{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2025,10,21]],"date-time":"2025-10-21T03:26:52Z","timestamp":1761017212904},"reference-count":0,"publisher":"American Physiological Society","issue":"5","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["Journal of Neurophysiology"],"published-print":{"date-parts":[[1994,11,1]]},"abstract":"<jats:p> 1. High-voltage-activated Ca2+ currents [ICa(HVA)] were studied in immunolabeled mouse retinal ganglion neurons (RGNs) to elucidate channel-specific components and their developmental changes in vitro. 2. Neurons were dissociated at postnatal day 5. RGNs were selected for electrophysiological measurements by vital labeling with an antibody against Thy-1.2. ICa(HVA) were recorded with patch electrodes in the whole cell configuration at a holding voltage (Vh) of -90 mV. 3. A total of 111 neurons was studied. On average, 13% of ICa(HVA) was reversibly blocked by 10 microM nifedipine, approximately 30% of the compound current displayed an irreversible block by 2.5 microM omega-conotoxin (omega-CTX) GVIA. The remainder current was resistant to both drugs, suggesting that the total ICa(HVA) was a mixture of at least three different components. 4. Developmental analysis revealed a significant increase of the omega-CTX-GVIA\/nifedipine-resistant component of ICa(HVA) (31% at day in vitro (DIV) 0\u20132, 70% at DIV 18\u201326) mainly at the expense of the omega-CTX-GVIA-sensitive current. No significant change was found in the nifedipine-sensitive component of ICa(HVA). 5. To characterize the Ca2+ current component that was resistant to both omega-CTX-GVIA and nifedipine at Vh -90 mV, three tests were performed. The P channel antagonist omega-agatoxin IVA (omega-Aga-IVA, 200 nM) completely failed to block ICa(HVA) in mouse RGNs. The novel Ca2+ channel blocker omega-CTX-MVIIC (5 microM) decreased the ICa(HVA) remaining after omega-CTX-GVIA treatment by only approximately 10%.(ABSTRACT TRUNCATED AT 250 WORDS) <\/jats:p>","DOI":"10.1152\/jn.1994.72.5.2542","type":"journal-article","created":{"date-parts":[[2017,12,25]],"date-time":"2017-12-25T04:21:13Z","timestamp":1514175673000},"page":"2542-2546","source":"Crossref","is-referenced-by-count":15,"title":["Retinal ganglion neurons express a toxin-resistant developmentally regulated novel type of high-voltage-activated calcium channel"],"prefix":"10.1152","volume":"72","author":[{"given":"T.","family":"Rothe","sequence":"first","affiliation":[{"name":"Developmental Neurobiology, Max Planck Institute for Psychiatry, Martinsried, Germany."}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"R.","family":"Grantyn","sequence":"additional","affiliation":[{"name":"Developmental Neurobiology, Max Planck Institute for Psychiatry, Martinsried, Germany."}],"role":[{"role":"author","vocabulary":"crossref"}]}],"member":"24","container-title":["Journal of Neurophysiology"],"original-title":[],"language":"en","link":[{"URL":"https:\/\/www.physiology.org\/doi\/pdf\/10.1152\/jn.1994.72.5.2542","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2019,9,9]],"date-time":"2019-09-09T05:20:44Z","timestamp":1568006444000},"score":1,"resource":{"primary":{"URL":"https:\/\/www.physiology.org\/doi\/10.1152\/jn.1994.72.5.2542"}},"subtitle":[],"short-title":[],"issued":{"date-parts":[[1994,11,1]]},"references-count":0,"journal-issue":{"issue":"5","published-print":{"date-parts":[[1994,11,1]]}},"alternative-id":["10.1152\/jn.1994.72.5.2542"],"URL":"https:\/\/doi.org\/10.1152\/jn.1994.72.5.2542","relation":{},"ISSN":["0022-3077","1522-1598"],"issn-type":[{"value":"0022-3077","type":"print"},{"value":"1522-1598","type":"electronic"}],"subject":[],"published":{"date-parts":[[1994,11,1]]}}}