotine stimulates -blocked by curare, muscles relaxation -skeletal muscle-type receptors (bungarotoxin binds, blocks irreversibly, causing paralysis) -neuron type receptors -nicotine is an agonist -found on skeletal muscles of automatic division of PNS and in CNS |
| gases |
|
-NO in learning/memory -neuronal damage during stroke -diffuses freely -binds to proteins -2-30 sec half life |
| opinoid peptides |
|
-enkephalins and endorphins (promotes sense of well-being) -mediate analgesia -pain relief |
| Substance P |
| -involved in pain pathways |
| amino acids are neurotransmitters |
|
-glutamate, aspartate--> excitatory in CNS; important in memory/learning -glycine, GABA--> inhibitory in CNS; Cl- channels open to hyperpolarize; valium enhances action; anesthetic action |
| biogenic amine neurotransmitters |
|
-catecholamines (NE, E, dopeamine) -serotonin -histimine -derived from single aas -all active in CNS |
| serotonin |
|
-derived from tryptophan -catabolized by MAO -excitatory for muscle -inhibitory for sensation -activity low during sleep, high during activity -LSD stimulates action, 5-HT receptors -psilocybin analog -prozac inhibits reuptake of serotonin -aka 5-HT |
| acetylecholine synthesis |
|
-choline plus acetyl CoA -mediated by coline acetyltranferase -choline small molecule that's recycled -takes place in axon terminal |
| acetylcholine |
|
-parasympathetic stimulation -(cardiac rate inhibitor, lower BP, GI stimulation) -neurotransmitter for neuromuscular junction (voluntary action for skeletal muscles) -2 post synaptic cholinergic receptors: muscarinic and nicotinic |
| PNS neurotransmitters |
| -ACh, NE, E |
| CNS neurotransmitters |
| -acetylecholine, amines, aas, purines, gases, peptides, lipids |
| chemical synapses |
|
-30-50nm -begins w/ AP -accounts for most delays in signal transduction -0.5msec -vast majority -initiates electrical response or 2nd messenger -neurotransmitter synthesis takes place in nerve cell body or axon terminal (terminal doesn't have organelles for protein synthesis) -vesicles "docked" at active zones along membrane closest to cleft |
| electrical synapse |
|
-2-3nm -gap junction -electrical current -crosses w/o chemicals -pass electrical current directly from one cell to cytoplasm of other via gap junctions -info flows in both directions -mainly in neurons of CNS -rapid conduction -also, chemical signal molecules diffuse b/w adjacent cells |
| postsynaptic cells |
| -can be neuron or non-neuron |
| too much/little K+ |
|
-shift resting membrane potential up -respond to smaller ESPSs if too low, won't respond to ESPSs as usual and muscle weakness occurs--> Gatorade! |
| MS |
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-demyelinating disease -fatigue, muscle weakness, loss of vision -autoimmune disorder? -depolarizations must be stronger to work |
| speed of APs |
|
-diameter of axon and reistance of axon membrane to ion leakage -larger diameter, less resistance -myelin sheath prevents ions from flowing out; limits contact w/ ECF Nodes: -each nodes has lots of Na+ voltage-gated channels -keep AP up as goes throgh axon -saltatory conduction lets APs jump from node to node |
| reasons potentials lose stength |
|
-current leak: + charges move out -cytoplasmic resistance: cytoplasm resists flow of electricity -must reach trigger zone at threshold voltage so Na+ voltage-gated channels open and AP occurs -or, just died out along axon |
| graded potentials |
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-open chemically gated ion channels -allows ions to enter/leave -or, mechanical stimuli -ex: K+ channels can close and depolarize the cell EPSP -stength of initial depolarization depends on how much charge enters teh cell (if more Na+ channels open) -diminish in stength |
| autonomic motor division |
|
- aka visceral nervous system b/c it controls various internal organs -divided into sympathetic and parasympathetic |
| PNS |
| -afferent and efferent |
| CNS |
|
brain and SC -integrate info of afferent PNS and determines if a response needed |
| long term depression |
|
-NO implicated -may be opposite of LTP |
| neuropeptides |
|
-endogenous opinoids: endorphins, enkephalons (analgesic actions reduce pain) Substance P: afferent( sensory) neurons; pain, nervous immune system link (arthritis) |
| MAO |
| -breaks down Serotonin, NE, and E |
| parkinson's disease |
|
-substantia nigra where dopamine produced -lack of dopamine -shakes, can't initiate mvt -L dopa therapy |
| dopamine |
|
-CNS -pleasure pthways -motor pathways -analogs: metamphetamine, peyote, -cocaine inhibits uptake of dopamine -parkinson's disease |
| ANS parasympathetic pathways |
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-distribution via cranial nerves and pelvic nerve from sacral region of SC -crancial nerves II, VII, IX, X< have 90% of body's parasympathetic fibers preganglionic fibers: ACh postganglionic fibers: ACh (cholinergic muscarinic receptors on target tissue |
| ANS sympathetic pathways |
|
-thoraiclumbar region of spine -use sympathetic chain ganglia via ventral root to blood vessles, sweat glands, hair -collateral ganglia to viscera (heart, GI, kidney) -runs parallel to spinal cord preganglionic fibers: ACh postganglionic fibers: NE (adrenergic receptors (a or b) on target tissue |
| somatic nervous sytem |
|
-ACh -nicotinic receptors |
| beta receptors for NE, E |
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-greater affinity for E b1: stimulates heart rate, contractility, kidney and fat lyposis b2: inhibits (relaxes smooth muscle) esp. in lung, heart, skeletal muscle, blood vessels |
| E, NE general action |
|
-sympathetic stimulation -cardiac rate stimulator, increase BP, inhibit GI tract -E, NE have different actions depending on receptor type |
| adrenergic fibers |
| -nerve tracts using E, NE |
| amine synthesis |
|
-from dietary tyrosine -tyrosine hydroxylase makes Dopa -Dopa decarboxylase makes dopamine -dopeamine B-hydroxylase makes NE -N-methyltransferase makes E (mostly a hormone) |
| zyban |
|
-general antidepressant -dopamine reuptake inhibitor |
| chantix |
|
-ACh antagonist/agonist -suicide noted |
| nicotrol |
| -nicotine replacement therapy for ACh receptor activation |
| alzheimers |
| -ACh synthesis down |
| myasthenia gravis |
| -few ACh receptors due to autoimmune degradation |
| botox |
| -prevents ACh release |
| sarin |
|
VX nerve gas -AChE inhibitor -asphyxiation -prevents mvt of diaphragm -2 part autoinjector: -atropine: blocks ACh stimulation -pralidoxime: regenerates bound AChE |
| temporal summation |
| -2 impulses in rapid succession |
| spatial summation |
| 2 impulses at same time |
| IPSP |
|
Fast: increase in Cl- conductance Slow: increase in K+ conductance |
| EPSP |
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-activating neurotransmitter mediated channels -moves cell closer to threshold -easier to depolarize -hypopolarizes cell Fast: increase in Na+ conductance Slow: decrease in K+ conductance |
| synaptic delay |
| -time neurotransmitter takes to cross synapse |
| antidromic |
| axon to cell body 0.1% |
| orthodromic |
| cell body to axon 99.9% |
| axon terminal |
| aka bouton aka presynaptic terminal |
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