Are histamine H2-receptor depressions of neuronal activity in tissue cultures from rat hypothalamus mediated through cyclic adenosine monophosphate?

Iontophoretic application of histamine H2-agonists depressed spontaneous firing of tuberal hypothalamic neurons in tissue culture. Perfusion with inhibitors of cyclic nucleotide phosphodiesterase increased the strength of these depressions, which persisted during perfusion with Ca2+-free medium. These results support a role of cyclic AMP as a mediator of histamine H2-elicited depressions of neuronal activity.