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29 Cards in this Set
- Front
- Back
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Is a ligand-gated ion channel dependent on the plasma membrane voltage?
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No.
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Where are LGIC's found?
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In the CNS and PNS
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Ionotropic vs. Metabotropic
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Ionotropic: the ion is the signal. FAST. Metabotropic: the receptor has to interact with 2nd messengers that take a slightly longer amount of time.
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4 prominent LGIC "ligands" or neurotransmitters
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ACh, Glutamate, GABA, Glycine
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Flow chart of neurotransmission
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Change in potential at presyn terminal -> Ca rushes in via volt channels -> Ca stimulates vesicles to release neurotransmitter -> NT binds to LGICs on postsyn cell -> signal propogates
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A neuron at rest
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Negative membrane potential
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Hyperpolarization and why?
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The membrane potential becomes more negative because the cell "loses positiveness"(K leaves, Cl enters, etc)
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Depolarization and why?
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The membrane potential becomes less negative because the cell "gains positiveness" (Na enters, Cl leaves, etc)
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On a graph, what does depolarization look like?
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A rising curve
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On a graph, what does hyperpolarization look like?
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A falling curve
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Flow chart of muscle contraction
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ACh binds to NACh receptors --> ion channel opens to let Na then K in --> depolarization eventually lets Ca in --> muscle contracts
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If a single ion (Cl, Na) is moving through a selective LGIC, what is the reversal potential of the membrane?
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Exactly equal to the Nernst potential for that ion.
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Why do we make a distinction between reversal potential and Nernst potential?
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A single ion likes to move the membrane towards its own Nernst potential. However, LGIC's are not single ion channels (usually). The balance of their Nernst values and permeability is the reversal potential.
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What is the reversal potential if both K (E = -104) and Na (E = +61) are moving through an open LGIC? Why?
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Around 0, oddly enough. You'd think it would be absolutely between the two Nernst values, but permeability also changes the balancing slightly.
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What is slow channel syndrome?
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When the LGIC stays open wayyy too long.
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Clinical presentation of slow channel syndrome.
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Myasthenis gravis, for example. If the LGIC stays open, the voltage dependent Na channels further on down the neuron inactivate and their refractory period is delayed.
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ACh blockers
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Tubocurarine, Vecuronium, Pancuronium, Rocuronium. COMPETITIVE PARALYTICS
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Irreversible ACh blocker
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alpha-bungarotoxin
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Is nicotine an ACh agonist?
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Yes
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How many subunits in the ACh receptor? What is the difference between the fetal and adult receptor?
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5. The gamma subunit is replaced by epsilon, which gives the receptor greater conductance.
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The three major classes of glutamate receptors.
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Kainate, AMPA, NMDA
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Why is NMDA current absent at hyperpolarized potentials? What happens as the potential becomes more positive?
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Mg is pulled into pore to block. Mg is released.
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Two special characteristics of NMDA receptor.
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1. Shuttles calcium
2. Requires glycine or D-serine as cofactors |
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Do AMPA and kainate allow calcium through their pore?
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No.
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What does Dr. Engisch want you to remember about the structure of glutamate receptors?
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They are diverse.
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What is the result of excess intracellular Ca?
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Cell death.
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Wha kind of channel is GABA?
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Anion selective, therefore inhibitory.
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What is the GABA-a channel? What is the membrane reversal potential where that channel is located?
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A chloride-selective channel. Identical to the Nernst potential for chloride.
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The two main allosteric potentiators of the GABA receptor?
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Barbituates and benzodiazepines.
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