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28 Cards in this Set
- Front
- Back
Parts of the potential
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Threshold
Subthreshold Resting potential Afterpotential Refractory period Regeneration |
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Speed of conduction is dependent on...
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diameter, and if mylenated
(passive current flow - active prop. only occurs at nodes of ranvier) |
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Stuff to know about giant squid axon
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1) Easy to use in experiments (Which is why Hodgekin/Huxley/Katz used it)
2) Unmyelinated 3) Very large diameter for fast AP propagation rate |
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Name another model system?
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Motor neuron in anterior horn of spinal chord
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Intracellular recording from brain slice/ record + stimulate axon slides
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You can use glass micro-pipettes to stimulate/record along axon
You find that hyperpolarizations provide no active response, but depolarization will result in action potentials |
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Action potentials vs graded potentials re:strength down axon
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strength remains same! (why?) All or nothing!
Graded potentials fade over axon |
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Why is there a threshold?
Why does action potential reverse? Why is there a hyperpolarizing afterpotential? |
1) Threshold due to Voltage gated Na+ channels (only open at certain depolarization)
Action potentials a function of voltage sensitive protein channels 2) depolarizes in both directions IF stimulated by electrode, because there's only a RELATIVE refractory period. Naturally, the absolute refractory period prevents it from going backward 3) Because K+ gates are slow, take a while to close |
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Voltage gated protein channels, provide another example
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Determine the electrical properties of cells, evolve, differ across tissue types, animals, etc.
Different cells are more or less active Cardiac sodium channel |
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Explain how action potentials propagate (are regenerated) along the axon
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1) Ionic current flows between neighboring membrane in inside/outside of cell (outside -> positive sides go to inner negative action potential, inside - positive action potential goes in both sides
2) Active membrane excites (depolarizes) neighboring inactive membrane - +ions move to either side 3) Refractory part (behind AP) remains unaffected 4) depolarization causes another AP |
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Absolute Refractory period
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Part where Na+ is inactivated (BUT DOES NOT CLOSE - this doesn't happen till it returns to resting potential)
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Explain what happens to action potential at terminals
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1) action potential travels down axon
2)Voltage gated Ca channels open, Ca2+ enters 3) Synaptic vesicles fuse with membrane/ release NT into cleft 4) Transmitter activates postsynaptic receptors 5) This triggers ionic currents (EPSP/IPSP) 6) Transmitter inactivated/removed, may activate presynaptic autoreceptors to decrease release |
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EPSP
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excitatory postsynaptic potential - produces a small local depolarization pushing the cell closer to threshold
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IPSP
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inhibitory postsynaptic potential - produces a small hyperpolarization pushing cell away from threshold
NEGATES EPSP! |
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Postsynaptic potentials are..
what do their effects depend on (what does reaching threshold depend on?) |
SMALL (much less than presynaptic recording), the summation of their charges (NET effect)
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What triggers postsynaptic neurons (2 things)? Explain how
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Electrical signals (not covered)
Neurotransmitters! 1) Activate (attach to) ligand gated ion channels 2) allow Na+ to move through channel into cell 3) Can trigger IPSP or EPSP |
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Equilibrium potential of Cl-
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is near resting potential, negative
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Temporal summation
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Summing of potentials at axon hillock that arrive at different times
Closer together in time they arrive = greater sumation/possibility of AP So, pattern of APs matter |
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Location of inputs (Spatial summation) - explain.
How does evolution relate? |
More near cell body = more potent
Near synapse = most potent More inputs simultaneous = stronger Evolution of neural morphology reflects this property (Betz cell layer 5 - very large = receives gigantic input from large area, can integrate a lot of info) |
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Striatial/subthalamic innervation of pallidal cells
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Example of spatial summation - how potent nerve can be depending on neuroanatomy
1) striatal inputs gives small terminal to each pallidal cell 2) Subthalamic innervates its terminals around all palidal cells, very potent (wraps itself around) 3) Striatal cells pick and choose which pallidal cells to innervate 4) Subthalamic neurons aim for max innervation |
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Betz cell/ Striatal and subthalamic innervation of pallidal cells
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Striatal neurons seem to pick
and choose particular dendrites on GPi cells to influence more than others STN iuputs to GPi wrap around target dendrites to maximize influence |
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Name 2 adaptive properties of most neural circuits, explain then
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Convergence: Where many cells send signals to one cell
Divergence: One cell sends signals to many cells Parallel, sequential, lateral interactions across units |
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Example of convergence/divergence
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Convergence from retinal receptor cell, bipolar cell, retinal ganglion cell (EYE)...across optic nerve...Divergence across thalamic and cortical cell (BRAIN)
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GABA
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A neurotransmitter that activates Cl- channels, Concentration of Cl- is high outside so they move out of cell to inside.
Hyperpolarizes cell closer to resting potential (inside becomes more negative), so it is harder for a EPSP to make it reach threshold |
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5 subunits of a gaba receptor
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1) Benzodiazepine site
2) Picrotoxin site 3) GABA site 4) Neurosteroid site 5) Barbiturate site (6) Alcohol/steroid sites |
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IF too much K+ in blood, you feel...
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not great, go to hospital (why?)
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Relative refractory period
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How K+ hyperpolarizes beyond resting potential, so a larger depolarization is needed (but AP is still possible, compared to absolute refractory period)
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Difference between spatial summation and convergence
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Spatial summation is more local (regards one neuron) than convergence (which is more general, talks about system)
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Which ions provide excitatory input, which are inhibitory
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Na+ = excitatory
K+ = excitatory? Cl- = inhibitory |