Data from Toyama University advance knowledge in schizophrenia
Data from Toyama University advance knowledge in schizophrenia
According to a study from Toyama, Japan, "Blockade of N-methyl-d-asparate (NMDA) receptors has been shown to produce some of the abnormal behaviors related to symptoms of schizophrenia in rodents and human. Neonatal treatment of rats with non-competitive NMDA antagonists has been shown to induce behavioral abnormality in a later period."
"The aim of this study was to determine whether brief disruption of NMDA receptor function during a critical stage of development is sufficient to produce sensorimotor-gating deficits in the late adolescence or early adulthood in the rat. Male pups received the NMDA receptor blocker MK-801 (0.13 or 0.20 mg/kg), or an equal volume of saline on postnatal day (PD) 7 through 10. The animals were tested twice for prepulse inhibition (PPI) and locomotor activity in pre- (PD 35-38) and post- (PD 56-59) puberty. Neonatal exposure to both doses MK-801 disrupted PPI in the adolescence and early adulthood. Low-dose MK-801 elicited long-term effects on startle amplitudes, whereas high-dose MK-801 did not. Neither dose of MK-801 showed a significant effect on spontaneous locomotor activity, whereas the high dose attenuated rearing. The results of this study suggest neonatal exposure to MK-801 disrupted sensorimotor gating in the adolescence and early adulthood stages," wrote T. Uehara and colleagues, Toyama University (see also Schizophrenia).
The researchers concluded: "These findings indicate that rats transiently exposed to NMDA blockers in neonatal periods are useful for the study of the pathophysiology and treatment of schizophrenia."
Uehara and colleagues published the results of their research in Psychopharmacology (Long-term effects of neonatal MK-801 treatment on prepulse inhibition in young adult rats. Psychopharmacology, 2009;206(4 Sp. Iss.):623-630).
For additional information, contact T. Uehara, Toyama University, Graduate School of Medicine & Pharmaceutical Science, Dept. of Neuropsychiatry, 2630 Sugitani, Toyama 9300194, Japan.
The publisher of the journal Psychopharmacology can be contacted at: Springer, 233 Spring St., New York, NY 10013, USA.
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