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Lecture 2

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Physiology 3120
Tom Stavraky

Hore – Lecture 2 Notes 6. -Excitatory postsynaptic potential produced by the transmitter upper left causing Na+ to rush in and the Axon Hillock becomes a region that is positive; at the same time, another synapse that is activated simultaneously that was an inhibitory synapse causes some flow of ions, usually Cl-, to come in making the Axon Hillock region more negative and the positive charge flows toward the inhibitory synapse which is now hyperpolarized and current will flow around there -Positive charge is the normal convention for current flow -Brain activity is the summation of excitatory and inhibitory activity over any given period -Neuron can either fire an AP or not -Axon area is an area of high electrical resistance so the currents go out the low resistance area, which is the axon hillock -Let’s assume that there are a number of excitatory inputs to this neuron; large current flow; large amount of depolarization in this region, which results in Na+ rushing in through these voltage-gated Na+ channels, and excitation postsynaptic potential, summation of all of them, get to threshold and we fire an action potential 7. -We’ve got an AP going down a myelinated nerve by saltatory conduction; AP is at the top node with all the positive charges -Node at top is depolarized b/c of the AP (large positive area compared to down below), there will be positive current flow to the bottom region; doesn’t go down the axon b/c it’s an area of high electrical resistance: instead flow out across the node region, which is just like the axon hillock (which is low electrical resistance and full of VG Na+ channels); consequently we get a depolarization down below, which opens the VG Na+ channels and Na+ rushes in and an action potential is generated at this next node (jumping from one node to the next node) and on it goes down the axon 8. -Can have branching or collateral; many neurons will have axons that branch considerably and these are called collaterals -Schematic shows one axon but there can be axons going off somewhere else -Local currents flowing into the terminal region; the AP may not invade the terminal, it doesn’t need to b/c the local current ahead of the action potential will bring in the depolarization to the terminal region; in this region there are VG Ca2+ channels, which will open up b/c of the depolarization, in will rush Ca2+, which will cause release of vesicles -At the synapse: effects divided into 3 1) transmitter (ex. Glutamate; produces excitation; one of the most important transmitters in the CNS) diffuses across the synaptic gap and acts on the receptor on the post synaptic surface; ex. Glutamate gated channel: when glutamate arrives it will cause opening of this channel (AMPA receptor; ionic receptor) through which Na+ and K+ can flow (Na+ comes in, K+ may come out); Na+ wins which produces a depolarization in this region of the postsynaptic cell, which then is an excitatory postsynaptic potential; if this was an inhibitory synapse it would be a different transmitter and it would act on different receptors to produce an IPSP; if there is enough of either one of these, then an AP could be generated -2) the same transmitter, glutamate, can act on a channel but in this case the particular channel being opened is an NMDA receptor, which under certain circumstances can open up and cause Ca2+ to come into the cell, which can cause activation of second messengers; NMDA receptors are common in the Hippocampus -Hippocampus (associated with the limbic system): cortex like structures at the top of the brain stem (one of them is the Hippocampus); important for memory (if you have damage in the Hippocampus you will have trouble laying down memories); a lot of NMDA receptors in the Hippocampus; where memories are stored; one mechanism that can help store the memory is synaptic plasticity (synaptic change); if you’re going to have a change in neuronal function something has to change -Long term potentiation (a type of synaptic plasticity): best cellular correlate of memory -So we can get activation of second messengers by this in flow of Ca2+ under certain circumstances where you want to lay down memory 3) you can have a peptide released (different molecule than the other 2 effects) (sometimes called a neuron modulator) and it can act on a receptor and affect G proteins and then you can have an Effector from this that could cause activation of second messengers -2 potential ways to activate second messengers -Second messengers: 1) regulates the sensitivity of existing ion channels (ex. Can change the sensitivity to allow more ions to flow through); probably changes in protein mechanisms; 2) can insert existing ion channels into the membrane (ion channels floating around in the cytoplasm, which will be activated by glutamate and inserted into the membrane, which changes the excitability status of the postsynaptic membrane); combining these two: for any amount of transmitter that is released, you will get a bigger excitation (more channels and greater sensitivity); 3) can have synthesized new ion channels (more of a long term thing) (altered gene expression) -First two can happen in minutes; some of these mechanisms can last for days or even a year; can get immediate, midterm and long-term changes in the excitability level of the neuron as a result of these 3 different effects -There are capacitant elements in the membrane, so you can have effective current flow without any ions going across -More than 100 molecules that are believed to act as transmitters in the CNS (gonna divide them arbitrarily into 5 categories): -Acetylcholine NMJ and also a transmitter in the cerebral cortex (where it’s associated wi
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