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Article

GABABR Modulation of Electrical Synapses and Plasticity in the Thalamic Reticular Nucleus

Department of Biological Sciences, Lehigh University, 111 Research Drive, Bethlehem, PA 18015, USA
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Author to whom correspondence should be addressed.
Academic Editor: Camillo Peracchia
Int. J. Mol. Sci. 2021, 22(22), 12138; https://doi.org/10.3390/ijms222212138
Received: 14 October 2021 / Revised: 31 October 2021 / Accepted: 5 November 2021 / Published: 9 November 2021
(This article belongs to the Special Issue Chemical Regulation of Gap Junction Channels and Hemichannels 2.0)
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 GABAB receptor activity, here we examined the impact of GABAB 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 GABAB receptor inactivation itself induces a modest depression of electrical synapses and occludes LTD induction by either paired bursting or metabotropic glutamate receptor (mGluR) activation. GABAB 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 GABAB 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. View Full-Text
Keywords: gap junction connexin36; LTD; GABAB receptor gap junction connexin36; LTD; GABAB receptor
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MDPI and ACS Style

Wang, H.; Haas, J.S. GABABR Modulation of Electrical Synapses and Plasticity in the Thalamic Reticular Nucleus. Int. J. Mol. Sci. 2021, 22, 12138. https://doi.org/10.3390/ijms222212138

AMA Style

Wang H, Haas JS. GABABR Modulation of Electrical Synapses and Plasticity in the Thalamic Reticular Nucleus. International Journal of Molecular Sciences. 2021; 22(22):12138. https://doi.org/10.3390/ijms222212138

Chicago/Turabian Style

Wang, Huaixing, and Julie S. Haas. 2021. "GABABR Modulation of Electrical Synapses and Plasticity in the Thalamic Reticular Nucleus" International Journal of Molecular Sciences 22, no. 22: 12138. https://doi.org/10.3390/ijms222212138

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