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Description : Check out this medical presentation on Neurology, which is titled "Synaptic transmission", to know about synaptic transmission and the communication between neurons.

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Published on : Aug 23, 2021 | Views : 522 | Downloads : 0

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Slide 1-

Synaptic transmission John Jacques
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Communication between neurons
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Communication between neurons Staggering diversity of synapse morphologies and types in the brain Fundamental process of synaptic transmission same A key quantity in neural circuits is the synaptic efficacy or strength, which varies over time. long-term potentiation and depression constitute the basis of learning and memory
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Arrival of an action potential Release of neurotransmitter Binds to receptors Generate a response in the postsynaptic neuron
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Reserve pool (80-95%) Recycling pool (5-20%) Readily-releasable pool (0.1-2%; 5-10 synapses per active zone) Docked vesicles lie close to plasma membrane (within 30 nm) Primed vesicles fuse with the plasma membrane by sustained depolarization high K+, elevated Ca++, hypertonic sucrose treatment Fusion release transmitter near calcium channels The ‘active zone’ Exocytosis Endocytosis
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Inhibitory Neurotransmitters: Glycine and GABA Excitatory Neurotransmitters: ACh and glutamate
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T(t): amount of transmitter released into the synaptic cleft at time t. N(t) available for release vesicles changes over time since the occupancy of the pool changes during neural activity p(t)release probability dramatically increases upon the arrival of a presynaptic AP Focus on the action of ionotropic receptors ion channel that opens when transmitter is bound
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Postsynaptic conductance proportional to the amount of transmitter released Equation 2 above peak conductance is denoted by gm Postsynaptic conductance
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Short term plasticity discuss biological background and plausibility Mechanistic aspects of these models Vesicle depletion and facilitation Use-dependent vesicle replenishment Receptor desensitization Stochasticity of synapses Outlook/Conclusion
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Synaptic depression and facilitation Depression: progressive reduction of the postsynaptic response during repetitive presynaptic activity Facilitation: an increase synaptic efficacy. Different mechanisms with different time constants Not mutually exclusive most synapses express some combination of these two mechanisms Variable between different neuron types
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STP: Factors located in the presynaptic terminal contain vesicles filled with neurotransmitter Opposed by the postsynaptic density (PSD) Area that contains a large number of different proteins implicated in synapse maintenance and plasticity contains the bulk of the neurotransmitter receptors mediating the postsynaptic response
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Opening of voltage gated calcium channels (VGCC) Intracellular concentration increase increases the probability of vesicle fusion with the cell membrane subsequent release of transmitter into the synaptic cleft (equation 1) activity-dependent; function of time. [Ca2+]i and release probability p not linear The release of a single vesicle smallest signal transmitted to the postsynaptic neuron spontaneous current small fraction in terminal in AZ
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Presynaptic vesicles are a limited resource during ongoing activity can lead to a suppression of the postsynaptic response model predicts an exponential decay of the postsynaptic response (A) Time constant order of seconds Faster decay- higher p steady state values decrease more slowly with increasing frequency (E) Suggests other mechanism
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Depression model counteracted by facilitation accumulation of residual calcium in the synaptic terminal causes rapid VGCC facilitation increases the release probability after each presynaptic spike Time constant : range of tens of milliseconds much faster than vesicle replenishment
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Vesicle replenishment accelerate after intensive stimulation. increase in intracellular calcium concentration Enhanced vesicle replenishment included in the depletion model adding some form of activity-dependent component to Equation (7) Use-dependent replenishment reflect faster recruitment due to more efficient endocytosis A main function of mechanism maintain the ability of a synapse to transmit during sustained periods of high activity
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Synaptic depression due to desensitization the state of the population of receptors D(t) (10) Recovery from desensitization order of tens of milliseconds only effective during intense episodes of activity desensitization important property of receptors contribute to synaptic depression during physiological activity levels
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Transmitter release postsynaptic current fluctuates from time to time. Changes in the synaptic parameters due to short term plasticity cause changes in the average postsynaptic response magnitude of the fluctuations measured by the coefficient of variation: (11) Stochasticity of synapses
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Theoretical models have contributed much to our understanding of synaptic transmission and short term plasticity Relationship between depletion and facilitation key variables in these models have direct measurable correlates Not straight forward to experimentally interfere with short term plasticity Valuable tool that enables analysis beyond the experimentally feasible. Short term plasticity may related to homeostatic effects or metabolic efficacy of synapses Outlook/Conclusion
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REFENCES Hennig, Matthias H. “Theoretical Models of Synaptic Short Term Plasticity.” Frontiers in Computational Neuroscience 7 (2013): 45. PMC. Web. 3 Oct. 2017. Destexhe, A., Mainen, Z. and Sejnowski, T. (1994). Synthesis of models for excitable membranes, synaptic transmission and neuromodulation using a common kinetic formalism. Journal of Computational Neuroscience, [online] 1(3), pp.195-230. Available at: https://www.ncbi.nlm.nih.gov/pubmed/8792231 [Accessed 2 Oct. 2017].
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QUESTIONS??