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Synapses Part 2

by: Eileen artigas

Synapses Part 2 NEUR 0010

Eileen artigas
Brown U

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Synapse Lecture Continued
Intro to Neuroscience
Michael Paradiso
Class Notes
Intoduction, to, neuroscience
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This 5 page Class Notes was uploaded by Eileen artigas on Tuesday September 27, 2016. The Class Notes belongs to NEUR 0010 at Brown University taught by Michael Paradiso in Fall 2016. Since its upload, it has received 6 views. For similar materials see Intro to Neuroscience in Neuroscience at Brown University.

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Date Created: 09/27/16
SYNAPSES PART TWO Interaction with post synaptic cell will alter the post synaptic cell’s membrane potential How fast does it happen? In which direction does it happen? Both depend on the type of receptor and the type of ion permeability that is going to end up being changed. How rapidly membrane potential changes in post synaptic cell 3 time frames: 1. Fast- milliseconds 2. Intermediate- seconds 3. Slow- seconds to minutes What direction? Depends on the ion whose permeability is changed For example: Change Na+ permeability- depolarizes Change K+ permeability- hyperpolarize Change Cl- permeability- hyperpolarize Change Ca++ permeability- depolarizes When receptors are stimulated, a molecular pathway which ultimately results in the change in permeability of one or more ions Receptors - Fastest mechanism- Ligand (or neurotransmitter) gated ion channel o Trans-membrane proteins, made up of multiple subunits o From top, donut shape, hole in middle (ion channel), the neurotransmitter will bind in the synaptic cleft portion and changes confirmation of the protein complex to make the hole open and allow one of the ions its selective to flow down concentration gradient Conversion of chemical signal back to electrical signal by causing passing of ios Ligand-gated ion channel receptors  Acetylcholine will usually gate Na+  Glutamate will usually gate Na+ or Ca2+  GABA will gate Cl- (hyperpolarization)  Glycine will gate Cl- (hyperpolarization) Many of these Ligand/NT gated ion channels have subtypes - Glutamate has- AMPA, NMDA, Kainate (have slightly different properties) - depending on where the receptor is and what role its playing you get the various effects that are mediated through glutamate - G-protein coupled receptor (GPCR's) (metabatropic) o All single plpeptide chain, no subunits (unlike 5 protein subunits in ligand gated receptors) o Transmembrane helixes go through membrane 7 times, form bundle o NT binds extracellularly o Very large family of receptors How do these receptors work? Why are they called G- protein coupled receptors? o Despite large variety of NT and hormones that act through these receptors, they all function in much the same way, involves the G- protein o G-protein made of alpha, beta, gamma subunit o Mark Rodbell, Alfred Gilman- shared Nobel prize in physiology and medicine for figuring out how G-coupled protein receptors work (1995) o Guanine-Nucleotide (G in G-coupled receptors)  2 Guanine-Nucleotides involved (play critical role in function of how chemical signal gets transmitted when it binds to a receptor)  Guanosine triphosphate- GTP  Guanosine diphosphate- GDP o o When there’s no NT in cleft, all parts floating in membrane of post synaptic cell, do not associate o Alpha subunit attached to GDP and beta-gamma subunit o When NT is released into the cleft, it binds to receptor and changes the shape or confirmation of receptor, alpha-beta-gamma subunits bind to it o That attachment event causes GTP/GDP exchange o GTP/GDP exchange reaction- GDP pops off, GTP comes on to alpha subunit, causes conformational change, alpha separates from beta- gamma subunits o Each subunit floats away and affects activity where it bumps into (effector protein) o Alpha-subunit has built within it GTPase- converts GTP back to GDP by removing one of the phosphate groups o GDP ends up bound to alpha subunit and inactivates it o Inactivated alpha subunit, cycles back to the top, re-associates with beta-gamma, turns off activation o As long as there is NT in cleft the cycle will keep running - Two things can happen that alter the activity of post-synaptic cell once you activate the g-coupled protein receptor o G-protein can have direct effects on a signaling partner Direct G- Protein Signaling  Muscarinic acetylcholine receptor, binds to receptor, GTP/GDP exchange reaction…. BUT in this case beta gamma subunit floats off and interacts/opens channel (takes seconds) o Or can act through an enzyme which makes other chemical messages and carries signal into the cell further: Intermediating Second Messengers-in this case alpha subunits interacts with enzyme, enzyme produces intermediate chemical second messengers, those second messengers have downstream effects (ultimately result in change in membrane potential) (i.e. Adenylyl cyclase) What's protein kinase? - Group of enzymes, alter the function of proteins - Activity of proteins is determined by conformation/ shape - Protein kinase takes ATP, removes the terminal phosphate from ATP and places it on protein, changing the activity of protein (might activate it, inhibit it, open it or close it if it’s a channel) - Process is called phosphorylation - *Protein phosphatase reverses this reaction - EPSP- excitatory-post synaptic potential - Opening a channel for sodium or calcium channel- depolarization IPSP- inhibitory- post synaptic potential - Opening a channel for chloride or potassium channel- hyperpolarization Receptors produce small EPSP or IPSP, not AP, just small depolarizations, hyperpolarizations Neuron collects all this input in dendritic tree and send message to spike initiation zone If depolarization at spike initiation zone goes from resting potential to around -40mv, you will fire AP in cell. Synaptic integration Mini’s and Quantal Release We think of synaptic transmission as being quantal, each packet is able to depolarize the post synaptic membrane by some fixed amount (about 0.5 mM) quantal release Mini's- miniature post-synaptic potentials, can add up and there's a summation of depolarization NMJ- if your motor neuron fires, you want your muscle to twitch, so quantal release at NMJ is very high, you almost always get enough of a depolarization to cause a muscle to twitch How does this integration occur? Spatial Summation- Synapses in close proximity to each other Temporal Summation- A single synapse with multiple trains of AP’s arriving one after another, release of more NT PROBLEM- Current easily leaks out of membrane because of the properties of the membrane Length constant Position on the membrane where depolarization is 37% of where it is at origin, initiating point (less depolarization can be measured further away from injection point because some of it has leaked out) Lambda- measure of how far the depolarization will spread If a cell has a way to increase the length constant- it will Increase probability that those small depolarizations will reach hillock with enough value to cause an action potential SOLUTION- Excitable dendrite Voltage gated sodium channels dispersed on membrane cause more depolarization- greater spread, small depolarization is enough to open one voltage gated sodium channel, causing more depolarization to reach over to next channel Excitable dendrite (vs. passive which doesn't have sodium channels)- one way of increasing length constant Another way of increasing length constant- cell can use G-coupled protein receptors What about IPSP? Hyperpolarizing Involved in controlling the excitability of the post synaptic cell- If excitatory synapse fires and inhibitory synapse fires, depolarization travels and then canceled out by inhibitory synapse and depolarization never reaches axon hillock Termination of Signaling Stop sending action potentials down terminal bouton Removal of NT- to stop activating receptors -diffusion- what’s been placed in synapse diffuses away (not very efficient but does allow for NT to be removed from cleft (used by peptide NT most) -degradation- chemically degrade so its no longer active (more effective0 enzyme sitting right next to receptor -reuptake -take NT backup into terminal buoton directly, transporters suck NT back up and remove them from cleft, packaged into vesicles Terminating events in postsynaptic cell - Just removing NT from cleft not enough to shut everything down, we’ve activated many intracellular processes (i.e. with g-protein coupled receptors) - G- protein coupled receptors- we’ve made second messengers; enzymes can break down the second messengers (cyclic AMP phosphosterase turns cyclic amp into 5’ AMP which cannot activate alpha subunit anymore) - Calcium- was also released by protein kinase process- How to get rid of it? ATPase in ER drives calcium back into ER, reduces calcium concentration on cytosol - Phosphorylated proteins- get rid of them, protein phosphatase come in and remove phosphate groups from proteins to original state of activity


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