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Lamotrigine blocks the initiation and expression of repeated high-dose methamphetamine-induced prepulse inhibition

Yasuya Nakato1, Tomohiro Abekawa, Koki Ito

  • 1Department of Psychiatry, Hokkaido University Graduate School of Medicine, North 15, West 7, Sapporo, Hokkaido 060-8638, Japan. nakatou@med.hokudai.ac.jp

Neuroscience Letters
|July 13, 2010
PubMed

Insights

Lamotrigine (LTG) prevents and reverses a long-lasting prepulse inhibition (PPI) deficit in a novel animal model of schizophrenia. This suggests LTG may help block neurocognitive decline in schizophrenia patients.

Area of Science:

  • Neuroscience
  • Psychopharmacology
  • Animal Models of Disease

Background:

  • Schizophrenia is characterized by cognitive deficits, including impaired prepulse inhibition (PPI), a measure of sensorimotor gating.
  • Conventional animal models often require stimulant challenge injections, unlike the proposed model which induces a lasting PPI deficit via repeated methamphetamine (METH) administration.
  • This study utilizes a novel psychostimulant-induced animal model to investigate potential therapeutic interventions for schizophrenia-related cognitive dysfunction.

Purpose of the Study:

  • To investigate the efficacy of lamotrigine (LTG) in preventing (initiation) and reversing (expression) a steady-state PPI deficit induced by repeated METH administration.
  • To assess LTG's effects on the initiation phase of the PPI deficit when co-administered with METH.
  • To evaluate LTG's impact on the established PPI deficit after a withdrawal period.

Main Methods:

  • A novel animal model was established using repeated METH administration to induce a long-lasting PPI deficit.
  • Lamotrigine (LTG) was administered either concurrently with METH to assess initiation or after a withdrawal period to assess expression of the PPI deficit.
  • Prepulse inhibition (PPI) was measured using the SR-LAB system at a specific prepulse intensity (68dB).

Main Results:

  • LTG significantly blocked the initiation of the PPI deficit induced by repeated METH administration at 68dB prepulse intensity.
  • LTG also prevented the expression of the established PPI deficit, indicating a reversal effect.
  • LTG did not affect the startle amplitude, suggesting a specific effect on PPI rather than general sensorimotor function.

Conclusions:

  • Repeated METH administration in rodents provides a valuable model for studying schizophrenia-related PPI deficits.
  • Lamotrigine (LTG) demonstrates potential as a therapeutic agent for schizophrenia by blocking the initiation and expression of neurocognitive deficits.
  • These findings suggest LTG could be beneficial in preventing progressive neurocognitive deterioration and recovering deficits in schizophrenia.

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