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UVM NSCI 110 - Metabotropic Receptors
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NSCI 110 1st Edition Lecture 13Outline of Last Lecture I. Temporal and spatial summation may lead to either hyperpolarization or depolarization of a neuronII. There are several crucial differences between an action potential and synaptic potentialIII. Synapses can be classified according to where on a neuron the release of neurotransmitters occursIV. Synaptic transmissiona. Docking and primingb. Action potential reaches axon terminali. Gated calcium channels openc. Transmitter is released and travels to post-synaptic membraneOutline of Current Lecture I. Metabotropic receptors and ionotropic receptors differ in their mechanisms of opening an ion channelII. Acetylcholine is synthesized in the pre-synaptic terminal in a specific sequence of stepsa. Eventually is broken down and taken back up by pre-synaptic terminalIII. Catcholamines are all derived from tyrosinea. The subsequent transmitter used by the neuron depends on the enzymes present at each step of the pathwayIV. Amino acids include glutamate and GABAV. A superfamily of receptors is involved in transporting glutamate across the membranea. NMDA and AMPA receptorsCurrent LectureI. A metabotropic receptor is not directly attached to the channel (unlike an ion channel)a. Coupled with the phosphorylation of G-proteins that induce conformational changes in the channelsII. Synthesis of Ach by the presynaptic terminala. Acetyl CoA carries acetate to the transmitter-synthesis siteb. ChAT (enzyme) transfers acetate to the choline to form Ach and coenzyme Ac. Once in the synaptic cleft, ACh is broken down by acetylcholinesterasei. Forms acetic acid and cholineii. These products go through reuptake and travel back into the presynaptic terminaliii. Choline transporter allows this transportation across the membraneThese notes represent a detailed interpretation of the professor’s lecture. GradeBuddy is best used as a supplement to your own notes, not as a substitute.III. Other common neurotransmittersa. Catecholaminesi. Tyrosine (from diet)  L-dopa  dopamine  norepinephrine  epinephrine1. Tyrosine hydroxylase is the rate limiting factor in this pathway2. If the third enzyme is not present in that synapse, dopamine will be the neurotransmitter used3. Forms a feedback systemb. Amino acidsi. Glutamate (excitatory) and GABA (inhibitory) are structurally very similar1. GABA is missing one carboxyl groupii. Glutamic acid decarboxylase (GAD) can turn glutamate into GABAiii. If the concentration is increased from 5 mM to about 20 mM of glutamate in a presynaptic terminal, glutamate will be used as the neurotransmitterIV. More on glutamate…a. Glutamate superfamily of receptorsi. NMDA (ionotropic)  exogenous1. Specific receptors for glutamate and NMDAii. AMPA (ionotropic)  exogenous1. Specific receptors for glutamate and AMPAiii. mGluR (metabotropic)b. NMDAi. Na+ > K+ >Ca 2+ (NMDA is a non-selective cation channel)1. Don’t normally have a current because a magnesium usually sits inthe pore and prevents ions from flowing throughii. NMDA receptors also have AMPA receptors nearby as partners1. Kainate receptors may also be involvediii. When glutamate binds to the AMPA receptor, ions influx through the channel1. Positive charge repolarizes the membrane in the immediate area and causes the magnesium ion to move and allow ions through the NMDA channel2. Causes a summation and allows a longer action potentiala. Important in learning and memory3. This is why the ionic current is voltage-dependentiv. At around 0 mV potassium starts flowing outward trying to reach equilibrium potentialc. Glutamate is not broken down in the synaptic clefti. Either goes through reuptake or absorbed by an adjacent astrocyte, where it is stored at glutamineii. Astrocyte then releases the molecule as glutaminase back into the presynaptic terminal so glutamate levels may be restorediii. GABA goes through the same process but is stored as glutamine and taken back up by the presynaptic terminal as glutamate, then converted into


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UVM NSCI 110 - Metabotropic Receptors

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