Activation of α1-adrenoceptors enhances excitatory synaptic transmission via a pre- and postsynaptic protein kinase C-dependent mechanism in the medial prefrontal cortex of rats

The physiological effects of α1‐adrenoceptors (α1‐ARs) have been examined in many brain regions. However, little is known about the mechanism of modulation on synaptic transmission by α1‐ARs in the medial prefrontal cortex (mPFC). The present study investigated how α1‐AR activation regulates glutama...

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Veröffentlicht in:The European journal of neuroscience 2014-04, Vol.39 (8), p.1281-1293
Hauptverfasser: Luo, Fei, Tang, Hua, Li, Bao-ming, Li, Si-hai
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container_title The European journal of neuroscience
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creator Luo, Fei
Tang, Hua
Li, Bao-ming
Li, Si-hai
description The physiological effects of α1‐adrenoceptors (α1‐ARs) have been examined in many brain regions. However, little is known about the mechanism of modulation on synaptic transmission by α1‐ARs in the medial prefrontal cortex (mPFC). The present study investigated how α1‐AR activation regulates glutamatergic synaptic transmission in layer V/VI pyramidal cells of the rat mPFC. We found that the α1‐AR agonist phenylephrine (Phe) induced a significant enhancement of the amplitude and frequency of miniature excitatory postsynaptic currents (mEPSCs). The facilitation effect of Phe on the frequency of mEPSCs involved a presynaptic protein kinase C‐dependent pathway. Phe produced a significant enhancement on the amplitude of α‐amino‐3‐hydroxy‐5‐methyl‐4‐isoxazolepropionic acid receptor (AMPA‐R)‐ and N‐methyl‐d‐aspartic acid receptor (NMDA‐R)‐mediated evoked excitatory postsynaptic currents (eEPSCs). Phe enhanced inward currents evoked by puff application of glutamate or NMDA. The Phe‐induced facilitation of AMPA‐R‐ and NMDA‐R‐mediated eEPSCs required, in part, postsynaptic Gq, phospholipase C and PKC. These findings suggest that α1‐AR activation facilitates excitatory synaptic transmission in mPFC pyramidal cells via both pre‐ and post‐synaptic PKC‐dependent mechanisms. Little is known about the mechanism of modulation on synaptic transmission by α1‐AR in the medial prefrontal cortex (mPFC). We found that α1‐AR activation enhances glutamatergic transmission in the mPFC by increasing the glutamate release from presynaptic terminals, via PKC‐dependent mechanism, and by enhancing the responsiveness of postsynaptic AMPA‐Rs and NMDA‐Rs, likely via Gq/PLC/PKC signaling pathway.
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Tang, Hua ; Li, Bao-ming ; Li, Si-hai</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c3445-b626a454deb104d5cd669ccd9ebaed28308d0758ab4f40d09a3bb7dc1ab35bb13</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2014</creationdate><topic>Adrenergic alpha-1 Receptor Agonists - pharmacology</topic><topic>Animals</topic><topic>Excitatory Postsynaptic Potentials</topic><topic>excitatory synaptic transmission</topic><topic>medial prefrontal cortex</topic><topic>Miniature Postsynaptic Potentials</topic><topic>Phenylephrine - pharmacology</topic><topic>Prefrontal Cortex - cytology</topic><topic>Prefrontal Cortex - metabolism</topic><topic>Prefrontal Cortex - physiology</topic><topic>Protein Kinase C - metabolism</topic><topic>Pyramidal Cells - drug effects</topic><topic>Pyramidal Cells - metabolism</topic><topic>Pyramidal Cells - physiology</topic><topic>rat</topic><topic>Rats</topic><topic>Rats, Sprague-Dawley</topic><topic>Receptors, Adrenergic, alpha-1 - metabolism</topic><topic>Receptors, AMPA - metabolism</topic><topic>Receptors, N-Methyl-D-Aspartate - metabolism</topic><topic>Synapses - metabolism</topic><topic>Synapses - physiology</topic><topic>α1-Adrenoceptor</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Luo, Fei</creatorcontrib><creatorcontrib>Tang, Hua</creatorcontrib><creatorcontrib>Li, Bao-ming</creatorcontrib><creatorcontrib>Li, Si-hai</creatorcontrib><collection>Istex</collection><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>MEDLINE - Academic</collection><jtitle>The European journal of neuroscience</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Luo, Fei</au><au>Tang, Hua</au><au>Li, Bao-ming</au><au>Li, Si-hai</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Activation of α1-adrenoceptors enhances excitatory synaptic transmission via a pre- and postsynaptic protein kinase C-dependent mechanism in the medial prefrontal cortex of rats</atitle><jtitle>The European journal of neuroscience</jtitle><addtitle>Eur J Neurosci</addtitle><date>2014-04</date><risdate>2014</risdate><volume>39</volume><issue>8</issue><spage>1281</spage><epage>1293</epage><pages>1281-1293</pages><issn>0953-816X</issn><eissn>1460-9568</eissn><abstract>The physiological effects of α1‐adrenoceptors (α1‐ARs) have been examined in many brain regions. However, little is known about the mechanism of modulation on synaptic transmission by α1‐ARs in the medial prefrontal cortex (mPFC). The present study investigated how α1‐AR activation regulates glutamatergic synaptic transmission in layer V/VI pyramidal cells of the rat mPFC. We found that the α1‐AR agonist phenylephrine (Phe) induced a significant enhancement of the amplitude and frequency of miniature excitatory postsynaptic currents (mEPSCs). The facilitation effect of Phe on the frequency of mEPSCs involved a presynaptic protein kinase C‐dependent pathway. Phe produced a significant enhancement on the amplitude of α‐amino‐3‐hydroxy‐5‐methyl‐4‐isoxazolepropionic acid receptor (AMPA‐R)‐ and N‐methyl‐d‐aspartic acid receptor (NMDA‐R)‐mediated evoked excitatory postsynaptic currents (eEPSCs). Phe enhanced inward currents evoked by puff application of glutamate or NMDA. The Phe‐induced facilitation of AMPA‐R‐ and NMDA‐R‐mediated eEPSCs required, in part, postsynaptic Gq, phospholipase C and PKC. These findings suggest that α1‐AR activation facilitates excitatory synaptic transmission in mPFC pyramidal cells via both pre‐ and post‐synaptic PKC‐dependent mechanisms. Little is known about the mechanism of modulation on synaptic transmission by α1‐AR in the medial prefrontal cortex (mPFC). We found that α1‐AR activation enhances glutamatergic transmission in the mPFC by increasing the glutamate release from presynaptic terminals, via PKC‐dependent mechanism, and by enhancing the responsiveness of postsynaptic AMPA‐Rs and NMDA‐Rs, likely via Gq/PLC/PKC signaling pathway.</abstract><cop>France</cop><pub>Blackwell Publishing Ltd</pub><pmid>24494713</pmid><doi>10.1111/ejn.12495</doi><tpages>13</tpages></addata></record>
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subjects Adrenergic alpha-1 Receptor Agonists - pharmacology
Animals
Excitatory Postsynaptic Potentials
excitatory synaptic transmission
medial prefrontal cortex
Miniature Postsynaptic Potentials
Phenylephrine - pharmacology
Prefrontal Cortex - cytology
Prefrontal Cortex - metabolism
Prefrontal Cortex - physiology
Protein Kinase C - metabolism
Pyramidal Cells - drug effects
Pyramidal Cells - metabolism
Pyramidal Cells - physiology
rat
Rats
Rats, Sprague-Dawley
Receptors, Adrenergic, alpha-1 - metabolism
Receptors, AMPA - metabolism
Receptors, N-Methyl-D-Aspartate - metabolism
Synapses - metabolism
Synapses - physiology
α1-Adrenoceptor
title Activation of α1-adrenoceptors enhances excitatory synaptic transmission via a pre- and postsynaptic protein kinase C-dependent mechanism in the medial prefrontal cortex of rats
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