Gender-Specific Alterations in Adult Sexual Behavior and Brain Neurotransmitters Following Prenatal Morphine Exposure
Studies of the consequences of fetal exposure to opiates demonstrate that prenatally morphine- and methadone-treated animals exhibit considerable developmental lags, altered motor activities, and impaired learning behavior ( Hutchings, 1993; Hutchings, Zmitrovitch, Brake, Malowany, Church, & Nero, 1992; Hutchings, Zmitrovitch, Brake, Church, & Malowany, 1993; Zagon, MacLaughlin, & Thompson, 1979a; 1979b). These developmental and behavioral effects appear to result from delays in brain DNA synthesis, cell proliferation, and synaptogenesis in exposed rat pups (Ricalde & Hammer, 1991; Hammer, 1993; Seatriz & Hammer, 1993; Slotkin, Whitmore, Salvaggio, & Seidler, 1979). It has been thought for some time that drugs exert their effects on organisms through interaction with specific receptors ( Langley, 1906). The influence of a specific drug on the developing brain is thus dependent on the presence of specific cellular recognition sites for the drug, the maturational state of the receptive sites, and the maturational state of neural circuitry. In rats, receptors for gonadal steroids, catecholamines, and endogenous opioids, all of which regulate the expression of adult sexual behaviors, begin to appear in the central nervous system (CNS) during the second half of gestation ( Antelman & Caggiula, 1977; Clendenin, Petriats, & Simon, 1976; Coyle & Pert, 1976; McEwen, 1978; Vito, Bates, & Fox, 1979). Thus, mid- to late gestational morphine exposure could potentially influence the development of those systems that have important roles in the display of adult sexual behavior.