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CU-Boulder PSYC 2012 - bio psych lecture 7 notes

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2/3/15 – Lecture 7 – Neurotransmitter Receptors and Post Synaptic Potentials- Goal: to discover how neurotransmitters produce effects on post- synaptic neurons- 2 Main Types of Neurotransmitter Receptorso Ionotropic: receptors is an ion channel, and binding of neurotransmitters directly opens or closes it and allows ions to flow into or out of the cell Ligand Gated Ion Channels: allows ions across cell membrane in response to neurotransmitter binding, once the neurotransmitter unbinds, the ion channel returns to itsprior (inactivates -> de-inactivates -> closed)- Non gated ion channels, voltage gated ion channels, and now ligand/chemical/neurotransmitter binding gated ion channelo Metabotropic: receptor is NOT an ion channel, and binding of neurotransmitters indirectly opens a separate ion channel by activating other intracellular proteins Binding of neurotransmitters activates an intracellular protein called a G Protein, then the neurotransmitter unbinds and G proteins are inactivated and ion channel returns to its closed state- G Protein either directly or indirectly (by activating an effector protein) opens of closes an ion channel In both cases … neurotransmitters binds to the receptor for only a short time and then comes off, so that ion channels only stay open for a short time- What happens when the neurotransmitter opens an ion channel?o Ions flow in/ out of the cell, resting membrane potential changes on post synaptic neuron The change in membrane potential in response to the neurotransmitter released by a singleaction potential on the presynaptic neuron is known as a Post – Synaptic Potential- Depending on the ion channel, it can make the inside of the cell more or less negativeo EPSPs and IPSPs Excitatory PSP: depolarization of postsynaptic membrane in which its resting membrane potential becomes less negative- Na+ channel goes in down its concentration gradient- Ca2+ channel goes in down its concentration gradient Inhibitory PSP: hyperpolarization of postsynaptic membrane in which its resting potential becomes more negative- K+ channel goes out down its concentration gradient- Cl- channel, chloride is high outside of the cell and wants to flow into the cell with its concentration gradiento Likes being where ever Na+ is Neurotransmitters can also operate in reverse and close the ion channels that were open- Closing the Na+ ion channel, hyperpolarizes the cell (IPSP)- Closing the Cl- ion channel, depolarizes the cell (EPSP) You can PREDICT was will happen to a neuron electrically if you know..- 1. If the ion channel is opened or closed by the NT- 2. What the concentration gradient is of the ion- 3. What the charge the ion has A SINGLE PSP is usually not sufficient to cause an action potential to the post synaptic cell- Rather, a single neuron has thousands of synapses producing excitatory and inhibitory inputs- The summation of PSPs from all over the post synaptic neuron’s is what you need tolook at to see if they will actually create an action potentialo The rate or pattern of action potential firing often conveys information in nervous system communication Single action potential, a few, or a crap ton very quickly, depends on the given time and the action potentials from the presynaptic neuronso Threshold Potential: the potential at which enough voltage gated Na+ channels open that the action potential becomes all – or – nothing  EPSPs bring the post synaptic neuron closer to threshold potential to fire an action potential IPSPs take it farther away from the threshold potential- Temporal Summation: addition of PSPs from the same neuron across time (Multipleinputs from the same source)o If Aps occurs on the same presynaptic neuron before the first EPSP decays back to resting potential on the post synaptic neuron, they will add on top of the previous EPSP and may reach threshold potential One action potential on presynaptic neuron = post synaptic neuron doesn’t reach threshold- BOOM… fizzle Multiple action potentials on presynaptic neuron = post synaptic neuron reaching its own threshold and releases an action potential- BOOM… BOOM… BOOM… BOOOOOOM- Spatial Summation: addition of PSPs from different neurons (many action potentialsfrom many different presynaptic neurons)o 2 EPSPs reach post synaptic neuron from two different presynaptic neurons at the same time, their sum might reach threshold potential Sometimes they wont add up though because some inputs will be excitatory and some will be inhibitoryo Receptor Agonists and Antagonists: chemicals that can act like neurotransmitters Agonists: mimic the effects of endogenous neurotransmitters by binding and inducing normal responses- Binds and makes the same effect as the neurotransmittero Nicotine: binds to and activates acetylcholine receptors, even when the neurotransmitter isn’t normally releasing Acetylcholine is involved with arousal and activation of voluntary muscles- Nicotine causes increased alertness and increased muscle jitters and rigid paralysis Antagonists: binds the receptor but doesn’t induce a response, rather blocks the natural ligand from binding and reduces the activity- Binds and blocks the receptor from being activatedo Curare: binds to acetylcholine receptors and prevents the binding of acetylcholine, if the levels are high enough it can totally block the acetylcholine from binding When blocking the acetylcholine receptors, it causes decreased alertness and flaccid paralysis Many drugs and toxins work as neurotransmitters agonists or antagonistso Termination of Synaptic Signaling: mechanisms by which the effects of neurotransmitters on post synaptic cells are terminated Degradation/ deactivation of neurotransmitters (like with acetylcholinesterase) Reuptake of neurotransmitters: transporter proteins that move the neurotransmitters back into the presynaptic neuron axon terminal Diffusion: movement of neurotransmitters away from the synapse Uptake by Glial Cells: broken


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