GABA<sub>B</sub>R Modulation of Electrical Synapses and Plasticity in the Thalamic Reticular Nucleus

Two distinct types of neuronal activity result in long-term depression (LTD) of electrical synapses, with overlapping biochemical intracellular signaling pathways that link activity to synaptic strength, in electrically coupled neurons of the thalamic reticular nucleus (TRN). Because components of b...

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Autores principales: Huaixing Wang, Julie S. Haas
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Lenguaje:EN
Publicado: MDPI AG 2021
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LTD
Acceso en línea:https://doaj.org/article/09ef2eaa38a6479883eb5eb17ed59b0a
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spelling oai:doaj.org-article:09ef2eaa38a6479883eb5eb17ed59b0a2021-11-25T17:53:43ZGABA<sub>B</sub>R Modulation of Electrical Synapses and Plasticity in the Thalamic Reticular Nucleus10.3390/ijms2222121381422-00671661-6596https://doaj.org/article/09ef2eaa38a6479883eb5eb17ed59b0a2021-11-01T00:00:00Zhttps://www.mdpi.com/1422-0067/22/22/12138https://doaj.org/toc/1661-6596https://doaj.org/toc/1422-0067Two distinct types of neuronal activity result in long-term depression (LTD) of electrical synapses, with overlapping biochemical intracellular signaling pathways that link activity to synaptic strength, in electrically coupled neurons of the thalamic reticular nucleus (TRN). Because components of both signaling pathways can also be modulated by GABA<sub>B</sub> receptor activity, here we examined the impact of GABA<sub>B</sub> receptor activation on the two established inductors of LTD in electrical synapses. Recording from patched pairs of coupled rat neurons in vitro, we show that GABA<sub>B</sub> receptor inactivation itself induces a modest depression of electrical synapses and occludes LTD induction by either paired bursting or metabotropic glutamate receptor (mGluR) activation. GABA<sub>B</sub> activation also occludes LTD from either paired bursting or mGluR activation. Together, these results indicate that afferent sources of GABA, such as those from the forebrain or substantia nigra to the reticular nucleus, gate the induction of LTD from either neuronal activity or afferent glutamatergic receptor activation. These results add to a growing body of evidence that the regulation of thalamocortical transmission and sensory attention by TRN is modulated and controlled by other brain regions. Significance: We show that electrical synapse plasticity is gated by GABA<sub>B</sub> receptors in the thalamic reticular nucleus. This effect is a novel way for afferent GABAergic input from the basal ganglia to modulate thalamocortical relay and is a possible mediator of intra-TRN inhibitory effects.Huaixing WangJulie S. HaasMDPI AGarticlegap junction connexin36LTDGABA<sub>B</sub> receptorBiology (General)QH301-705.5ChemistryQD1-999ENInternational Journal of Molecular Sciences, Vol 22, Iss 12138, p 12138 (2021)
institution DOAJ
collection DOAJ
language EN
topic gap junction connexin36
LTD
GABA<sub>B</sub> receptor
Biology (General)
QH301-705.5
Chemistry
QD1-999
spellingShingle gap junction connexin36
LTD
GABA<sub>B</sub> receptor
Biology (General)
QH301-705.5
Chemistry
QD1-999
Huaixing Wang
Julie S. Haas
GABA<sub>B</sub>R Modulation of Electrical Synapses and Plasticity in the Thalamic Reticular Nucleus
description Two distinct types of neuronal activity result in long-term depression (LTD) of electrical synapses, with overlapping biochemical intracellular signaling pathways that link activity to synaptic strength, in electrically coupled neurons of the thalamic reticular nucleus (TRN). Because components of both signaling pathways can also be modulated by GABA<sub>B</sub> receptor activity, here we examined the impact of GABA<sub>B</sub> receptor activation on the two established inductors of LTD in electrical synapses. Recording from patched pairs of coupled rat neurons in vitro, we show that GABA<sub>B</sub> receptor inactivation itself induces a modest depression of electrical synapses and occludes LTD induction by either paired bursting or metabotropic glutamate receptor (mGluR) activation. GABA<sub>B</sub> activation also occludes LTD from either paired bursting or mGluR activation. Together, these results indicate that afferent sources of GABA, such as those from the forebrain or substantia nigra to the reticular nucleus, gate the induction of LTD from either neuronal activity or afferent glutamatergic receptor activation. These results add to a growing body of evidence that the regulation of thalamocortical transmission and sensory attention by TRN is modulated and controlled by other brain regions. Significance: We show that electrical synapse plasticity is gated by GABA<sub>B</sub> receptors in the thalamic reticular nucleus. This effect is a novel way for afferent GABAergic input from the basal ganglia to modulate thalamocortical relay and is a possible mediator of intra-TRN inhibitory effects.
format article
author Huaixing Wang
Julie S. Haas
author_facet Huaixing Wang
Julie S. Haas
author_sort Huaixing Wang
title GABA<sub>B</sub>R Modulation of Electrical Synapses and Plasticity in the Thalamic Reticular Nucleus
title_short GABA<sub>B</sub>R Modulation of Electrical Synapses and Plasticity in the Thalamic Reticular Nucleus
title_full GABA<sub>B</sub>R Modulation of Electrical Synapses and Plasticity in the Thalamic Reticular Nucleus
title_fullStr GABA<sub>B</sub>R Modulation of Electrical Synapses and Plasticity in the Thalamic Reticular Nucleus
title_full_unstemmed GABA<sub>B</sub>R Modulation of Electrical Synapses and Plasticity in the Thalamic Reticular Nucleus
title_sort gaba<sub>b</sub>r modulation of electrical synapses and plasticity in the thalamic reticular nucleus
publisher MDPI AG
publishDate 2021
url https://doaj.org/article/09ef2eaa38a6479883eb5eb17ed59b0a
work_keys_str_mv AT huaixingwang gabasubbsubrmodulationofelectricalsynapsesandplasticityinthethalamicreticularnucleus
AT julieshaas gabasubbsubrmodulationofelectricalsynapsesandplasticityinthethalamicreticularnucleus
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