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Prenatal IV Cocaine: Alterations in Auditory Information Processing
Charles F Mactutus1, Steven B Harrod, Lauren L Hord
1Behavioral Neuroscience Program, Department of Psychology, University of South Carolina Columbia, SC, USA.
Insights
Prenatal cocaine exposure in rats alters auditory processing and startle responses in offspring. This suggests long-lasting effects on the central noradrenergic system, impacting attention and sensory information processing.
Area of Science:
- Neuroscience
- Developmental Psychology
- Pharmacology
Background:
- Prenatal exposure to substances like cocaine can lead to long-term neurodevelopmental deficits.
- Clinical observations of altered startle responses in infants exposed to cocaine prenatally suggest impacts on attentional processing.
- Neurophysiological evidence indicates prenatal cocaine exposure may alter brainstem transmission times.
Purpose of the Study:
- To investigate the effects of prenatal cocaine exposure on auditory information processing in offspring.
- To examine auditory startle response (ASR), habituation, and prepulse inhibition (PPI) following in utero cocaine exposure.
- To determine if cocaine-induced alterations in auditory processing persist into adulthood.
Main Methods:
- Administered cocaine hydrochloride (0.5–3.0 mg/kg) or saline to pregnant Long-Evans rats via IV from gestation day 8-20.
- Assessed auditory startle response (ASR), habituation, and prepulse inhibition (PPI) in offspring at postnatal days 18-20 and adulthood (90-100 days).
- Utilized an alpha(2)-adrenergic receptor antagonist (Idazoxan) to probe noradrenergic system involvement.
Main Results:
- Prenatal cocaine exposure did not affect maternal/litter parameters or offspring growth.
- Offspring exhibited increased ASR in a sex-dependent manner at both juvenile and adult stages.
- Prenatal cocaine exposure retarded within-session habituation and altered PPI response functions.
- Idazoxan enhanced ASR, with diminished enhancement observed at higher prenatal cocaine doses, suggesting noradrenergic pathway involvement.
Conclusions:
- In utero cocaine exposure, mimicking recreational use patterns, induces persistent alterations in auditory information processing.
- These findings suggest prenatal cocaine exposure leads to dysfunction in the central noradrenergic circuitry.
- The observed changes in auditory processing may underlie deficits in attentional processing seen in humans exposed to cocaine prenatally.
Abstract:
One clue regarding the basis of cocaine-induced deficits in attentional processing is provided by the clinical findings of changes in the infants' startle response; observations buttressed by neurophysiological evidence of alterations in brainstem transmission time. Using the IV route of administration and doses that mimic the peak arterial levels of cocaine use in humans, the present study examined the effects of prenatal cocaine on auditory information processing via tests of the auditory startle response (ASR), habituation, and prepulse inhibition (PPI) in the offspring. Nulliparous Long-Evans female rats, implanted with an IV access port prior to breeding, were administered saline, 0.5, 1.0, or 3.0 mg/kg/injection of cocaine HCL (COC) from gestation day (GD) 8-20 (1×/day-GD8-14, 2×/day-GD15-20). COC had no significant effects on maternal/litter parameters or growth of the offspring. At 18-20 days of age, one male and one female, randomly selected from each litter displayed an increased ASR (>30% for males at 1.0 mg/kg and >30% for females at 3.0 mg/kg). When reassessed in adulthood (D90-100), a linear dose-response increase was noted on response amplitude. At both test ages, within-session habituation was retarded by prenatal cocaine treatment. Testing the females in diestrus vs. estrus did not alter the results. Prenatal cocaine altered the PPI response function across interstimulus interval and induced significant sex-dependent changes in response latency. Idazoxan, an α(2)-adrenergic receptor antagonist, significantly enhanced the ASR, but less enhancement was noted with increasing doses of prenatal cocaine. Thus, in utero exposure to cocaine, when delivered via a protocol designed to capture prominent features of recreational usage, causes persistent, if not permanent, alterations in auditory information processing, and suggests dysfunction of the central noradrenergic circuitry modulating, if not mediating, these responses.
