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Lecture Notes on Synaptic Integration and Transmission

by: Rebeka Jones

Lecture Notes on Synaptic Integration and Transmission BIOH 313-001

Marketplace > Montana State University > Cell Biology and Neuroscience > BIOH 313-001 > Lecture Notes on Synaptic Integration and Transmission
Rebeka Jones
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Includes figures from lecture slides
Noudoost, Behrad
Class Notes
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This 15 page Class Notes was uploaded by Rebeka Jones on Thursday October 13, 2016. The Class Notes belongs to BIOH 313-001 at Montana State University taught by Noudoost, Behrad in Fall 2016. Since its upload, it has received 10 views. For similar materials see Neurophysiology in Cell Biology and Neuroscience at Montana State University.

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Date Created: 10/13/16
Synaptic Integration For the worm experiment you need a worm, electrode, amplifier, and a data analyzer. • Synaptic vesicles: Elementary units of synaptic transmission – Quantum: An indivisible unit *the unit of change in a vesicle is defined by a single number – Miniature postsynaptic potential or Miniature endplate potential – Quantal analysis: Used to determine number of vesicles that are released during neurotransmission • Neuromuscular junction: Between 100 and 400 synaptic vesicles are released for each AP (1-several vesicles at each active zone in an endplate) > EPSP of ~40mV • CNS synapse: Single vesicle, EPSP of few tenths of a millivolt The drops are influx of ions which causes the channels to open If you have something that drops twice there are two channels If you increase the current, you increase the amount of neurotransmitter 2 When you stimulate E1 or E2 you see a big jump if you stimulate them shortly after you see to individual jumps. If you stimulate E1 and I then add together and I will take away from E1. If you stimulate E1 and E2 it reaches action potential 3 *synaptic delay = how long it takes for the voltage to open the gate in the presynaptic cell to notice a change in the postsynaptic cell Sometimes if the EPSP is too much you may get two action potentials 4 *When an EPSP travels down the channel and meets and Inhibitory channel that is open the EPSP leaks out of the channel *reversal potential = the potential where the direction of the flux changes…this is what cause the inhibitory channels to open in shunting Important concepts Simple inhibition happens due to hyperpolarization Simple inhibition has a subtractive nature 5 Shunting inhibition happens due to change in leaks (resistance) Shunting inhibition has a divisive nature (reduces magnitude) The neural code The stimuli need to be encoded to create a response - going from response to stimuli is decoding Rate Code – motor system – how many hertz for the action – rate determines force *we have neurons that are tuned to different actions the cells have to work together to create a full action. Feature code - 6 spike trigger average – take what was happening before the action potential and take an average of all of the spikes to figure out what caused the neuron to fire patterns of the spikes matter too Ensemble code – information is encoded as the join activity of several or many nerve cells, rather than as the activity of a single nerve cell in isolation (this will be covered more later) 7 Synaptic Transmission Chapter 6 readings will not be on exam only chapters 4&5 readings and chapter 6 lecturing along with 4&5 lectures You need to be able to explain why firing frequency of depolarization affects action potentials So after the absolute refractory period there is the relative refractory period. If you have enough depolarization you can activate another action potential. When you have greater current it reaches threshold faster making more action potentials. *Watch movies on D2L under Synaptic transmission During synaptic transmission calcium goes into the cell which causes vesical fusion and transmitter release the receptor channels open and Na+ enter the postsynaptic cell and vesicles recycle. Recycling -simple diffusion -Reuptake into the presynaptic terminal (by the action of specific neurotransmitter transporter proteins) once inside -destroyed -reloaded into vesicles -Reuptake in glial cells (using transporters) -Enzymatic destruction in the synaptic cleft Neurotransmitters act either directly or indirectly on ion channels that regulate current flow in neurons Ionotropic receptor – directly gated Made of 4-5 subunits 2 functional domains –binding site and extracellular mediate rapid post synaptic affect Metabotropic receptor – indirectly gated Do not have ion channels – affect other channels through activation of g proteins Extracellular bind site Intracellular binding site Typically produces much slower responses 2 *indirect gating is more complex All receptors for chemical transmitters have two biochemical feautu res in common - They are membrane-spanning proteins. The region exposed to the external environment of the cell reconizes and bind the reanmitter from the pre-synaptic cell - They carry out an effector funaction within the target cell. The receptors typically influence the opening or closing of ion channesl Ionotropic receptors (directly gated) - ACh receptor o nicotinic (nAch) o Muscarinic (mAch) 3 • Upon release of ACh from the motor nerve terminal, the membrane at the end-plate depolarizes rapidly. • The excitatory postsynaptic potential in the muscle cell is called the end-plate potential. • The amplitude of the end- plate potential is very large; stimulation of a single motor cell produces a synaptic potential of about 70 mV. • This change in potential usually is large enough to rapidly + activate the voltage-gated Na channels in the junctional folds. • This converts the end-plate potential into an action potential, which propagates along the muscle fiber. (In contrast, in the central nervous system most presynaptic neurons produce postsynaptic potentials less than 1 mV in amplitude, so that input from many presynaptic neurons is needed to generate an action potential there.) *potassium also fluxes through the ach-gated channel but for simplicity we are ignoring it 4 End-Plate Potential - Endplate potentials (EPPs) are the depolarizations of skeletal muscle fibers caused by neurotransmitters binding to the postsynaptic membrane in the neuromuscular junction - They are called “end plates” because terminal of muscle fibers have large saucer like appearance - In the absence of an action potential, acetylcholine vesicles spontaneously leak into the neuromuscular junction and cause very small depolarizations in the postsynaptic membrane. This small response (~0.4mV) is called a miniature end plate potential (MEPP) and is generated by one acetylcholine-containing vesicle. End plate current depends on four factors - Total number of Ach receptors - Their probability to open 5 - Channels conductance - Driving force If you have more channels the potentials will be larger. Greater amount of Ach increases the probability open (release more neurotransmitter. By long term changes in the postsynaptic cell you may have changes in the channel conductance or changing the resting membrane potentials. This is important because it gives you an idea of how to change the efficacy of the synapse. Metabotropic receptors - G-protein Coupled Receptors o Alpha and Beta adrenergic receptors o Muscarinic Acetylcholine o GABA B Receptor Tyrosine Kinases - Hormones - Growth factors - Neuropeptides 6 - They are slow: Direct gating of ion channels through ionotropic receptors usually is rapid—on the order of milliseconds—because it involves a change in the conformation of only a single macromolecule. In contrast, indirect gating of ion channels through metabotropic receptors is slower in onset (tens of milliseconds to seconds) and longer lasting (seconds to minutes) because it involves a cascade of reactions, each of which takes time. -They have a wider range of action: Ionotropic receptors function as simple on-off switches. Their main job is either to excite a neuron to fire an action potential or to inhibit the neuron from firing an action potential. Because these channels open only when they bind a transmitter available in the synaptic cleft, they are normally localized to the postsynaptic membrane. Ligand-gated channels do not participate in setting the resting potential of a cell or in generating and conducting an action potential. In contrast, metabotropic receptors, by virtue of their ability to recruit freely diffusible intracellular second messengers, can act on channels that are located throughout the cell soma, dendrites, axons, and even presynaptic terminals and growth cones. As a result, a variety of channel types are affected by these indirect-acting receptors, including resting channels, voltage-gated channels that generate the action potential and that provide Ca influx for neurotransmitter release, and ligand-gated channels. - They can both open and close a channel: A third important difference is that metabotropic synaptic actions can not only increase channel opening, they can also decrease channel opening. Ionotropic channels only open a channel. *difference between two channels. - They do not mediate rapid behaviors; they usually modulate: the slow synaptic actions of metabotropic receptors normally are insufficient to cause a cell to fire an action potential. Consequently, they do not normally mediate rapid behaviors, as do the ionotropic receptors. However, they can greatly influence the electrophysiological properties of a cell, including changes in resting potential, input resistance, length and time constants, threshold potential, action potential duration, and repetitive firing 7 characteristics. Thus, the actions of metabotropic receptors are often referred to as modulatory synaptic actions. 8


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