Prenatal cocaine exposure enhances long-term potentiation induction in rat medial prefrontal cortex

Chiung Chun Huang, Ying Ching Liang, Kuei Sen Hsu

研究成果: Article同行評審

10 引文 斯高帕斯(Scopus)


Prenatal exposure to cocaine has been reported to produce long-lasting cognitive deficits, but the underlying mechanisms remain largely unknown. Here, we report that the induction of long-term potentiation (LTP) at excitatory synapses onto layer V pyramidal neurons in the medial prefrontal cortex (mPFC) is facilitated in rats exposed to cocaine in utero (3 mg/kg, intravenous twice daily during embryonic days 10-20). This facilitated LTP is caused by a reduction of A-type γ-aminobutyric acid (GABAA) receptor-mediated inhibition of mPFC pyramidal neurons. Biochemical experiments revealed a significant decrease in the surface expression of GABAA receptor α1 subunits and total protein levels of γ2 and δ subunits in mPFC slices from rats exposed to cocaine in utero. Prenatal cocaine exposure also leads to enhanced mPFC pyramidal neuronal excitability. However, the development of behavioural sensitization to repeated cocaine administration was impaired in rats that were exposed to cocaine in utero. These results suggest that prenatal cocaine exposure causes a long-lasting reduction of GABAergic inhibition in mPFC layer V pyramidal neurons, leading to an increased susceptibility of excitatory synapses to LTP induction during the postnatal period.

頁(從 - 到)431-443
期刊International Journal of Neuropsychopharmacology
出版狀態Published - 2011 五月

All Science Journal Classification (ASJC) codes

  • Pharmacology
  • Psychiatry and Mental health
  • Pharmacology (medical)

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