Alterations in the development of catecholamine turnover induced by perinatal methadone: Differences in central vs. peripheral sympathetic nervous systems

Abstract

Administration of methadone to pregnant and nursing rats slows synaptogenesis of central cathcholaminergic systems in the offspring but accelerates the onset of synaptic function in peripheral sympathetic pathways. Norepinephrine turnover, assessed by inhibiting catecholamine biosynthesis with alpha-methyl-p-tyrosine, was elevated in cardiac sympathetic nerve terminals in rats exposed perinatally to methadone. In contrast, turnover was unchanged in noradrenergic and dopaminergic systems in the brain. Similar results were obtained when methadone was given directly to the pups during postnatal life. These data suggest that opiate-induced alterations of impulse flow and transmitter turnover in a given neuron population may determine whether the effects of perinatal methadone exposure result in facilitation or inhibition of synaptic development.