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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.

Frontiers in Psychiatry
|July 13, 2011
PubMed
Summary

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.

Keywords:
auditory startledose–responsehabituationidazoxanintravenous administrationnorepinephrineprenatal cocaineprepulse inhibition

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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.