GIRK2 splice variants and neuronal G protein-gated K+ channels: implications for channel function and behavior

Abstract Many neurotransmitters directly inhibit neurons by activating G protein-gated inwardly rectifying K+ (GIRK) channels, thereby moderating the influence of excitatory input on neuronal excitability. While most neuronal GIRK channels are formed by GIRK1 and GIRK2 subunits, distinct GIRK2 isofo...

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Autores principales:	Ezequiel Marron Fernandez de Velasco, Lei Zhang, Baovi N. Vo, Megan Tipps, Shannon Farris, Zhilian Xia, Allison Anderson, Nicholas Carlblom, C. David Weaver, Serena M. Dudek, Kevin Wickman
Formato:	article
Lenguaje:	EN
Publicado:	Nature Portfolio 2017
Materias:	Medicine R Science Q
Acceso en línea:	https://doaj.org/article/71558560ec304bf5a09b60698ab9c399
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spelling	oai:doaj.org-article:71558560ec304bf5a09b60698ab9c3992021-12-02T16:08:12ZGIRK2 splice variants and neuronal G protein-gated K+ channels: implications for channel function and behavior10.1038/s41598-017-01820-22045-2322https://doaj.org/article/71558560ec304bf5a09b60698ab9c3992017-05-01T00:00:00Zhttps://doi.org/10.1038/s41598-017-01820-2https://doaj.org/toc/2045-2322Abstract Many neurotransmitters directly inhibit neurons by activating G protein-gated inwardly rectifying K+ (GIRK) channels, thereby moderating the influence of excitatory input on neuronal excitability. While most neuronal GIRK channels are formed by GIRK1 and GIRK2 subunits, distinct GIRK2 isoforms generated by alternative splicing have been identified. Here, we compared the trafficking and function of two isoforms (GIRK2a and GIRK2c) expressed individually in hippocampal pyramidal neurons lacking GIRK2. GIRK2a and GIRK2c supported comparable somato-dendritic GIRK currents in Girk2 −/− pyramidal neurons, although GIRK2c achieved a more uniform subcellular distribution in pyramidal neurons and supported inhibitory postsynaptic currents in distal dendrites better than GIRK2a. While over-expression of either isoform in dorsal CA1 pyramidal neurons restored contextual fear learning in a conditional Girk2 −/− mouse line, GIRK2a also enhanced cue fear learning. Collectively, these data indicate that GIRK2 isoform balance within a neuron can impact the processing of afferent inhibitory input and associated behavior.Ezequiel Marron Fernandez de VelascoLei ZhangBaovi N. VoMegan TippsShannon FarrisZhilian XiaAllison AndersonNicholas CarlblomC. David WeaverSerena M. DudekKevin WickmanNature PortfolioarticleMedicineRScienceQENScientific Reports, Vol 7, Iss 1, Pp 1-15 (2017)
institution	DOAJ
collection	DOAJ
language	EN
topic	Medicine R Science Q
spellingShingle	Medicine R Science Q Ezequiel Marron Fernandez de Velasco Lei Zhang Baovi N. Vo Megan Tipps Shannon Farris Zhilian Xia Allison Anderson Nicholas Carlblom C. David Weaver Serena M. Dudek Kevin Wickman GIRK2 splice variants and neuronal G protein-gated K+ channels: implications for channel function and behavior
description	Abstract Many neurotransmitters directly inhibit neurons by activating G protein-gated inwardly rectifying K+ (GIRK) channels, thereby moderating the influence of excitatory input on neuronal excitability. While most neuronal GIRK channels are formed by GIRK1 and GIRK2 subunits, distinct GIRK2 isoforms generated by alternative splicing have been identified. Here, we compared the trafficking and function of two isoforms (GIRK2a and GIRK2c) expressed individually in hippocampal pyramidal neurons lacking GIRK2. GIRK2a and GIRK2c supported comparable somato-dendritic GIRK currents in Girk2 −/− pyramidal neurons, although GIRK2c achieved a more uniform subcellular distribution in pyramidal neurons and supported inhibitory postsynaptic currents in distal dendrites better than GIRK2a. While over-expression of either isoform in dorsal CA1 pyramidal neurons restored contextual fear learning in a conditional Girk2 −/− mouse line, GIRK2a also enhanced cue fear learning. Collectively, these data indicate that GIRK2 isoform balance within a neuron can impact the processing of afferent inhibitory input and associated behavior.
format	article
author	Ezequiel Marron Fernandez de Velasco Lei Zhang Baovi N. Vo Megan Tipps Shannon Farris Zhilian Xia Allison Anderson Nicholas Carlblom C. David Weaver Serena M. Dudek Kevin Wickman
author_facet	Ezequiel Marron Fernandez de Velasco Lei Zhang Baovi N. Vo Megan Tipps Shannon Farris Zhilian Xia Allison Anderson Nicholas Carlblom C. David Weaver Serena M. Dudek Kevin Wickman
author_sort	Ezequiel Marron Fernandez de Velasco
title	GIRK2 splice variants and neuronal G protein-gated K+ channels: implications for channel function and behavior
title_short	GIRK2 splice variants and neuronal G protein-gated K+ channels: implications for channel function and behavior
title_full	GIRK2 splice variants and neuronal G protein-gated K+ channels: implications for channel function and behavior
title_fullStr	GIRK2 splice variants and neuronal G protein-gated K+ channels: implications for channel function and behavior
title_full_unstemmed	GIRK2 splice variants and neuronal G protein-gated K+ channels: implications for channel function and behavior
title_sort	girk2 splice variants and neuronal g protein-gated k+ channels: implications for channel function and behavior
publisher	Nature Portfolio
publishDate	2017
url	https://doaj.org/article/71558560ec304bf5a09b60698ab9c399
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GIRK2 splice variants and neuronal G protein-gated K+ channels: implications for channel function and behavior

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