Repetitive synaptic activity leads to calcium-dependent secretion of endogenous CGRP and subsequent increase of quantal size in mouse neuromuscular junctions

2018 ◽  
Author(s):  
Polina Bogatcheva
Keyword(s):  
Neuromuscular Junctions ◽  
Synaptic Activity ◽  
Subsequent Increase ◽  
Calcium Dependent ◽  
Quantal Size

Bidirectional Control of Quantal Size by Synaptic Activity in the Hippocampus

Science ◽  
1996 ◽  
Vol 271 (5253) ◽  
pp. 1294-1297 ◽  
Author(s):  
S. H. R. Oliet ◽  
R. C. Malenka ◽  
R. A. Nicoll
Keyword(s):  
Synaptic Activity ◽  
Quantal Size

Characterization of postsynaptic Ca2+ signals at the Drosophila larval NMJ

2011 ◽  
Vol 106 (2) ◽  
pp. 710-721 ◽  
Author(s):  
Sunil A. Desai ◽  
Gregory A. Lnenicka
Keyword(s):  
Transmitter Release ◽  
Postsynaptic Membrane ◽  
Synaptic Activity ◽  
Synaptic Efficacy ◽  
Single Action ◽  
Synaptic Homeostasis ◽  
Multiple Transcripts ◽  
Quantal Size ◽  
Intracellular Ca ◽  
Larval Neuromuscular Junction

Postsynaptic intracellular Ca2+ concentration ([Ca2+]i) has been proposed to play an important role in both synaptic plasticity and synaptic homeostasis. In particular, postsynaptic Ca2+ signals can alter synaptic efficacy by influencing transmitter release, receptor sensitivity, and protein synthesis. We examined the postsynaptic Ca2+ transients at the Drosophila larval neuromuscular junction (NMJ) by injecting the muscle fibers with Ca2+ indicators rhod-2 and Oregon Green BAPTA-1 (OGB-1) and then monitoring their increased fluorescence during synaptic activity. We observed discrete postsynaptic Ca2+ transients along the NMJ during single action potentials (APs) and quantal Ca2+ transients produced by spontaneous transmitter release. Most of the evoked Ca2+ transients resulted from the release of one or two quanta of transmitter and occurred largely at synaptic boutons. The magnitude of the Ca2+ signals was correlated with synaptic efficacy; the Is terminals, which produce larger excitatory postsynaptic potentials (EPSPs) and have a greater quantal size than Ib terminals, produced a larger Ca2+ signal per terminal length and larger quantal Ca2+ signals than the Ib terminals. During a train of APs, the postsynaptic Ca2+ signal increased but remained localized to the postsynaptic membrane. In addition, we showed that the plasma membrane Ca2+-ATPase (PMCA) played a role in extruding Ca2+ from the postsynaptic region of the muscle. Drosophila melanogaster has a single PMCA gene, predicted to give rise to various isoforms by alternative splicing. Using RT-PCR, we detected the expression of multiple transcripts in muscle and nervous tissues; the physiological significance of the same is yet to be determined.

scholarly journals Essential Functions of the Transcription Factor Npas4 in Neural Circuit Development, Plasticity, and Diseases

2020 ◽  
Vol 14 ◽  
Author(s):  
Jian Fu ◽  
Ouyang Guo ◽  
Zhihang Zhen ◽  
Junli Zhen
Keyword(s):  
Transcription Factor ◽  
Neural Circuit ◽  
Second Messenger ◽  
Synaptic Activity ◽  
Postsynaptic Potentials ◽  
Calcium Dependent ◽  
Neural Information ◽  
Formation Function ◽  
Second Messenger Pathways ◽  
Circuit Formation

Signaling from the synapse to nucleus is mediated by the integration and propagation of both membrane potential changes (postsynaptic potentials) and intracellular second messenger cascades. The electrical propagation of postsynaptic potentials allows for rapid neural information processing, while propagating second messenger pathways link synaptic activity to the transcription of genes required for neuronal survival and adaptive changes (plasticity) underlying circuit formation and learning. The propagation of activity-induced calcium signals to the cell nucleus is a major synapse-to-nucleus communication pathway. Neuronal PAS domain protein 4 (Npas4) is a recently discovered calcium-dependent transcription factor that regulates the activation of genes involved in the homeostatic regulation of excitatory–inhibitory balance, which is critical for neural circuit formation, function, and ongoing plasticity, as well as for defense against diseases such as epilepsy. Here, we summarize recent findings on the neuroprotective functions of Npas4 and the potential of Npas4 as a therapeutic target for the treatment of acute and chronic diseases of the central nervous system.

Neuromuscular transmission in dystrophic mice

1977 ◽  
Vol 40 (4) ◽  
pp. 836-843 ◽  
Author(s):  
S. Carbonetto
Keyword(s):  
Neuromuscular Transmission ◽  
Neuromuscular Junctions ◽  
Large Population ◽  
Muscle Fibers ◽  
Dystrophic Muscle ◽  
Quantum Content ◽  
Quantal Size ◽  
Significant Difference ◽  
Release Of Acetylcholine ◽  
Dystrophic Mice

1. Neuromuscular transmission was studied in the extensor digitorum-longus muscle of dystrophic mice (strain 129/ReJ) by means of intracellular recording techniques. 2. In a large population of normal and dystrophic muscle fibers tested, the incidence of transmission failure was about 2% and showed no significant difference between the two groups. 3. Quantal size and quantum content of dystrophic junctions were found to be normal. This was true even of nerve terminal on apparently atrophied muscle fibers. 4. The facilitation ratio at dystrophic junctions was not significantly different from normal. 5. Dystrophic neuromuscular junctions exhibited an abnormality high frequency of giant spontaneous potentials. Application of tetrodotoxin (10(-6) M) and curare (10(-6) M) indicated that these potentials were caused by impulse-independent release of acetylcholine. 6. Neuromuscular transmission in dystrophic mice was found functionally normal and unrelated to the degenerative state of the muscle.

scholarly journals Activity-dependent, homeostatic regulation of neurotransmitter release from auditory nerve fibers

2015 ◽  
Vol 112 (20) ◽  
pp. 6479-6484 ◽  
Author(s):  
Tenzin Ngodup ◽  
Jack A. Goetz ◽  
Brian C. McGuire ◽  
Wei Sun ◽  
Amanda M. Lauer ◽  
...  
Keyword(s):  
Auditory Nerve ◽  
Neurotransmitter Release ◽  
High Reliability ◽  
Downstream Processing ◽  
Nerve Fibers ◽  
Synaptic Activity ◽  
Quantal Size ◽  
Activity Dependent ◽  
The Brain ◽  
Homeostatic Response

Information processing in the brain requires reliable synaptic transmission. High reliability at specialized auditory nerve synapses in the cochlear nucleus results from many release sites (N), high probability of neurotransmitter release (Pr), and large quantal size (Q). However, high Pr also causes auditory nerve synapses to depress strongly when activated at normal rates for a prolonged period, which reduces fidelity. We studied how synapses are influenced by prolonged activity by exposing mice to constant, nondamaging noise and found that auditory nerve synapses changed to facilitating, reflecting low Pr. For mice returned to quiet, synapses recovered to normal depression, suggesting that these changes are a homeostatic response to activity. Two additional properties, Q and average excitatory postsynaptic current (EPSC) amplitude, were unaffected by noise rearing, suggesting that the number of release sites (N) must increase to compensate for decreased Pr. These changes in N and Pr were confirmed physiologically using the integration method. Furthermore, consistent with increased N, endbulbs in noise-reared animals had larger VGlut1-positive puncta, larger profiles in electron micrographs, and more release sites per profile. In current-clamp recordings, noise-reared BCs had greater spike fidelity even during high rates of synaptic activity. Thus, auditory nerve synapses regulate excitability through an activity-dependent, homeostatic mechanism, which could have major effects on all downstream processing. Our results also suggest that noise-exposed bushy cells would remain hyperexcitable for a period after returning to normal quiet conditions, which could have perceptual consequences.

The structure of the ventral nerve cord of Caenorhabditis elegans

1976 ◽  
Vol 275 (938) ◽  
pp. 327-348 ◽  
Keyword(s):  
Caenorhabditis Elegans ◽  
Synaptic Input ◽  
Neuromuscular Junctions ◽  
Nerve Ring ◽  
Motor Neurone ◽  
The Body ◽  
Synaptic Activity ◽  
Linear Sequence ◽  
Motor Neurones ◽  
Longitudinal Fibre

The nervous system of Caenorhabditis elegans is arranged as a series of fibre bundles which run along internal hypodermal ridges. Most of the sensory integration takes place in a ring of nerve fibres which is wrapped round the pharynx in the head. The body muscles in the head are innervated by motor neurones in this nerve ring while those in the lower part of the body are innervated by a set of motor neurones in a longitudinal fibre bundle which joins the nerve ring, the ventral cord. These motor neurones can be put into five classes on the basis of their morphology and synaptic input. At any one point along the cord only one member from each class has neuromuscular junctions. Members of a given class are arranged in a regular linear sequence in the cord and have non-overlapping fields of motor synaptic activity, the transition between fields of adjacent neurones being sharp and well defined. Members of a given class form gap junctions with neighbouring members of the same class but never to motor neurones of another class. Three of the motor neurone classes receive their synaptic input from a set of interneurones coming from the nerve ring. These interneurones can in turn be grouped into four classes and each of the three motor neurone classes receives its synaptic input from a unique combination of interneurone classes. The possible developmental and functional significance of these observations is discussed.

scholarly journals CaMKII Is Involved in the Choline-Induced Downregulation of Acetylcholine Release in Mouse Motor Synapses

Acta Naturae ◽  
2017 ◽  
Vol 9 (4) ◽  
pp. 110-113 ◽  
Author(s):  
A. E. Gaydukov ◽  
O. P. Balezina
Keyword(s):  
Protein Kinase ◽  
Nicotinic Acetylcholine Receptors ◽  
Acetylcholine Receptors ◽  
Inhibitory Effect ◽  
Synaptic Activity ◽  
Ach Release ◽  
Calcium Dependent ◽  
Calcium Calmodulin Dependent ◽  
Kinase C ◽  
Dependent Protein

We investigated the involvement of calcium-dependent enzymes, protein kinase C (PKC) and calcium-calmodulin-dependent protein kinase II (CaMKII), in the signaling pathway triggered by the activation of presynaptic alpha7-type nicotinic acetylcholine receptors by exogenous choline, leading to downregulation of the evoked acetylcholine (ACh) release in mouse motor synapses. Blockade of PKC with chelerythrine neither changed the evoked release of ACh by itself nor prevented the inhibitory effect of choline. The CaMKII blocker KN-62 did not affect synaptic activity but fully prevented the choline-induced downregulation of ACh release.

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