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Blockade of N- and Q-type Ca2+ channels inhibit K+-evoked [3H]acetylcholine release in rat hippocampal slices
| Content Provider | Semantic Scholar |
|---|---|
| Author | Saydoff, J. A. Zaczek, Robert C. |
| Copyright Year | 1996 |
| Abstract | In the present study, we examined the contribution of specific Ca2+ channels to K(+)-evoked hippocampal acetylcholine (ACh) release using [3H]choline loaded hippocampal slices. [3H]ACh release was Ca(2+)-dependent, blocked by the nonspecific Ca2+ channel blocker verapamil, but not by blockade of L-type Ca2+ channels. The N-type Ca2+ channel blocker omega-conotoxin GVIA (omega-CgTx GVIA; 250 nM) inhibited [3H]ACh release by 44% and the P/Q-type Ca2+ channel blocker omega-agatoxin IVA (omega-Aga IVA; 400 nM) inhibited [3H]ACh release by 27%, with the combination resulting in a nearly additive 79% inhibition. Four hundred or one thousand nM omega-Aga IVA was necessary to inhibit [3H]ACh release. omega-Conotoxin MVIIC (omega-CTx-MVIIC) was used after first blocking N-type Ca2+ channels with omega-CgTx GVIA (1 microM). Under these conditions, 500 nM omega-CTx-MVIIC led to a nearly maximal inhibition of the omega-CgTx GVIA-insensitive [3H]ACh release. Based on earlier reports about the relative sensitivity of cloned and native Ca2+ channels to these toxins, this study indicates that N- and Q-type Ca2+ channels primarily mediate K(+)-evoked hippocampal [3H]ACh release. |
| Starting Page | 283 |
| Ending Page | 286 |
| Page Count | 4 |
| File Format | PDF HTM / HTML |
| DOI | 10.1016/0361-9230(96)00071-8 |
| Alternate Webpage(s) | https://api.elsevier.com/content/article/pii/0361923096000718 |
| Alternate Webpage(s) | https://www.sciencedirect.com/science/article/pii/0361923096000718?dgcid=api_sd_search-api-endpoint |
| PubMed reference number | 8842414 |
| Alternate Webpage(s) | https://doi.org/10.1016/0361-9230%2896%2900071-8 |
| Journal | Medline |
| Volume Number | 40 |
| Journal | Brain Research Bulletin |
| Language | English |
| Access Restriction | Open |
| Content Type | Text |
| Resource Type | Article |
