Perinatal morphine administration affects neuronal growth in the developing animal. Neuronal packing density was reduced by morphine treatment in both primary somatosensory cortex and preoptic area of the hypothalamus. However, glial packing density was increased, but only in hypothalamus, which could reflect greater severity of opiate-induced neurotoxicity in hypothalamus. Cortical pyramidal neurons show morphine-induced reduction of basilar dendritic growth limited to late-developing terminal branches. This effect is completely reversed by concurrent naltrexone administration. This selective effect could be caused by morphine acting at opiate receptors to inhibit extrinsic determinants of dendritic growth (e.g., afferent supply). The ontogeny of opiate receptors is also affected by perinatal morphine administration in a regionally-dependent manner. Mureceptors are downregulated by morphine in hypothalamus, but not in cortex. Differential maturity of receptors in these regions could be a factor in such differential drug effects. Therefore, different critical periods for opiate action in different regions of the developing brain could exist.