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Gene expression profiling in the developing rat brain exposed to ketamine.

Q Shi1, L Guo, T A Patterson

  • 1Division of Systems Toxicology, National Center for Toxicological Research, US Food and Drug Administration, 3900 NCTR Road, Jefferson, AR 72079, USA.

Neuroscience
|January 19, 2010
PubMed
Summary
This summary is machine-generated.

Ketamine exposure in young rats increases N-methyl-d-aspartate (NMDA) receptors, leading to overstimulation and enhanced neuronal apoptosis. This study reveals a mechanism for ketamine

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Area of Science:

  • Neuroscience
  • Molecular Biology
  • Pharmacology

Background:

  • Ketamine, an N-methyl-d-aspartate (NMDA) receptor antagonist, is known to cause neuronal apoptosis in developing brains.
  • The precise molecular mechanisms underlying ketamine-induced neurotoxicity remain under investigation.

Purpose of the Study:

  • To investigate the effects of ketamine exposure on gene expression and receptor signaling pathways in the developing rat brain.
  • To elucidate the role of NMDA receptor up-regulation in ketamine-induced neuronal apoptosis.

Main Methods:

  • Postnatal day 7 rats received multiple subcutaneous doses of ketamine.
  • Frontal cortical RNA was analyzed using gene expression microarrays (Illumina Rat Ref-12 Expression BeadChips).
  • Ingenuity Pathway Analysis, quantitative polymerase chain reaction (Q-PCR), and in situ hybridization were employed to validate findings.

Main Results:

  • Ketamine treatment led to differential gene expression, particularly in genes related to cell death, differentiation, and receptor activity.
  • Pathway analysis indicated significant perturbations in NMDA-type glutamate, GABA, and dopamine receptor signaling.
  • Q-PCR and in situ hybridization confirmed the significant up-regulation of NMDA receptor subunits and mRNA signaling.

Conclusions:

  • Prolonged ketamine exposure in developing neurons results in the up-regulation of NMDA receptors.
  • This up-regulation enhances the glutamatergic system's sensitivity to endogenous glutamate, triggering increased neuronal apoptosis.
  • Findings support a mechanism where ketamine disrupts normal neuronal development through NMDA receptor overstimulation.