5-HT2A/2C receptor-mediated hypopnea in the newborn rat: Relationship to Fos immunoreactivity

Previous data derived from anesthetized, decerebrate, or in vitro preparati ons suggested that 5-HT2 receptor activation might be responsible for respi ratory dysfunction. Such a mechanism has not yet been documented in the int act animal, but might be of clinical relevance to the apneic spells of the premature infant. In the present investigation on conscious newborn rats we analyzed the respiratory response to the activation of 5-HT2A/2C receptors by the agonist 1-(2.5-dimethoxy-4-iodophenyl)-2-aminopropane (DOI), and we delineated central structures possibly involved in this response, using Fo s expression as a marker of neuronal activation. We demonstrated that intra peritoneal injection of 5 mg/kg DOI produced a long-lasting decrease in res piratory frequency and tidal volume, which could be blocked by the antagoni st ritanserin. Fos immunohistochemistry suggested that the rostral ventrola teral medulla and the lateral paragigantocellular nucleus might have a key role in the respiratory response to 5-HT2 receptor activation, In addition, double immunostaining for Fos and tyrosine hydroxylase suggested that the contribution of catecholaminergic neurons to this response mi-ht be modest and indirect.