{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2025,9,17]],"date-time":"2025-09-17T15:48:38Z","timestamp":1758124118121,"version":"3.32.0"},"reference-count":0,"publisher":"Maximum Academic Press","issue":"3","license":[{"start":{"date-parts":[[2000,5,1]],"date-time":"2000-05-01T00:00:00Z","timestamp":957139200000},"content-version":"unspecified","delay-in-days":0,"URL":"https:\/\/www.cambridge.org\/core\/terms"}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["Vis Neurosci"],"published-print":{"date-parts":[[2000,5]]},"abstract":"<jats:p>Catfish cone horizontal cells contain a voltage-gated \nL-type calcium channel that is modulated by activation \nof metabotropic glutamate receptors (mGluRs). Activation \nof group I mGluRs with the mGluR I agonist, (S)-3,5-dihydroxyphenylglycine \n[(S) 3,5-DHPG], potentiated peak calcium current \namplitude, shifted the membrane potential corresponding \nto peak current activity, and widened the calcium current's \nactivation range. In this study, we have examined the mechanisms \nlinking activation of the mGluRs with \u201cup-regulation\u201d \nof calcium current activity. Under whole-cell voltage-clamp \nconditions favoring expression of the L-type calcium current, \nwe provide evidence that activation of mGluRs initiate \nthe diacylglyceral (DG) second messenger pathway to activate \nprotein kinase C (PKC) and up-regulate calcium channel \nactivity. This evidence was based on results using a number \nof PKC activators and inhibitors. PKC activators mimicked \nthe effect of (S) 3,5-DHPG on calcium current activity. \nUp-regulation of the calcium channel by PKC activators \nor (S) 3,5-DHPG was eliminated if PKC inhibitors were present. \nThese results also demonstrated that activation of group \nI mGluRs were linked to a pertussis toxin sensitive G-protein. \nWhen the GTP analog, guanosine 5-0-(3-thiotriphosphate \n(GTP\u03b3S), was allowed to diffuse into voltage-clamp \ncells, up-regulation of the calcium channel occurred and \nmimicked the effect of (S) 3,5-DHPG. However, when pertussis \ntoxin (PTX) was allowed to diffuse into the cell along \nwith GTP\u03b3S, GTP\u03b3S failed to modulate calcium current \nactivity. IP<jats:sub>3<\/jats:sub> (inositol 1,4,5 triphosphate) \nis a second product produced by activation of group I mGluRs. \nOnce formed, IP<jats:sub>3<\/jats:sub> can trigger calcium release \nfrom IP<jats:sub>3<\/jats:sub>-sensitive intracellular stores. To \ndetermine if the IP<jats:sub>3<\/jats:sub> second messenger system \nwas involved in up-regulation of calcium channel, (S) 3,5-DHPG \nwas applied to voltage-clamped cone horizontal cells containing \ndifferent concentrations of the calcium buffer, EGTA. Low \nconcentrations of EGTA failed to buffer calcium released \nfrom intracellular stores. In the presence of low EGTA \nconcentrations, (S) 3,5-DHPG's enhancement of the \ncalcium current amplitude was reduced. Inhibition of the \ncalcium current amplitude in low concentrations of EGTA \nwas eliminated in the presence of the intracellular calcium \nstore blocker, heparin. These results suggest that both \nthe DG and IP<jats:sub>3<\/jats:sub> second messenger pathways are \ninvolved in modulation of the voltage-gated calcium channel \nin catfish cone horizontal cells. The DG pathway up-regulates \nthe voltage-gated calcium channel activity whereas calcium \nreleased from IP<jats:sub>3<\/jats:sub> intracellular stores inhibits \npeak current amplitude.<\/jats:p>","DOI":"10.1017\/s0952523800173134","type":"journal-article","created":{"date-parts":[[2002,7,27]],"date-time":"2002-07-27T13:39:16Z","timestamp":1027777156000},"page":"473-482","source":"Crossref","is-referenced-by-count":14,"title":["Second messenger pathways involved in up-regulation of an \nL-type calcium channel"],"prefix":"10.48130","volume":"17","author":[{"given":"CINDY L.","family":"LINN","sequence":"first","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]}],"member":"27968","published-online":{"date-parts":[[2000,5,1]]},"container-title":["Visual Neuroscience"],"original-title":[],"language":"en","link":[{"URL":"https:\/\/www.cambridge.org\/core\/services\/aop-cambridge-core\/content\/view\/S0952523800173134","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2025,1,2]],"date-time":"2025-01-02T20:00:25Z","timestamp":1735848025000},"score":1,"resource":{"primary":{"URL":"https:\/\/www.cambridge.org\/core\/product\/identifier\/S0952523800173134\/type\/journal_article"}},"subtitle":[],"short-title":[],"issued":{"date-parts":[[2000,5]]},"references-count":0,"journal-issue":{"issue":"3","published-print":{"date-parts":[[2000,5]]}},"alternative-id":["S0952523800173134"],"URL":"https:\/\/doi.org\/10.1017\/s0952523800173134","relation":{},"ISSN":["0952-5238","1469-8714"],"issn-type":[{"type":"print","value":"0952-5238"},{"type":"electronic","value":"1469-8714"}],"subject":[],"published":{"date-parts":[[2000,5]]}}}