Central respiratory depression constitutes a major clinical problem of infancy. Treatment of newborns with prostaglandins or opiates as well as severe hypoxia depress the medullary neuronal network that mediates breathing movements. Disturbed respiratory network function is also involved in subsets of sudden infant death syndrome. Using in vitro models of perinatal rodents, we analyze the cellular mechanisms of drug-induced and endogenous respiratory depression. We combine electrophysiological recording of membrane potentials and currents with digital imaging of intracellular signalling factors in presumably rhythmogenic 'pre-Botzinger Complex' respiratory neurons. The aim of the research is to develop a novel pharmacological strategy to treat respiratory diseases. Based upon our current results, we will concentrate on clinically-applicable drugs that block inwardly-rectifying K+ channels of the pre-Botzinger Complex neurons via the cAMP-protein kinase-A pathway.