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62 Cards in this Set
- Front
- Back
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what is the organelle composition of the presynaptic nerve terminus?
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mitochondria rich for energy, many vessicles, few lysosomes, and no ribosomes (proteins must be transported down axon from cell body)
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where does synthesis of the NT's usually occur?
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in the presynaptic terminus. It may uptake a complete NT or it may uptake precursors and use enzymes to make the NT.
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Does the reuptake system in pre synaptic neurons place the NT's directly into the storage vesicles?
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No there is a second system that puts them into the vesicles.
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Release of NT's is primarily via exocytosis. What NT's may use transporter systems to be released?
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amino acid NT's
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Describe uptake 1.
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It is reuptake to the presynaptic cell via a sodium dependent mechanism that has a much greater affinity for the NT in order to halt signaling quickly.
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Describe uptake 2.
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This is uptake of NT that "escaped" the synapse. It is sodium independent and is carried out by glial cells and other neurons. Its likened to a garbage disposal.
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describe the "kiss and run" theory of excocytosis.
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vesicles are emptied partially of NT and then recycled with some contents via endocytosis
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describe electrical synapses
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presynaptic and postsynaptic neurons are connected via gap junctions and ions travel through to potentiate the signal
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what is the role of presynaptic autoreceptors?
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feedback to alter release of NT.
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what are the advantages and disadvantages of chemical neurotransmission?
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advantages include signal amplification, positive or negative responses, graded responses, and chemical coding
disadvantages include the complex machinery with high energy demands. |
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how are peptide NT's transported?
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they are made in the cell body and must be transported down to the synapse. this is time consuming and thus these are not used as often as the typical amine receptors
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1. how are peptide NT's released?
2. Whats their speceficity and their affinity? 3. How are they inactivated? |
1. via exocytosis
2. they have a very high affinity because they are very specefic to their receptor 3. via degradation not reuptake. |
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what is dale's principle?
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All terminals of the same neuron release the same NT or NT's. (thus cholinergic, adrenergic, etc.)
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What are 4 requirements for maintaining the Vm?
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electrical neutrality, selective permeability of membrane, osmotic neutrality, and active transport of sodium and potassium.
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What is the most permeable ion and why?
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potassium because of potassium leak channels.
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1. What is the general nernst equation?
2. what is the shortcut at 20 C for z of +/- 1? 3. At 37 C at +/- 1? |
1. Eion (eq. potential) =
(RT)/(zF)xln([ion out]/[ion in]) 2. +/- 58 log(ionout/ionin) 3. same as above with 61.5 instead of 58. |
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If the membrane was only permeable to potassium, what would the Vm equal?
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The equillibrium potential of potassium.
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What is the equillibriums potentials of 1. sodium, 2. potassium, 3. chloride, 4. calcium
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1.-90
2.60 3.-75 4.120 |
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why is the equillibrium potential of cations usually about 0?
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Because Na and K channels are open at the same time allowing Na in and K out
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Why isn't Vm equal to the Ek?
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Na is also slighlty permeable thus depolarizing Vm to -70
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what is the goldman hodkin kate equation telling us?
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it uses all ion species in one equation to determine the Vm
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what are the neuro permeabilities and concentration ratios of the following?
1.potassium 2.sodium 3.chloride |
1. P=1, in/out = 40
2. P=1/25, out/in = 10 3. P=1/15, out/in = 10-30 |
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How many sodiums go outside and potassiums inside the cell per ATP via the Na/K pump?
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3 Na out and 2 K in
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what are two consequences of the Ns/K pump and how does it maintain the membrane potential?
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It makes the Vm -3 mV less and it maintains osmotic balance by preventing swelling (more sodium out, thus water follows). If K and Na were allowed to leak in and out, the Vm would reach 0,; the pump prevents this.
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an advantage of the patch clamp method is that it allows...
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study of small cells and/or single ion channles
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how many transmembrane domains do the votlage gated ion channels have and where is the pore located?
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6 domains and the pore is located between S5 and S6
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what transmembrane segment of voltage gated channels contains the M gate AKA the voltage sensor? How does this sensor work to open the voltage gated channel?
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It is located on the S4 domain. As the cell is depolarized in response to opening of ligand gated channels, the interior side of the membrane becomes more positive; the voltage sensor is near the inside of the membrane and it contains positive amino acids. Thus it is pushed towards the exterior in response to depolarization, opening the channel and furthering depolarization.
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The movement of the M gate (voltage sensor) in voltage gated channels creates a current called what?
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The gating current (Ig)
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What is the difference between inactivated state of Na voltage gated channels and the closed state?
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The inactivated state is caused by the insertion of the H gate (inactivation ball) on the cytosolic side. The channel is still technically open not closed, but now it is blocked.
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What kind of voltage gated channels lack an inactivation ball?
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Delayed rectifier channels.
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what ensures that AP's are all or none?
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large sodium current and large number of voltage gated sodium channels
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what toxins block the voltage gated sodium channels on the extracellular surface?
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tetrodotoxin from the puffer fish, saxitoxin from the clam, and red tide toxins
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what toxin opens the voltage gated Na channel and then blocks it?
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ciguatera toxin
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where do local anasthetics block the voltage gated Na channel?
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on the inside
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why do scorpion toxins hurt?
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they induce slow inactivation in voltage gated sodium channels (prolonged opening)
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what toxins activate voltage gated sodium channels at a more -Vm and then block inactivation?
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lipid solubl toxins including batrachotoxin and pyrethrins
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what is an example of a delayed rectifyer channel?
(they do not inactivate) |
voltage sensitive K channel
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define the threshold of an AP.
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the Vm that will illicit an AP 50% of the time.
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what is responsible for the overshoot to +40 in AP's?
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Na+ influx is trying to reach +60 but it is inactivated too quickly.
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What is the time called when the Na channels are inactivated (blocked by the H gate)?
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the absolute refractory period
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what is the advantage to the absolute refractory period?
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it prevents the AP from going in reverse (it must spread forward because the voltage gated channels behind it are unexcitable)
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What causes the first downward slope of the AP?
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the leak channels
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what causes the undershoot in the AP?
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Voltage gated K channels open and close slowly. Closing slowly prolongs the hyperpolarization as the Vm tries to reach -90mV, the Ek.
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What is the relative refractory period?
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this is the undershoot of the AP from the VS K+ channels. It takes more stimulus at this time to illicit an AP (bc we need more depolarization).
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mammalian myelinated axons do not use what kind of voltage sensitive channels?
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They do not use VS K+ channels, the delayed rectifyers. They only use potassium leak channels, thus the undershoot is negligable and the relative refractory period is much shorter.
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what kind of synapses experience a synaptic delay?
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chemical synapses have a delay bc of release of NT whereas electrical synapses do not.
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Voltage gated Ca2+ channels in the presynaptic terminus are slow to activate; what is physiologically significat about this?
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These channels can "open more" in response to an increased frequency of action potentials. Thus more Ca2+ influx and thus more NT released and thus a stronger signal.
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How are AP's and synaptic transmission modulated?
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AP's are frequency modulated (they are all or none). Synaptic transmission is amplitude modulated (more NT means bigger signal)
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Define synaptic delay.
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The time between between the onset of presynaptic AP's and the onset of postsynaptic AP's.
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What is the cause of synaptic delays?
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Ca2+ channels in the presynaptic terminus are slow openers.
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what aspect of some ionotropic receptors on the postsynaptic terminus may increase the synaptic delay?
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The ionotropic receptor is coupled to a transducer like a G protein.
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The NT's GABAa and Gly act on what kind of receptors? Do they stimulate influx or efflux at -70mV? What is the overall effect on Vm?
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They stimulate ionotropic Cl- channels. Cl- influxes and causes hyperpolarization (IPSP) at a Vm of -70.
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The NT Glu acts on what kind of receptors? Do they stimulate influx or efflux at -70mV? What is the overall effect on Vm?
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It acts on ionotropic cation channels (mainly Na and K, some Ca2+). Na and Ca influx and K efflux at -70mV resulting in depolarization (EPSP)
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The NT Ach acts on nicotinic receptors. What ion(s) changes permeability? Do they influx or efflux at resting Vm? What is the overall effect on Vm?
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Na will influx and K will efflux at resting Vm. Thus a depolarization will occur. This is an EPSP or an EPP at neuromuscular junctions.
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The GABAb NT acts on what kind of receptors? What is the result, and is this inhibitory or excitatory?
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It acts on metabotropic receptors that also allow K+ permeability. Thus K+ effluxes (very slowly) at resting Vm causing an inhibitory effect. But a Gi protein is also stimulated.
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Ach acts on muscarinic receptors causing what kind of meatabotropic effect? What ion also becomes permeant? What is the result.
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Gi proteins are stimulated. K+ ions are made permeant, thus an efflux at resting Vm. This is an inhibitory effect. (Note that it is much slower than the EPSP at the nicotinic receptors).
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What specefically does Ca2+ do at the sites of exocytosis?
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It phosphorylates proteins on vesicles and it recruits vesicles reserved pool to the docked pool.
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What does the fact that the safety factor is high in EPPs and muscle stimulation mean?
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An EPP will illicit muscle stimulation no matter what bc the amplitude of stimulation from an EPP is always large enough to cause depolarization that stimulates muscle movement.
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How do myasthenic diseases cause muscle weakness?
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They reduce the safety factor for neurotransmission, thus not each EPP will illicit muscle contraction.
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How does Lambert Eaton Myasthenic Syndrome produce muscle weakness?
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Ab's destroy Ca2+ channels, thus fewer vesicles of NT are released. Thus there are fewer MEPPs and thus the EPP is smaller.
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How does myasthenia gravis produce muscle weakness?
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Ab's destroy Ach receptors, thus there is less stimulation, leading to smaller MEPP's and thus smaller EPP's.
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Contrats how LEMs and myasthenia gravis differ after frequent stimulation?
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LEMs patients will have improvement due to more Ach in the cleft, while gravis patients will fail more often because the already small number of Ach receptors have already been activated...
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