Prenatal cocaine exposure: Decreased sensitization to cocaine and decreased striatal dopamine transporter binding in offspring

Augmentation of Cocaine-Sensitized Dopamine Release in the Nucleus Accumbens of Adult Mice following Prenatal Cocaine Exposure

“…Glatt et al [2004] also demonstrated a significant increase in basal DA efflux in the presence of the selective DA-reuptake blocker nomifensine suggesting a developmental down-regulation of the dopamine transporter, a finding supported by other studies of dopamine transporter expression after prenatal cocaine exposure [Byrnes et al, 1993;Fang and Ronnekleiv, 1999;Salvatore et al, 2004]. There are conflicting findings on the effect of prenatal cocaine exposure on stimulated DA release.…”

“…Using operant or instrumental conditioning techniques, increased intravenous self-administration of cocaine [Keller et al, 1996b;Rocha et al, 2002] and increased potentiation of rewarding electrical selfstimulation by cocaine [Lin and Kellogg, 1996;Malanga et al, 2008] have been demonstrated in adult animals following early developmental exposure to cocaine. Conversely, locomotor sensitization with repeated non-contingent cocaine administration [Byrnes et al, 1993;Crozatier et al, 2003;Guerriero et al, 2005] and conditioned place-preference to a cocaine-paired environment [Heyser et al, 1992;Malanga et al, 2007] are diminished in adult mice exposed to cocaine in utero. Thus, there is an apparent divergence of effects of prenatal cocaine exposure on reward-relevant behaviors, with an increase in the potency of cocaine on operant or instrumental learning and a decrease in its potency on Pavlovian or associational learning.…”

Acute and chronic methylphenidate dose–response assessment on three adolescent male rat strains

“…None of our experimental groups exhibited behavioral sensitization, while there were some reports [3,6,8,31] that showed that adolescent rats exhibited sensitization to the locomotor activating effects of cocaine. In these experiments, the drug injection and the recording were performed in test cages, while in the present study drug treatment and recordings were performed in the rats' home cages.…”

“…Some investigators reported that younger animals treated chronically with stimulants rarely exhibited behavioral sensitization [3,8], while others reported the presence of sensitization to the locomotor effects of cocaine [31]. Since each of the above reports used different rat strains and different drug regimens of cocaine and amphetamine but none involved MPD, the present study used three different rat strains of the same age and the same protocol with three different MPD concentrations for a dose-response assessment and strain comparison.…”

Prenatal Exposure to Cocaine Increases the Rewarding Potency of Cocaine and Selective Dopaminergic Agonists in Adult Mice

“…Investigations employing operant behavioral measures of reward in adult animals following prenatal exposure to cocaine or other drugs of abuse are comparatively limited; however, increased intravenous self-administration of cocaine following gestational cocaine exposure [19,20] and increased potentiation of rewarding electrical self-stimulation by cocaine following neonatal cocaine exposure [21] have been demonstrated. Conversely, chronic non-contingent cocaine administration to adult animals exposed to cocaine in utero results in less locomotor sensitization [22][23][24] and impaired development of conditioned place-preference [25]. Therefore, an apparent dissociation exists between the effects of prenatal cocaine exposure on the subsequent potency of cocaine in adulthood using operant methods compared to classical methods.…”