Two independent forms of activity-dependent potentiation regulate electrical transmission at mixed synapses on the Mauthner cell

Roger Cachope, Alberto E. Pereda

Research output: Contribution to journalArticle

8 Citations (Scopus)

Abstract

Mixed (electrical and chemical) synaptic contacts on the Mauthner cells, known as Club endings, constitute a valuable model for the study of vertebrate electrical transmission. While electrical synapses are still perceived by many as passive intercellular channels that lack modifiability, a wealth of experimental evidence shows that gap junctions at Club endings are subject to dynamic regulatory control by two independent activity-dependent mechanisms that lead to potentiation of electrical transmission. One of those mechanisms relies on activation of NMDA receptors and postsynaptic CaMKII. A second mechanism relies on mGluR activation and endocannabinoid production and is indirectly mediated via the release of dopamine from nearby varicosities, which in turn leads to potentiation of the synaptic response via a PKA-mediated postsynaptic mechanism. We review here these two forms of potentiation and their signaling mechanisms, which include the activation of two kinases with well-established roles as regulators of synaptic strength, as well as the functional implications of these two forms of potentiation. Special Issue entitled Electrical Synapses.

Original languageEnglish (US)
Pages (from-to)173-182
Number of pages10
JournalBrain Research
Volume1487
DOIs
StatePublished - Dec 3 2012

Fingerprint

Electrical Synapses
Synapses
Calcium-Calmodulin-Dependent Protein Kinase Type 2
Endocannabinoids
Gap Junctions
N-Methyl-D-Aspartate Receptors
Vertebrates
Dopamine
Phosphotransferases

Keywords

  • Auditory
  • CaMKII
  • Connexin 36
  • Dopamine
  • Endocannabinoid
  • Gap junction
  • Long-term potentiation
  • NMDA
  • PKA

ASJC Scopus subject areas

  • Neuroscience(all)
  • Clinical Neurology
  • Developmental Biology
  • Molecular Biology

Cite this

Two independent forms of activity-dependent potentiation regulate electrical transmission at mixed synapses on the Mauthner cell. / Cachope, Roger; Pereda, Alberto E.

In: Brain Research, Vol. 1487, 03.12.2012, p. 173-182.

Research output: Contribution to journalArticle

@article{c685bb4c3cdc4b0b87ed523d21268f15,
title = "Two independent forms of activity-dependent potentiation regulate electrical transmission at mixed synapses on the Mauthner cell",
abstract = "Mixed (electrical and chemical) synaptic contacts on the Mauthner cells, known as Club endings, constitute a valuable model for the study of vertebrate electrical transmission. While electrical synapses are still perceived by many as passive intercellular channels that lack modifiability, a wealth of experimental evidence shows that gap junctions at Club endings are subject to dynamic regulatory control by two independent activity-dependent mechanisms that lead to potentiation of electrical transmission. One of those mechanisms relies on activation of NMDA receptors and postsynaptic CaMKII. A second mechanism relies on mGluR activation and endocannabinoid production and is indirectly mediated via the release of dopamine from nearby varicosities, which in turn leads to potentiation of the synaptic response via a PKA-mediated postsynaptic mechanism. We review here these two forms of potentiation and their signaling mechanisms, which include the activation of two kinases with well-established roles as regulators of synaptic strength, as well as the functional implications of these two forms of potentiation. Special Issue entitled Electrical Synapses.",
keywords = "Auditory, CaMKII, Connexin 36, Dopamine, Endocannabinoid, Gap junction, Long-term potentiation, NMDA, PKA",
author = "Roger Cachope and Pereda, {Alberto E.}",
year = "2012",
month = "12",
day = "3",
doi = "10.1016/j.brainres.2012.05.059",
language = "English (US)",
volume = "1487",
pages = "173--182",
journal = "Brain Research",
issn = "0006-8993",
publisher = "Elsevier",

}

TY - JOUR

T1 - Two independent forms of activity-dependent potentiation regulate electrical transmission at mixed synapses on the Mauthner cell

AU - Cachope, Roger

AU - Pereda, Alberto E.

PY - 2012/12/3

Y1 - 2012/12/3

N2 - Mixed (electrical and chemical) synaptic contacts on the Mauthner cells, known as Club endings, constitute a valuable model for the study of vertebrate electrical transmission. While electrical synapses are still perceived by many as passive intercellular channels that lack modifiability, a wealth of experimental evidence shows that gap junctions at Club endings are subject to dynamic regulatory control by two independent activity-dependent mechanisms that lead to potentiation of electrical transmission. One of those mechanisms relies on activation of NMDA receptors and postsynaptic CaMKII. A second mechanism relies on mGluR activation and endocannabinoid production and is indirectly mediated via the release of dopamine from nearby varicosities, which in turn leads to potentiation of the synaptic response via a PKA-mediated postsynaptic mechanism. We review here these two forms of potentiation and their signaling mechanisms, which include the activation of two kinases with well-established roles as regulators of synaptic strength, as well as the functional implications of these two forms of potentiation. Special Issue entitled Electrical Synapses.

AB - Mixed (electrical and chemical) synaptic contacts on the Mauthner cells, known as Club endings, constitute a valuable model for the study of vertebrate electrical transmission. While electrical synapses are still perceived by many as passive intercellular channels that lack modifiability, a wealth of experimental evidence shows that gap junctions at Club endings are subject to dynamic regulatory control by two independent activity-dependent mechanisms that lead to potentiation of electrical transmission. One of those mechanisms relies on activation of NMDA receptors and postsynaptic CaMKII. A second mechanism relies on mGluR activation and endocannabinoid production and is indirectly mediated via the release of dopamine from nearby varicosities, which in turn leads to potentiation of the synaptic response via a PKA-mediated postsynaptic mechanism. We review here these two forms of potentiation and their signaling mechanisms, which include the activation of two kinases with well-established roles as regulators of synaptic strength, as well as the functional implications of these two forms of potentiation. Special Issue entitled Electrical Synapses.

KW - Auditory

KW - CaMKII

KW - Connexin 36

KW - Dopamine

KW - Endocannabinoid

KW - Gap junction

KW - Long-term potentiation

KW - NMDA

KW - PKA

UR - http://www.scopus.com/inward/record.url?scp=84869508673&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=84869508673&partnerID=8YFLogxK

U2 - 10.1016/j.brainres.2012.05.059

DO - 10.1016/j.brainres.2012.05.059

M3 - Article

VL - 1487

SP - 173

EP - 182

JO - Brain Research

JF - Brain Research

SN - 0006-8993

ER -