| First Author | Aourz N | Year | 2014 |
| Journal | CNS Neurosci Ther | Volume | 20 |
| Issue | 7 | Pages | 662-70 |
| PubMed ID | 24685142 | Mgi Jnum | J:345562 |
| Mgi Id | MGI:6872814 | Doi | 10.1111/cns.12259 |
| Citation | Aourz N, et al. (2014) Cortistatin-14 mediates its anticonvulsant effects via sst2 and sst3 but not ghrelin receptors. CNS Neurosci Ther 20(7):662-70 |
| abstractText | Cortistatin (CST)-14, a neuropeptide that is structurally and functionally related to somatostatin-14 (SRIF) binds all five somatostatin receptor subtypes (sst1-sst5). Using in vivo microdialysis and telemetry-based electroencephalographic recordings, we provide the first experimental evidence for anticonvulsive effects of CST-14 in a pilocarpine-induced seizure model in rats and mice and for the involvement of sst2 and sst3 receptors in these anticonvulsant actions of CST-14. Both receptor subtypes are required for the anticonvulsant effects of CST-14 given that co-perfusion of a selective sst2 antagonist (cyanamid15486) or a selective sst3 antagonist (SST3-ODN-8) reversed anticonvulsant effect of CST-14, and this, independently of each other. Next, as the ghrelin receptor has been proposed as a target for the biological effects of CST-14, we used ghrelin receptor knockout mice and their wild type littermates to study the involvement of this receptor in the anticonvulsive actions of CST-14. Our results show a significant decrease in seizure duration in both genotypes when CST-14 treated mice were compared with corresponding control animals receiving only pilocarpine. In addition, this CST-14-induced decrease was comparable in both genotypes. We here thus provide the first evidence that ghrelin receptors are not involved in mediating anticonvulsant actions of CST-14 in vivo. |
