Neonatal rats do not have functional splanchnic nerve connections to the adrenal medulla until approximately one week of postnatal age, yet they are able to respond to some drugs or stresses by releasing adrenal catecholamines. Reserpine (5 mg/kg s.c.) resulted in significant loss (20-40%) of neonatal catecholamines within 4 h; unlike the acute effects of reserpine in the adult, depletion was not prevented by pretreatment with a nicotinic blocking agent, demonstrating that the effect in the neonate is non-neurogenic. Depletion did not result simply from inhibition of catecholamine storage by reserpine, but rather, the non-neurogenic depletion represented net movement of the amines from the storage granules into the extracellular space, as evaluated by the subcellular distribution of catecholamines. These results suggest that the non-neurogenic mechanism represents release of catecholamines. The immature response mechanism disappeared by 11 days of age and was replaced by a completely neurogenic release, demonstrating that the special mechanism is lost within several days of the onset of functional innervation of the adrenal. Experiments also were carried out to test whether endogenous opioids and/or opiate receptors are involved in the non-neurogenic mechanism. Naloxone (5 mg/kg s.c.) potentiated the depletion of catecholamines by reserpine, while methadone (2.5 mg/kg s.c.) inhibited the non-neurogenic response. In contrast, no potentiation of release by naloxone or inhibition by methadone was seen in adult rats. Thus, opiate receptors may modulate only the immature secretory mechanism.
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