Chemical synapse

Summary

Chemical synapses are biological junctions through which neurons' signals can be sent to each other and to non-neuronal cells such as those in muscles or glands. Chemical synapses allow neurons to form circuits within the central nervous system. They are crucial to the biological computations that underlie perception and thought. They allow the nervous system to connect to and control other systems of the body. At a chemical synapse, one neuron releases neurotransmitter molecules into a small space (the synaptic cleft) that is adjacent to another neuron. The neurotransmitters are contained within small sacs called synaptic vesicles, and are released into the synaptic cleft by exocytosis. These molecules then bind to neurotransmitter receptors on the postsynaptic cell. Finally, the neurotransmitters are cleared from the synapse through one of several potential mechanisms including enzymatic degradation or re-uptake by specific transporters either on the presynaptic cell or on some o

Official source

https://en.wikipedia.org/wiki/Chemical_synapse

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The aim of this study is to contribute to understand the physiology of the Olfactory System through detailed microcircuit investigation, adopting advanced electrophysiological and anatomical techniques. Multiple patch clamp recordings allow understanding the structural foundations supporting the network architecture, the biophysical rules adopted by the microcircuit connectivity and the fine dynamic of the synaptic transmission. The study focuses on the Olfactory Bulb microcircuit as a first neuronal processor of sensory inputs. The excitatory elements of the Olfactory Bulb microcircuit are anatomically defined by affiliation to the same receptive field: the Glomerulus. A correlated subthreshold activity between microcircuit elements defines the physiological signature of the microcircuit. We experimentally addressed three fundamental issues: origin of the correlated subthreshold activity, connectivity rules and dynamic of the synaptic transmission. In the first study we attribute the origin of correlated subthreshold activity to a class of pacemaker cells responsible for the synchronization of the population onset and acting therefore as a timer of the microcircuit response. In the second study we investigated the connectivity rules supporting the interaction between excitatory cells. The tight apposition between gap junctions and chemical synapses on the excitatory cells dendrites allows gap junctions to propagate postsynaptic potentials toward surrounding compartments. The result of the propagation is represented by an enhancement in the amplification of the sensory information and an increase in the speed of the reaction time. In the third study we extensively analyzed the mechanisms of the synaptic transmission and the activity dependent properties of synapses, revealing a potential role for the short-term plasticity in the development of the sensory processing. The results of our investigation are going to constitute the foundation of a database available for high definition multi-compartmental modeling of the Olfactory Bulb network.

EPFL2009

Identification of Signaling Mechanisms Determining the Development of Large Excitatory Synapses in the Lower Auditory System

Le Xiao

In the brainstem auditory circuit of mammals and birds, excitatory synapses with extraordinarily large size have evolved, which ensure fast membrane potential signaling mediated by large, multiquantal excitatory postsynaptic currents (EPSCs). The so-called "calyx of Held" synapses are formed by the globular bushy cells (GBCs) in the ventral cochlear nucleus (VCN) onto the contralateral medial nucleus of the trapezoid body (MNTB) neurons. One the other hand, the spherical bushy cells (SBCs) in the VCN project to the lateral superior olive (LSO), where they form small bouton-like synapses. Therefore, the lower auditory brainstem circuits constitute an example of synapse-specificity, in which presynaptic neuron pools are connected through highly specific synapses to their postsynaptic partner neurons. Calyx of Held synapses are formed at postnatal day 2 - 4 in rodents in a target-cell specific manner and prior to the onset of hearing. The molecular signaling pathways which drive the formation of these synapses are unknown. Here we identify bone morphogenetic protein (BMP) signaling as an essential signaling pathway in the development of calyces of Held. Through unbiased genome-wide transcriptome analyses in rats and mice, BMPs were identified as candidates for diffusible signaling molecules which are expressed at a higher level in the MNTB (the target area of calyces of Held), as compared to the LSO. The microarray analysis was validated by quantitative PCR (qPCR) and in-situ hybridisation. A conditional knock-out (KO) of BMP-receptor 1a (BMPR1a) in the lower auditory system, in the genetic background of a conventional KO of BMP-receptor 1b (BMPR1b), was then used to address the role of BMP-receptor signaling for calyx of Held formation in vivo. Genetically knocking out BMPR1a/1b activity in the auditory brainstem led to a drastic deficit at the calyx of Held synapses both morphologically and functionally, as well as to the persistence of multiple innervation of MNTB neurons. This study therefore shows that BMP signaling drives the development of the large calyx of Held synapses. The study offers a possible mechanism for the specificity of a large excitatory synapse formation in the central nervous systems (CNS). In addition, the study shows a novel function of BMP signaling in synaptogenesis in the mammalian CNS.

EPFL2011

Homeostatic regulation of axonal Kv1.1 channels accounts for both synaptic and intrinsic modifications in the hippocampal CA3 circuit

Mickael Maurice Zbili

Homeostatic plasticity of intrinsic excitability goes hand in hand with homeostatic plasticity of synaptic transmission. However, the mechanisms linking the two forms of homeostatic regulation have not been identified so far. Using electrophysiological, imaging, and immunohistochemical techniques, we show here that blockade of excitatory synaptic receptors for 2 to 3 d induces an up-regulation of both synaptic transmission at CA3-CA3 connections and intrinsic excitability of CA3 pyramidal neurons. Intrinsic plasticity was found to be mediated by a reduction of Kv1.1 channel density at the axon initial segment. In activity-deprived circuits, CA3-CA3 synapses were found to express a high release probability, an insensitivity to dendrotoxin, and a lack of depolarization-induced presynaptic facilitation, indicating a reduction in presynaptic Kv1.1 function. Further support for the down-regulation of axonal Kv1.1 channels in activity-deprived neurons was the broadening of action potentials measured in the axon. We conclude that regulation of the axonal Kv1.1 channel constitutes a major mechanism linking intrinsic excitability and synaptic strength that accounts for the functional synergy existing between homeostatic regulation of intrinsic excitability and synaptic transmission.

NATL ACAD SCIENCES2021

EPFL2009

Identification of Signaling Mechanisms Determining the Development of Large Excitatory Synapses in the Lower Auditory System

Le Xiao

EPFL2011