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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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) |
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gap junction connexin36 LTD GABA<sub>B</sub> receptor Biology (General) QH301-705.5 Chemistry QD1-999 |
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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 |
_version_ |
1718411843183050752 |