Does corticotropin releasing factor act via a calcium-dependent mechanism?
The widespread distribution of CRF in the brain suggests a possible role of this peptide as a neuromodulator. An interaction with calcium-dependent conductances, as observed in hippocampal slices, could explain the action of CRF in different brain structures. In the present study, the calcium antagonist, verapamil, was found to block the excitatory action of CRF on neuronal discharge activity. This supports the hypothesis that CRF blocks a calcium-dependent potassium conductance, which represents a resting component of neuronal activity, thereby enhancing ion fluxes into the cell.
D000200:Action Potentials / Q000187:drug effects; D000818:Animals; D002110:Caffeine / Q000494:pharmacology; D002118:Calcium / Q000502:physiology*; D003346:Corticotropin-Releasing Hormone / Q000037:antagonists & inhibitors / Q000494:pharmacology*; D006624:Hippocampus / Q000187:drug effects* / Q000502:physiology; D066298:In Vitro Techniques; D007473:Ion Channels / Q000187:drug effects; D011188:Potassium / Q000378:metabolism; D051381:Rats; D014700:Verapamil / Q000494:pharmacology
D007473:Ion Channels; D002110:Caffeine; D003346:Corticotropin-Releasing Hormone; D014700:Verapamil; D011188:Potassium; D002118:Calcium