Literature DB >> 8251011

Cytosolic Ca2+ gradients, Ca2+ binding proteins and synaptic plasticity.

H Kasai1.   

Abstract

Trains of spikes encoded by presynaptic neurons are decoded into rises in cytosolic Ca2+ concentration both in presynaptic terminals and in postsynaptic dendrites. Intracellular [Ca2+] rises trigger neurotransmitter release and also induce short- and long-term modifications of synaptic efficacy. These modifications can be potentiation or depression depending on the intensity of stimuli. A dynamic mechanism, "dynamic decoding", is proposed to understand the multiplicity of the functions of Ca2+, based on recent knowledge of Ca2+ binding proteins and of the dynamics of Ca2+ signaling. The dynamic model is in many ways superior to static models, and may be applied to various neuronal functions including the induction of long-term plasticity in cerebral cortex.

Entities:  

Mesh:

Substances:

Year:  1993        PMID: 8251011     DOI: 10.1016/0168-0102(93)90002-8

Source DB:  PubMed          Journal:  Neurosci Res        ISSN: 0168-0102            Impact factor:   3.304


  4 in total

1.  [Ca2+]i elevations detected by BK channels during Ca2+ influx and muscarine-mediated release of Ca2+ from intracellular stores in rat chromaffin cells.

Authors:  M Prakriya; C R Solaro; C J Lingle
Journal:  J Neurosci       Date:  1996-07-15       Impact factor: 6.167

2.  CaV2 channel subtype expression in rat sympathetic neurons is selectively regulated by α2δ subunits.

Authors:  Mallory B Scott; Paul J Kammermeier
Journal:  Channels (Austin)       Date:  2017-09-21       Impact factor: 2.581

3.  Intracellular calcium regulates agrin-induced acetylcholine receptor clustering.

Authors:  L J Megeath; J R Fallon
Journal:  J Neurosci       Date:  1998-01-15       Impact factor: 6.167

Review 4.  Presynaptic nanodomains: a tale of two synapses.

Authors:  Lu-Yang Wang; George J Augustine
Journal:  Front Cell Neurosci       Date:  2015-01-26       Impact factor: 5.505

  4 in total

北京卡尤迪生物科技股份有限公司 © 2022-2023.