Synaptic Transmission in the Nervous System

2020 ◽  
pp. 106-120
e-Neuroforum ◽  
2017 ◽  
Vol 23 (4) ◽  
Author(s):  
Jens Rettig ◽  
David R. Stevens

AbstractThe release of neurotransmitters at synapses belongs to the most important processes in the central nervous system. In the last decades much has been learned about the molecular mechanisms which form the basis for this fundamental process. Highly regulated exocytosis, based on the SNARE (soluble N-ethylmaleimide-sensitive attachment protein receptor) complex and its regulatory molecules is the signature specialization of the nervous system and is shared by neurons and neuroendocrine cells. Cells of the immune system use a similar mechanism to release cytotoxic materials from secretory granules at contacts with virally or bacterially infected cells or cancer cells, in order to remove these threats. These contact zones have been termed immunological synapses in reference to the highly specific targeted exocytosis of effector molecules. Recent findings indicate that mutations in SNARE or SNARE-interacting proteins are the basis of a number of devastating immunological diseases. While SNARE complexes are ubiquitous and mediate a wide variety of membrane fusion events it is surprising that in many cases the SNARE proteins involved in immunological synapses are the same molecules which mediate regulated exocytosis of transmitters and hormones in neurons and neuroendocrine cells. These similarities raise the possibility that results obtained at immunological synapses may be applicable, in particular in the area of presynaptic function, to neuronal synapses. Since immunological synapses (IS) are assembled and disassembled in about a half an hour, the use of immune cells isolated from human blood allows not only the study of the molecular mechanisms of synaptic transmission in human cells, but is particularly suited to the examination of the assembly and disassembly of these “synapses” via live imaging. In this overview we discuss areas of similarity between synapses of the nervous and immune systems and in the process will refer to results of our experiments of the last few years.


1976 ◽  
Vol 4 (3) ◽  
pp. 199-202 ◽  
Author(s):  
T. A. Torda ◽  
P. W. Gage

Thiopentone and pentobarbitone reduce the time constant of decay of miniature end-plate currents when applied in anaesthetic concentrations to the neuromuscular junction. Such an effect at central synapses would lead to failure of synaptic transmission in the central nervous system and may reflect a common mode of action of many anaesthetic drugs.


1958 ◽  
Vol 192 (3) ◽  
pp. 447-452 ◽  
Author(s):  
Sadayuki F. Takagi ◽  
Yutaka Oomura

The effect of nicotine on synaptic transmission in the frog and cat spinal cord was studied. Both a regular wick electrode and a microelectrode of the Ling-Gerard type were used. The reflex activity of the bullfrog spinal cord is facilitated by 0.01% nicotine solution, but is depressed and abolished by 0.1% solution. In the cat, intravenous administration of 150 mg/kg fails to block reflex activity, but topical application does block. The intracellular potential, of both frog and cat motoneurones, shows no change in the synaptic potential after application of the drug, but the spike appears after a shorter synaptic delay and one or more additional spikes appear. When the synaptic delay becomes sufficiently short, however, all spikes suddenly disappear, leaving the still unchanged synaptic potential. Occasionally the synaptic delay is again increased just before the spike potentials disappear. The excitability of a frog motoneurone was measured, by a recording microelectrode, before and after nicotine application. The drug first increased and then decreases excitability. Epinephrine can restore a reflex discharge depressed or abolished by nicotine. It is concluded that high concentrations of nicotine block synaptic transmission in the central nervous system, acting on the cell body but not on the synaptic potential.


2019 ◽  
Vol 25 (5) ◽  
pp. 408-419 ◽  
Author(s):  
Jessica A. Fawley ◽  
Michael C. Andresen

Nervous system communication relies on neurotransmitter release for synaptic transmission between neurons. Neurotransmitter is contained within vesicles in presynaptic terminals and intraterminal calcium governs the fundamental step of their release into the synaptic cleft. Despite a common dependence on calcium, synaptic transmission and its modulation varies highly across the nervous system. The precise mechanisms that underlie this heterogeneity, however, remain unclear. The present review highlights recent data that reveal vesicles sourced from separate pools define discrete modes of release. A rich diversity of regulatory machinery may further distinguish the different forms of vesicle release, including presynaptic proteins involved in trafficking, alignment, and exocytosis. These multiple vesicle release mechanisms and vesicle pools likely depend on the arrangement of vesicles in relation to specific calcium entry pathways that create compartmentalized spheres of calcium influence (i.e., domains). This diversity permits release specialization. This review details examples of how individual neurons rely on multiple calcium sources and unique regulatory schemes to provide differential release and discrete modulation of neurotransmitter release from specific vesicle pools—as part of network signal integration.


2017 ◽  
Vol 1 (3) ◽  
Author(s):  
Vito Di Maio ◽  
Francesco Ventriglia ◽  
Silvia Santillo

Synaptic transmission is the basic mechanism of information transfer between neurons not only in the brain, but along all the nervous system. In this review we will briefly summarize some of the main parameters that produce stochastic variability in the synaptic response. This variability produces different effects on important brain phenomena, like learning and memory, and, alterations of its basic factors can cause brain malfunctioning.


Physiology ◽  
1996 ◽  
Vol 11 (4) ◽  
pp. 161-166
Author(s):  
H Ohmori

Hair cells transduce mechanical information into electrical signal and, via afferent synapse, transmit it to the central nervous system (CNS). Hair cells receive cholinergic efferent innervation from the CNS, and a long-lasting membrane hyperpolarization is produced by activation of Ca2+-activated K+ channels. Acetylcholine may facilitate afferent synaptic transmission by suppressing K+ channels on the afferent nerve terminal.


2010 ◽  
Vol 38 (6) ◽  
pp. 1527-1530 ◽  
Author(s):  
Joel D. Richter

Synapses, points of contact between axons and dendrites, are conduits for the flow of information in the circuitry of the central nervous system. The strength of synaptic transmission reflects the interconnectedness of the axons and dendrites at synapses; synaptic strength in turn is modified by the frequency with which the synapses are stimulated. This modulation of synaptic strength, or synaptic plasticity, probably forms the cellular basis for learning and memory. RNA metabolism, particularly translational control at or near the synapse, is one process that controls long-lasting synaptic plasticity and, by extension, memory formation and consolidation. In the present paper, I review some salient features of translational control of synaptic plasticity.


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