Group II metabotropic glutamate receptors depress synaptic transmission onto subicular burst firing neurons.

The subiculum (SUB) is a pivotal structure positioned between the hippocampus proper and various cortical and subcortical areas. Despite the growing body of anatomical and intrinsic electrophysiological data of subicular neurons, modulation of synaptic transmission in the SUB is not well understood....

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Autores principales:	Michael Kintscher, Jörg Breustedt, Stéphanie Miceli, Dietmar Schmitz, Christian Wozny
Formato:	article
Lenguaje:	EN
Publicado:	Public Library of Science (PLoS) 2012
Materias:	Medicine R Science Q
Acceso en línea:	https://doaj.org/article/5fdf062d237b4fcdb6d8bdbd1070be82
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spelling	oai:doaj.org-article:5fdf062d237b4fcdb6d8bdbd1070be822021-11-18T07:05:58ZGroup II metabotropic glutamate receptors depress synaptic transmission onto subicular burst firing neurons.1932-620310.1371/journal.pone.0045039https://doaj.org/article/5fdf062d237b4fcdb6d8bdbd1070be822012-01-01T00:00:00Zhttps://www.ncbi.nlm.nih.gov/pmc/articles/pmid/22984605/?tool=EBIhttps://doaj.org/toc/1932-6203The subiculum (SUB) is a pivotal structure positioned between the hippocampus proper and various cortical and subcortical areas. Despite the growing body of anatomical and intrinsic electrophysiological data of subicular neurons, modulation of synaptic transmission in the SUB is not well understood. In the present study we investigated the role of group II metabotropic glutamate receptors (mGluRs), which have been shown to be involved in the regulation of synaptic transmission by suppressing presynaptic cAMP activity. Using field potential and patch-clamp whole cell recordings we demonstrate that glutamatergic transmission at CA1-SUB synapses is depressed by group II mGluRs in a cell-type specific manner. Application of the group II mGluR agonist (2S,1'R,2'R,3'R)-2-(2, 3-dicarboxycyclopropyl)glycine (DCG-IV) led to a significantly higher reduction of excitatory postsynaptic currents in subicular bursting cells than in regular firing cells. We further used low-frequency stimulation protocols and brief high-frequency bursts to test whether synaptically released glutamate is capable of activating presynaptic mGluRs. However, neither frequency facilitation is enhanced in the presence of the group II mGluR antagonist LY341495, nor is a test stimulus given after a high-frequency burst. In summary, we present pharmacological evidence for presynaptic group II mGluRs targeting subicular bursting cells, but both low- and high-frequency stimulation protocols failed to activate presynaptically located mGluRs.Michael KintscherJörg BreustedtStéphanie MiceliDietmar SchmitzChristian WoznyPublic Library of Science (PLoS)articleMedicineRScienceQENPLoS ONE, Vol 7, Iss 9, p e45039 (2012)
institution	DOAJ
collection	DOAJ
language	EN
topic	Medicine R Science Q
spellingShingle	Medicine R Science Q Michael Kintscher Jörg Breustedt Stéphanie Miceli Dietmar Schmitz Christian Wozny Group II metabotropic glutamate receptors depress synaptic transmission onto subicular burst firing neurons.
description	The subiculum (SUB) is a pivotal structure positioned between the hippocampus proper and various cortical and subcortical areas. Despite the growing body of anatomical and intrinsic electrophysiological data of subicular neurons, modulation of synaptic transmission in the SUB is not well understood. In the present study we investigated the role of group II metabotropic glutamate receptors (mGluRs), which have been shown to be involved in the regulation of synaptic transmission by suppressing presynaptic cAMP activity. Using field potential and patch-clamp whole cell recordings we demonstrate that glutamatergic transmission at CA1-SUB synapses is depressed by group II mGluRs in a cell-type specific manner. Application of the group II mGluR agonist (2S,1'R,2'R,3'R)-2-(2, 3-dicarboxycyclopropyl)glycine (DCG-IV) led to a significantly higher reduction of excitatory postsynaptic currents in subicular bursting cells than in regular firing cells. We further used low-frequency stimulation protocols and brief high-frequency bursts to test whether synaptically released glutamate is capable of activating presynaptic mGluRs. However, neither frequency facilitation is enhanced in the presence of the group II mGluR antagonist LY341495, nor is a test stimulus given after a high-frequency burst. In summary, we present pharmacological evidence for presynaptic group II mGluRs targeting subicular bursting cells, but both low- and high-frequency stimulation protocols failed to activate presynaptically located mGluRs.
format	article
author	Michael Kintscher Jörg Breustedt Stéphanie Miceli Dietmar Schmitz Christian Wozny
author_facet	Michael Kintscher Jörg Breustedt Stéphanie Miceli Dietmar Schmitz Christian Wozny
author_sort	Michael Kintscher
title	Group II metabotropic glutamate receptors depress synaptic transmission onto subicular burst firing neurons.
title_short	Group II metabotropic glutamate receptors depress synaptic transmission onto subicular burst firing neurons.
title_full	Group II metabotropic glutamate receptors depress synaptic transmission onto subicular burst firing neurons.
title_fullStr	Group II metabotropic glutamate receptors depress synaptic transmission onto subicular burst firing neurons.
title_full_unstemmed	Group II metabotropic glutamate receptors depress synaptic transmission onto subicular burst firing neurons.
title_sort	group ii metabotropic glutamate receptors depress synaptic transmission onto subicular burst firing neurons.
publisher	Public Library of Science (PLoS)
publishDate	2012
url	https://doaj.org/article/5fdf062d237b4fcdb6d8bdbd1070be82
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Group II metabotropic glutamate receptors depress synaptic transmission onto subicular burst firing neurons.

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