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Definition
| Measurement of teh charge difference across a lipid membrane. |
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Definition
| The charge difference in a resting cell. |
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Definition
| For a particular ion, the potential at which there would be no net movement. |
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| The absolute value of the membrane potential decreases; the sides of the membrane become more similar in voltage. (so, becomes less negative from the resting potential) |
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Definition
| The absolute value of the membrane potential increases; the voltages on each side of the membrane are further from one another. (physiologically, this is becoming more negative than the resting potential) |
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Definition
| A return to the original resting potential from a hyper or depolarized state. |
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| Change direction of the charge, a reversal of the charge. (the membrane potential becomes positively charged.) |
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Definition
| An electrical signal that can traval (propagate) down an axon. Action potentials always involve an overshoot. Action potentials are non decremental, cannot sum, have a refractory period, and are "all or nothing", either you hit the threshold or you do not. |
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Term
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Definition
| Vary in magnitude according to stimulus, are decremental, can sum, and have no refractory period. |
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Term
| Potassium voltage gated channels |
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Definition
| Negative feedback - These channels open when the cell depolarizes. Potassium flows out of the cell, increasing negative charge, which repolarizes the cell. They open and close slowly. |
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Term
| Sodium Voltage Gated Ion Channels |
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Definition
| These have two gates, an activation gate and an inactivation gate. This channel is a positive feedback channel, when it is depolarized up to its threshold it opens up the activation gate and begins closing the inactivation gate. Na rushes into the cell, further depolarizing the cell. Eventually (slowly) the inactivation gate completely closes. Then the activation gate closes, and the inactivation gate opens again, at this point the channel has reset. |
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Term
| How does an action potential propagate down an axon? |
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Definition
| Through sodium ion channels. One sodium ion channel is activated through ligand gated ion channels which initially caused it to depolarize enough to reach threshold. It then depolarizes the adjacent sodium ion channel, and it deactivates. This signal travels down the axon as each sodium ion channel bumps the adjacent one to its threshold. It doesn't go in the reverse direction because it takes time for the Na channel to reset its inactivation and activate gate. |
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Term
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Definition
| Myelin is insulation around the axons. It increases the speed at which action potentials can travel. |
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Definition
| region of contact between the neuron and its target |
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| What are the two types of synapses, and define them / describe them. |
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| Electrical (minority of synapses) - very fast synapse, membranes are almost touching. Involves gap junctions (protein channels that link membranes of two cells to allow direct ion flow between them) Can have directionality but no range of signal, either full on or full off. Chemical are not as fast as electrical. They have vesicles which then diffuse through synaptic cleft and bind to target receptors.(usually ligand gated ion channels) |
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| Describe Otto Loewi's Experiment |
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Definition
| 2 frog hearts, each in a jar of Ringer's solution (mimics bodily fluids). One heart had vagus nerve attached to it, slowing the heart rate down when stimulated. The two jars were connected so that the fluid from jar 1 went into jar 2. Heart 2 slowed down a few seconds after heart 1 slowed down, proving that a chemical traveled through the liquid and is also involved in the slowing of the heart rate. This proved there was chemical synapses, not only electrical. We now know the chemical was acetyl choline. |
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| What are the advantages of Chemical Synpases? |
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Definition
| amplification of the signal, can both stimulate and inhibit target. Integration - multiple inputs to a single neuron. Guaranteed 1-way communication. Easier to create and get rid of. |
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Term
| How do we identify if a chemical is a neurotransmitter? |
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Definition
1. Found at synaptic cleft.
2. Calcium dependent release into syn. clft.
3. Artificial application, adding it artificially gives expected response.
4. Has a mechanism for its removal ie either enzymes that get rid of it.
5. Drugs agonist vs antagonist |
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| Define Agonist and Antagonist in terms of both skeletal cell and nerve cell neurotransmitters. |
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Definition
Agonist - binds to same receptor, has same effect (mimics)
Antagonist - for nerve cells, it binds to same receptor but blocks the effect. For muscle, it binds to same receptor and has the opposite effect. |
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Term
| Describe the life cycle of a neurotransmitter |
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Definition
1. Creation and release through calcium ion channels. Neuro T. in vesicles that go to synaptic cleft when ca ion channels are open.
2. Bind to receptors and induce response.
3. When response is no longer needed, they are no longer produced and either diffuse out of the cleft, are degraded by enzymes, or "reuptake" to be used again. |
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Term
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Definition
| open ligand-gated ion channels, once you reach threshold they activate the voltage gated ion channels (action potentials) These are fast, turn on turn off quickly. |
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Term
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Definition
| G-protein coupled receptors, slower. When stopping you need to restore G-protein to original position, remove the second messenger, and invactivate the enzymes. |
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| Largest and most wellstudied synapse. Skeletal muscle synapse (easier to get to). Uses acetyl choline. |
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| How is acetyl choline made and broken down? |
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Definition
glucose -> pyruvate -> acetyl CoA (+choline) -> acetyl choline -> receptors
Broken down by acetylcholine esterase into acetate and choline for reuptake. |
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