SMS 201: Lecture 25 PDF

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Lecture notes for SMS 201 with Dr. Sarah Lindsay. ...

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****know whats happening in phases of an action potential ● Action potential - generated down length of axon, came to end of nerve and needs to get across a gap to the next nerve or muscle cell, ect. ● That gap between nerve cells is called a synapse ● Electrical signals from action potentials are transported directly from neurons to other cells ONLY in electrical synapses. ● Channels between cells of a gap junction transmit ions rapidly between adjacent nerve cells ● More common in vertebrates, especially in the brain ● Giant axons in squid and some crustaceans form electrical synapses with postsynaptic cells (allowing for fast escapes) ● *** Chemical synapses transfer action potentials indirectly and generally are more common. *** ● What is an electrical synapse? ○ Place where electrical signals communicate - electrical signal coming from action potential ○ Electrical synapses are direct, chemical synapses (more common) are indirect ■ Needs an intermediate step ● Neuromuscular junctions transfer the action potential through a chemical synapse ○ Involves a chemical ○ pre-synaptic and post-synaptic membrane - gap in between is synapse ○ In a chemical synapse, voltage-gated calcium membranes, neurotransmitters (pre-synaptic cell) also come into play ○ Post synaptic cell contains ligand gated ion channels ○ neurotransmitter binds to ^channel, causes chemical change and opens it ○ Ligand channels change sodium and ion concentrations inside the cell and generate another action potential ● How does a chemical synapse work? ○ 1. Action potential arrives at axon terminal and ○ 2. opens voltage gated Ca2+ channels near the synaptic terminal. Ca2+ influx causes: ○ 3. Synaptic vessels containing neurotransmitter to fuse with presynaptic membrane of axon terminal, releasing neurotransmitters into synaptic cleft ○ 4. Diffuse across cleft to the next cell and bind to receptors on ligand gated ion channels, opening them so ions can diffuse through them (causing postsynaptic potential) ■ If channel specific to sodium, it rushes in and causes depolarization becomes positively charged ■ If potassium, hyperpolarization occurs ○ 5. Neurotransmitter eventually released from receptor and may be degraded by enzymes; channel then closes ○ PSP = post-synaptic potential - if it reaches threshold will generate another action potential ● The chemical synapse acts as a one-way valve

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Nerve impulse transmission is unidirectional in a given neuronal pathway because neurotransmitters are only produced in the pre-synaptic neuron and neurotransmitter receptors are restricted to the postsynaptic membrane ○ Can get different kind of postsynaptic potentials - either: ■ Excidatory (EPSP) , depolarizing ■ Inhibitory (IPSP) , hyperpolarizing The excitatory postsynaptic potential is a graded potential that increases with increasing stimulus (ex more transmitter molecules opening more ligand-gated Na+ channels) ○ If enough ligand-gated channels open to depolarize the membrane to threshold, then … action potential generated Summation of postsynaptic potentials ○ Temporal summation (summation over time): same cell recieves multiple repeated stimuli from same neuron in increasingly rapid succession - gets to threshold → action potential ○ Spatial summation: nearby synapses are all stimulated at the same time and their subthreshold stimuli sum to reach threshold - gets to threshold → action potential There are multiple synapses and it gets complicated ○ Some of those presynaptic cells are producing excitatory postsynaptic potentials, and some creating inhibitory posysynaptic potentials ○ Stimuli A, B, C are from excitatory synapses; Stimuli D, E are from inhibitory synapses and produce inhibitory postsynaptic potentials (IPSPs) which are hyperpolarizing. EPSPs and IPSPs can offset each other. Neurotransmitters: ○ Contain nitrogen ○ Can be excitatory or inhibitory depending on the postsynaptic receptor ○ Ach (acetylcholine) is most common ○ Amino acid neurotransmitters active in vertebrate CNS and PNS; some induce metamorphosis in marine invertebrates ○ Neuropeptides usually stimulate metabotropic receptors like olfactory and taste receptors ■ Metabotropic receptors: slower, involve 2nd messengers ■ Ionotropic receptors: fast acting ○ Nitric oxide made on demand Drugs and toxins can interfere with nervous systems ○ Some nerve gases & insecticides inhibit cholinesterase, causing unrelenting stimulation of postsynaptic receptors for acetylcholine ○ Curare (d-tubocurarine), extracted from a South American tree and used as blowdart poison, blocks receptor sites for acetylcholine ○ Batrachotoxin from South American frogs is used as a dart or arrow poison; it blocks closing of the inactivation gates on voltage-gated Na+ channels ○ LSD binds to receptor sites for serotonin in the reticular formation of the brain, which regulates information going to the cortex, itself responsible for thought and imagination

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Puffer fish (fugu) contains tetrodotoxin(TTX) ○ Blocks post-synaptic voltage gated Na+ channels ○ Causes paralysis of respiratory muscles ○ Used in research to study Na+ channels ○ Enjoyed as delicacy by some, but must be prepared carefully…. ○ No antidote!! Dinoflagellates such as Alexandrium species produce saxitoxin (STX), a neurotoxin that blocks voltage gated Na+ channels. ○ Some shellfish that eat the algae can be partially paralyzed: susceptible clams cannot retract siphons or burrow. ○ BUT single mutation affecting one amino acid in the protein that forms the channel changes its shape enough to eliminate the effect of STX so that the clam is resistant to STX – it can burrow even when loaded with STX. STX can be passed to humans eating such clams. ○ Clams resistant to STX occur in higher frequencies in populations often subject to harmful algal blooms. Sensitive pop: 86% couldn’t burrow when exposed to STX Resistant pop.: 10% couldn’t burrow when exposed to STX [Dr. Laurie Connell, SMS] ○ Other clams (e.g. butter clams) concentrate ingested saxitoxin in siphon tips to deter browsing predators. Some cone snails use venomous harpoons in the proboscis to subdue fish ○ Omega-conopeptide, a cone snail toxin, has been developed as the drug Prialt, a painkiller ○ Prialt blocks voltage-gated Ca2+ channels in peripheral neurons that convey “pain signals” to the CNS. ○ The signal is stopped in the PNS and does not generate an awareness of pain in CNS. Note that voltage-gated Ca2+channels are presynaptic ****review the last few slides in this lecture...