{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2025,10,30]],"date-time":"2025-10-30T10:49:05Z","timestamp":1761821345775},"reference-count":0,"publisher":"Wiley","issue":"3","license":[{"start":{"date-parts":[[1996,8,1]],"date-time":"1996-08-01T00:00:00Z","timestamp":838857600000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["The Journal of Physiology"],"published-print":{"date-parts":[[1996,8]]},"abstract":"<jats:p>1. We have previously reported that activation of group II\u2010like metabotropic glutamate receptors (mGluRs) in rat hippocampus results in a potentiation of the accumulation of cAMP elicited by activation of G\u2010protein Gs\u2010coupled receptors. This large increase in cAMP levels results in release of cAMP or a cAMP metabolite and depression of synaptic transmission at the Schaffer collateral\u2010CA1 pyramidal cell synapse through activation of A1 adenosine receptors. 2. Consistent with these studies, we report that antagonists of group II mGluRs block both the potentiation of cAMP accumulation elicited by activation of mGluRs and the depression of synaptic transmission induced by coactivation of mGluRs and beta\u2010adrenergic receptors. 3. In situ hybridization studies suggest that of the cloned group II mGluRs only mGluR\u20103 mRNA is present in area CA1. Interestingly, mGluR\u20103 appears to be present predominantly in glia in this region. Thus, we tested the hypothesis that mGluRs coupled to potentiation of cAMP accumulation were present on glia rather than neurons in area CA1. 4. The selective group II mGluR agonist 2S,1'R,2'R,3'R\u20102(2,3\u2010dicarboxycyclo\u2010propyl)glycine (DCG\u2010IV) failed to enhance cAMP\u2010mediated electrophysiological responses to the beta\u2010adrenergic receptor agonist isoprenaline (Iso) in CA1 pyramidal cells, suggesting that mGluRs coupled to potentiation of cAMP accumulation may not be present in these cells. 5. Pre\u2010incubation of hippocampal slices with either of the selective glial toxins L\u2010alpha\u2010aminoadipic acid (L\u2010AA) or fluorocitrate (FC) blocked mGluR\u2010mediated potentiation of cAMP accumulation. However, L\u2010AA and FC had no discernible effects on viability of CA1 pyramidal cells, or cAMP\u2010mediated electrophysiological effects in these neurons. 6. Pre\u2010incubation of hippocampal slices with the neurotoxin kainate resulted in disruption of neuronal transmission and degeneration of neurons in area CA1, but had no effect on mGluR\u2010mediated potentiation of cAMP accumulation. 7. Pre\u2010incubation of hippocampal slices with the cAMP\/cAMP metabolite transport blocker probenicid blocked the depression of synaptic transmission elicited by coapplication of Iso and DCG\u2010IV, while having no significant effect on cAMP accumulation elicited by these agonists. 8. Taken together, these data suggest that mGluRs coupled to potentiation of cAMP accumulation are present on glia rather than neurons in area CA1 of hippocampus. This suggests that a novel form of glial\u2010neuronal communication may exist, since activation of these mGluRs in concert with beta\u2010adrenergic receptors results in depression of synaptic transmission.<\/jats:p>","DOI":"10.1113\/jphysiol.1996.sp021529","type":"journal-article","created":{"date-parts":[[2014,12,17]],"date-time":"2014-12-17T07:49:50Z","timestamp":1418802590000},"page":"743-755","source":"Crossref","is-referenced-by-count":56,"title":["Novel glial\u2010neuronal signalling by coactivation of metabotropic glutamate and beta\u2010adrenergic receptors in rat hippocampus."],"prefix":"10.1113","volume":"494","author":[{"given":"D G","family":"Winder","sequence":"first","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"P S","family":"Ritch","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"suffix":"4th","given":"R W","family":"Gereau","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"P J","family":"Conn","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]}],"member":"311","published-online":{"date-parts":[[1996,8]]},"container-title":["The Journal of Physiology"],"original-title":[],"language":"en","link":[{"URL":"https:\/\/api.wiley.com\/onlinelibrary\/tdm\/v1\/articles\/10.1113%2Fjphysiol.1996.sp021529","content-type":"unspecified","content-version":"vor","intended-application":"text-mining"},{"URL":"https:\/\/physoc.onlinelibrary.wiley.com\/doi\/pdf\/10.1113\/jphysiol.1996.sp021529","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2023,10,26]],"date-time":"2023-10-26T19:02:31Z","timestamp":1698346951000},"score":1,"resource":{"primary":{"URL":"https:\/\/physoc.onlinelibrary.wiley.com\/doi\/10.1113\/jphysiol.1996.sp021529"}},"subtitle":[],"short-title":[],"issued":{"date-parts":[[1996,8]]},"references-count":0,"journal-issue":{"issue":"3","published-print":{"date-parts":[[1996,8]]}},"alternative-id":["10.1113\/jphysiol.1996.sp021529"],"URL":"https:\/\/doi.org\/10.1113\/jphysiol.1996.sp021529","archive":["Portico"],"relation":{},"ISSN":["0022-3751","1469-7793"],"issn-type":[{"value":"0022-3751","type":"print"},{"value":"1469-7793","type":"electronic"}],"subject":[],"published":{"date-parts":[[1996,8]]}}}