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Neurotransmission
| Question | Answer |
|---|---|
| Resting Membrane Potential | the electrical charge difference across a plasma membrane. It is -70mV in an unstimulated, resting neuron |
| what does a RMP of -70mV imply about the membrane of a neuron? how does entering sodium ions change this? | means there are more negatively charged particles on the inside than on the outside of the membrane. Na+ coming in through membrane/diffusing across the soma depolarizes (makes more positive inside) |
| SPP | Sodium potassium pump: mechanism that uses ATP to push relatively more sodium out (than the amount of potassium it takes in), allowing outside of membrane to be slightly more positive than inside. |
| what does SPP move in and out of cell, specifically? | SPP pumps 3 Na+ out for every 2K+ it brings in |
| SPP must work continually to restore equilibrium of ions in cell. What two functions does it serve? | 1)continually compensates for ion leakage (1 in a million sodium will occassionally leak in, K+ leaks out.) 2) every signal genratd by a neurn slightly upsts the distr of Na+ & K+. Once nerve transmission is complete, SPP switches Na+ & K+ back 2 strt po |
| action potential | a rapid & more dramatic up-and-down shift in membrane voltage in which PM briefly reverses electrical polarity. produced by voltage-gated ion channels in membrane, it has a self-propagating effect that produces a traveling wave of excitation in neurons |
| where do action potentials occur? | APs occur only where there is a high enough density of voltage-gated channes, i.e. in the axon hillock or "trigger zone" |
| draw an action potential | start w graph of voltage vs time. dotted lines at -70 mV (RMP), -55 (threshold pot) and +30 (peak of voltage). straight at -70, slowly climbs 2 thresh, spikes 2 +30 (depolariz) & falls back down (repolariz), neg. overshoot (hyperpolar) then back to RMP |
| depolarization: definition and when does it happen during AP | any shift in elect pot across plasma membrane toward a voltage more pos than RMP(occurs when Na+ ions flood into membrane). on graph =from RMP thru the local pot approaching threshold and all the way to its peak at +30 mV when Na+ gates finally close |
| repolarization: definition and when does it happen during AP | reattainment of the RMP after neuron has depolarized. happens when K+ flood out of cell (from peak voltage back to RMP) |
| hyperpolarization: definition and when and why does it happen during AP | shift in elect pot across plasma memb 2 a value more neg than RMP, tending 2 inhibit a nerve cell from firing. after repolariz back 2 RMP, there is a brief negative overshoot due to K+ channels closing more slowly (more K+ exits than amount of Na+ entered |
| threshold potential | the minimum local potential voltage needed to open voltage-gated channels at the trigger point/axon hillock. |
| in AP graph, explain the steadily rising line from RMP to threshold | Na+ ions arrive at axon hillock, depolarizing membrane at that point. appears as a steadily rising local potential |
| in AP graph, explain the steeply shooting line up to peak | DEPOLARIZATON: local potential is able to meet threshold at the region of the axon hilock. Neuron now "fires" or produces AP. voltage-gated S chan open quickly, while K ch open more slowly. membrane voltage rises rapidly. |
| explain a positive feedback loop in terms of rapidly rising membrane voltage during | neuron is depolarized to threshold and "fires": Na+ channels open at axon hillock. Na+ floods into cell, further depolarizes the membrane, stimulates still more voltage-gated Na channels to open and admit even more Na+ etc etc |
| explain the peak of the AP graph | as rising potential passes 0 mV, Na+ channels are inactivated and begin to close. By the time they close and Na+ flow ceases, the voltage peaks at approx +30 mV. membrane is now pos on inside and neg on outside (polarity has reversed compared to RMP) |
| explain steeply declining line of AP graph | "REPOLARIZATION: by the time voltage peaks, slow K+ channels are now fully open. K+ ions, repelled by the positive ICF, flood out of the cell, repolarizing the membrane |
| explain the dip below RMP on AP graph, and how is it remedied? | HYPERPOLARIZATION K channels stay open longer than Na+ channels. = slightly more K+ flows out of cell than amount of Na+ entered. causes slight neg overshoot past RMP. it is eventually fixed by SPPs, Na+ leaking in and astrocytes removing xtracellular K+ |
| local potential what is it and how does it lead to AP | a short-range change in voltage across a neuron's membrane. incoming Na+ diffuses for short distances along the inside of plasma membrane. produces a current that travels from pt of stim towards the trigger zone. |
| explain a synapse, what kind of potential does it generate. | Interaction of a stimulant or neurotransmitter (ACh) with its receptors in the postsynaptic membrane opens chemically regulated gates & depolarizes that region of the membrane (creating excitatory postsynaptic potential) |
| EPSP | excitatory postsynaptic potentials: depolarize the postsynaptic membrane and make a neuron more likely to "fire" or produce an AP. |
| draw an EPSP | -70 and -55 dotted. two small waves, one slightly higher but neither reaches threshold, always reverses to RMP. arrows marking 2 stimuli. |
| example of neurotransmitter that sends off EPSP | ACh |
| IPSP | inhibitory postsynaptic potentials. hyperpolarize the postsyn memb, making it more neg (i.e. from -70 to -90). this inhibits a neuron, making it less sensitive and less likely to produce an AP. |
| two examples of neurotransmitters that send of IPSPs, how do they do this? | GABA & glycine: both open Cl- channels. |
| GABA | most prevalent neurotransmitter in brain. opens Cl- channels. involved in motor control |
| example of why you would need IPSPs. | if you want to flex your arm using your bicep, you want to inhibit your triceps (the extendor) |
| draw an IPSP | start at RMP and decline toward -90. |
| compare stimulus-to-voltage relationship in local and AP | local is GRADED while AP is all or none |
| compare reversibility in local and AP | local is reversible and AP is irreversible |
| compare strength of voltage over distance in local and AP | local is decremental, AP is nondecremental |
| compare distance of effect for local and AP | local is local and AP is self-propagating |
| compare voltage change in local and AP | local can be positive (depolarizing) voltage change (ex: EPSPs) or negative (hyperpolarizing) voltage change (ex: IPSPs). while APs always begin with depolarization |
| compare the location of local vs APs (where are they produced) | local potentials are produced by gated channels on dendrites & soma. APs are produced by voltage-gated channels on trigger zone (axon hillock) & along the axon |
| local potentials are graded. what does this mean | strength of signal voltage is proportional to stimulus strength |
| APs are all or none. what does this mean? | an AP either does not occur at all OR the neuron fires and exhibits the same peak voltage regardless of stimulus strength. (this only happens if stimulus depolarizes the neuron to threshold). |
| local potentials are reversible. what does this mean? | they return to RMP if stimulation ceases before threshold is reached |
| APs are irreversible. what does this mean? | an AP goes to completion once it begins |
| local potentials are decremental. what does this mean? | signal strength grows weaker with distance |
| APs are nondecremental. what does this mean? | signal maintains the same strength, regardless of distance |
| local potentials are "local" only, what does this mean? | a LP has effects for only a short distance from its point of origin. |
| APs are self-propagating. how does this relate to distance? | AP has effects a great distance from point of origin |
| refractory period | period of time (during an AP and shortly thereafter) in which it is difficult or impossible to restimulate that region of a neuron to fire again. |
| what are the 2 phases of the refractory period? | absolute refractory period and relative refractory period |
| absolute refractory period: | during the time that sodium gates are open, the membrane cannot respond to any subsequent stimulus, regardless of its strength. |
| relative refractory period, definition and when does it end? | if a second stimulus is applied while potassium gates are open (membrane is repolarizing), only a strong stimulus can depolarize the membrane & produce a 2nd AP. this period ends after hyperpolarization is finished |
| draw absolute and relative refractory periods | draw the AP graph. absolute is zone when sodium gates are open (so from when it reaches threshold to right after peak when they close). relative zone is while potassium gates are open, so from beginning of repolarization all the way ot end of hyperpolariz |
| explain signal conduction in unmyelinated nerve fibers ..continues until traveling signal reaches end of axon | these fibers have voltage-gat chan along its entire length. when AP occurs at trigg zone, Na floods in and diffuses for short distance just beneath PM. the resulting depol excites v-gated chan immediately distal to AP, and new AP is produced. chain rxn... |
| an action potential in progress: what does this imply about that specific region of unmyelinated fiber? | implies that the membrane polarity is reversed a this region. |
| since depolarization will excite voltage gated channels nearby, why doesn't a signal travel backwards towards soma? | there is a refractory membrane that trails just behind the AP; since it is difficult to restimulate this region to fire again, this prevents the nerve signal from going backward towards the soma |
| there are regions of unmyelinated fiber that consist of "excitable membrane" what does this mean? | these regions are fully polarized, and ready to respond to stimulus. |
| is an AP a traveling nerve signal? explain | AP is NOT a nerve signal. the AP itself is an electrical current but does not travel along an axon rather, it stimulates production of a new AP in the membrane just ahead of it. |
| nerve signal | traveling wave of excitation produced by self-propagating action potentials (its a chain rxn of APs) |
| APs in unmyelinated fibers: pro and con? | these are slower in unmyelinated fibers, but they will cover extensive distances since they are self-propagating and don't lose strength. |
| explain why the nerve signal is not like electricity through a wire, and more like a burning fuse. | elec thru a wire loses strength. the NS is nondecr, it is an elect current but prod from separate, self-prop APs that are regenerated along the axon's length. They R prop w/out decreasing amplitude (signal maintains same strength regardless of distance) |
| saltatory conduction | signal conduction in myelinated fibers |
| signal conduction in myelinated fibers is: | saltatory conduction |
| explain saltatory conduction. what happens at nodes of Ranvier? | ions can be exchanged with ECF only at the nodes of Ranvier. At these points, the Na+ inflow generates self-propagating AP's down the exposed axon's length. (nondecremental, but slow) |
| explain saltatory conduction, what happens at internodes? | nerve signal travels by rapid diff of Na+ along inside of the insulated axolemma until it reaches the next node of Ranvier. (this process is fast but decremental) at this point the diffusing Na+ causes excitation of volt-reg gates & will generate next AP |
| explain the jumping grasshopper | APs only occur at the nodes of Ranvier, therefore the traveling nerve signal (i.e. the chain rxn of APs at these nodes) appears to "jump" from node to node. |
| how many neurotransmitters are there? | there are 100 substances known to be neurotransmitters |
| neurotransmitters in CNS? | ACh, NE, DA, GABA |
| ACh | acetylcholine. 1st known neurotransmitter |
| NE | norepinephrine |
| DA | dopamine |
| which neurotransmitters produce EPSPs and which produce IPSPs? | excitatory: ACh, NE, DA inhibitory: GABA |
| neurotransmitter | a chemical in the distal end of an axon; when a nerve signal reaches this point it triggers release of NT into synaptic cleft, which stim a new wave of electr activity in the postsynaptic neuron |
| presynaptic neuron | signals arrive at the synapse by way of the presynaptic neuron, (which releases neurotransmitter) |
| postsynaptic neuron | the next neuron which responds to release of NT, generating a new chain rxn of APs down its fiber. |
| draw a typical synapse ..opening producing local EPSP that travels downward toward axon hillock | end bulb, synaptic gap, dendrite. label pre and post synaptic membr. arrows show elect signal, Ca++ channel opening, multiple vesicles w NT, Ca causes ves 2 open, NT cross cleft and fit w receptors, enzymes breaking down, pieces going back inNa chan.. |
| describe Ca gates in synapse | arrival of nerve signal at end bulb opens voltage-gated calcium channels |
| describes Ca effect in synapse | Ca enters the bulb & triggers exocytosis of the synaptic vesicles, releasing ACh |
| describe path of ACh once released | ACh diffuses across synaptic cleft and binds to receptors in the post syn M. this changes perm of membr. causing channels to open and allowing Na to flow in and K to flow out |
| explain production of EPSP by ACh, what happens to Na flow? | as Na enters cell, spreads along inside of p mem & depolarizes it, producing a local pot = EPSP. like other LPs, if this is strong and persistent enough (enough Na current makes 2 ax hill) it opens V-gated chann in T zone and causes postsyn neuron 2 fire |
| explain AChE, what is it and what is its role in cholinergic synapse? | enzyme "acetylcholine esterase" breaks down acetylcholine in synaptic gap. broken down bits are then taken back into end bulb and remade |
| cholinergic synapses.. | use ACh |
| adrenergic synapses: | use NE |
| what synapse uses ACh? | cholinergic synapse |
| what synapse uses NE | adrenergic synapse |
| summation what is it and where does it occur? | additive effect; process of adding up postsynaptic potentials and responding to their net effect. occurs in the trigger zone |
| what two summations are EPSPs capable of? | temporal summation & spacial summation |
| temporal summation | same place on dendrite, one after the other. (a single presynaptic neuron stimulates postsynaptic neuron so intensely that its EPSPs add up to threshold at the trigger zone and make it fire |
| draw temporal summation on the cell | draw neuron, 3 arrows to one dendrite |
| draw temporal summation on a graph | start at -70, 3 stairsteps to threshold (show three arrows point to three separate stimuli at diff times) |
| spatial summation | same time, different places on dendrites (multiple inputs stimulate postsyn neuron, each may only produce mod stim but collectively they prod enough EPSPs to add up to threshold at the trigger zone and make it fire |
| draw spatial summation on nerve | draw neuron w three different arrows pointint to three different dendrites at same time |
| draw spatial summation on graph | flat line at RMP, then straight up to threshold (one arrow shows collective stimuli at same time) |
| neurons routinely work in groups to modify each other's actions. what 2 process do they use to do such? | facilitation & presynaptic inhibition |
| facilitation | one neuron enhances the effects of another neuron |
| example of facilitation? | neuropeptides (closely related to neurotransmitters), these reg or mod the actions of neurotransmitters. 2 neuropeptides are substance P and endorphins |
| 2 neuropeptides? | substance P and endorphins |
| substance P | a neuropeptide. found in sensory nerves & spinal cord. facilitates transmission of pain sensation to brain |
| endorphins | neuropeptides. inhibit the perception of pain to brain |
| presynaptic inhibition | the amount of excitatory neurotransmitter (i.e. ACh) released at an end bulb is decreased or stopped by another inhibiting neuron. |
| draw presynaptic inhibition | draw neurons I II and III. inhibitory neuron I has axoaxonal synapse, show release of neurotransmitter to axon of II. arrows down II are inhhibited by -IPSP. show no neurotransmitter relased by II |
| axoaxonal synapse | presynaptic end bulb synapses w axon of postsynaptic neuron |
| axonal transport | the two-way passage of proteins, organelles & other materials along an axon. |
| why does axonal transport exist? | all proteins needed by a neuron must be made in soma, yet many are needed by axon so the materials must be transported. |
| anterograde transport | movement away from soma down the axon |
| movement away from soma down the axon: | anterograde transport |
| retrograde transport | movement up the axon toward the soma |
| movement up the axon toward the soma? | retrograde transport |
| slow axonal transport: what is the rate & which direction can it go | .5-10 mm/day. anterograde only |
| fast axonal transport: what is the rate and which direction can it go | 200-400 mm/day. anterograde & retrograde |
| how does nervous system get invaded? which pathogens do this? | some pathogens exploit fast axonal transport process (retrograde) to invade nervous system. i.e. herpes, rabies, tetanus and polio |
| how many SPPs in a typical neuron? how many ions are transported? what does this mean? | 1 million SPPs in a typical neuron, which transport nearly 200 million ions/second. SO Na+ and K+ depolarization and repolarization can be corrected very quickly |
| SPP & ATP? implication for brain? | the SPP accounts for about 70% of the ATP (energy) requirement of the nervous system. This is why the brain demands such high levels of glucose and oxygen, and why you would go unconscious after mere minutes without oxygen (nervous system is VERY active |
| explain why APs are not "conducted", also implication for distance | they are "propagated". each one is a separate, complete event that is regenerated along the axon's length. has effects great distance from point of origin. |
| explain nondecremental | APs are propagated without decreasing amplitude. signal maintains same strength regardless of distance traveled |
| during resting stage, what is going on? | during resting stage (-70mV), all voltage-gated Na and K channels are closed. (leakage channels are always open) |
| propagation rates of thin, unmyelinated fibers | can send info up to 2 meters/sec. |
| walking grasshopper? | analogy for signal conduction of thin, unmyelinated fibers (very slow) |
| jumping grasshopper? | analogy for signal conduction of thick, myelinated fibers (very fast, signal appears to "jump" from node to node |
| what are signals in unmyelinated fibers used for? | these mediate/send slower visceral responses |
| example of signal in unmyelinated fiber | autonomic fibers to smooth muscle and heart |
| propagation rates of thick, myelinated fibers (how does this compare to unmyelinated) | send info from 70-120 meters/sec. they are 30x faster! |
| what are signals in myelinated fibers used for? | involved in quick stretch reflexes in skeletal muscle (such as postural muscles, which are a quick response by skeletal muscle to correct posture) |
| how much ACh is in a synaptic vesicle?what does this do? | synaptic vesicles contain up to 10,000 molecules ACh each. so ACh will very quickly diffuse out by exocytosis, cross the narrow synaptic cleft & binds to receptor proteins which are built into post-synaptic membrane |
| excitatory neurotransmitters: do they produce APs? | they do not directly produce APs, they produce depolarizations (or local potentials, EPSPs) that will indirectly produce APs if strong or persistent enough. |
| flaccid paralysis | muscles are completely relaxed, cannot move |
| spastic paralysis | all muscles are completely contracted, clenched, so cannot move |
| what two chemical agents/toxins can affect nerve transmission? | curare & tetrodotoxin. |
| what 5 diseases affect nerve transmission? | botulism, polio, tetanus, MG (myasthenia gravis) and MS (multiple sclerosis) |
| curare | arrowhead poison used by So American natives to hunt. Blocks ACh receptors in muscle (by mimicking ACh). causes flaccid paralysis (diaphragm stops working) |
| botulism | disease. (botulin= toxin, the most potent microbrial toxin known. It blocks the relase of ACh in presynaptic membrane. flaccid paralysis. |
| polio | virus that destroys motor neurons, kills cell body. flaccid paralysis |
| tetrodotoxin | toxin comes from the skin and internal organs of the puffer fish. Highly specific sodium channel blocker. flaccid paralysis |
| tetanus | disease i.e. "lock jaw". the toxin is tetanospasmin. it blocks receptors at inhibitory synapses in nerve pathways supplying skeletal muslce. resulting in muscle seizures and spasms. causes spastic paralysis. |
| what is the toxin of botulism? | botulin |
| toxin of tetanus? | tetanospasmin |
| MG | myasthenia gravis. progressive degenerative autoimmune disease, leads to generalized muscle weakness. body develop antibodies to neuromuscular junction area. (takes down the receptors). |
| MS | multiple sclerosis. progressive degenerative auto immune disease, leads to generalized muscle weakness. myelin sheaths are destroyed. |
Created by:
kalmetina
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