Maternal cocaine addiction. II: An animal model for the study of brainstem mechanisms operative in sudden infant death syndrome.

Respiratory control abnormalities are mechanistic in Sudden Infant Death Syndrome (SIDS). In particular, arousal form sleep is an important component of respiratory regulation. Cocaine alters central neurotransmitter metabolism, particularly the monoamines. The locus coeruleus, the major Norepinephrine (NE) neuronal system, is involved in arousal from sleep related apnea and has extensive forebrain and brainstem projections. Thus, it is plausible that in utero cocaine exposure disrupts the normal maturation of transmitters and/or brain structures essential to sleep related respiratory regulation. Infants exposed to cocaine in utero may have an increased incidence of SIDS. We propose that cocaine use in pregnancy alters the normal maturation of centers and/or neurotransmitters involved in respiratory regulation thereby altering postnatal respiratory control. We hypothesize that the increased incidence of SIDS in cocaine exposed infants may be secondary to deficits in arousal. The study of prenatal brain development and of postnatal respiratory control in rabbit pups exposed to cocaine in utero will provide a useful model for the study of mechanisms operative in SIDS.