کد مقاله | کد نشریه | سال انتشار | مقاله انگلیسی | نسخه تمام متن |
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6284934 | 1615172 | 2011 | 4 صفحه PDF | دانلود رایگان |
Lamotrigine (LTG) is sometimes co-administered with antipsychotic drugs for the treatment of schizophrenia. Nevertheless, the pharmacological basis of LTG use for schizophrenia has not been reported. Our group recently proposed a new psychostimulant animal model that might reflect the progressive pathophysiology of schizophrenia. Results obtained using that model show that LTG blocks the initiation and expression of repeated high-dosage methamphetamine-induced prepulse inhibition deficit in rats (Nakato et al., 2010, Neurosci. Lett. [25]). Using the model, the effect of LTG (30Â mg/kg) on methamphetamine (METH, 2.5Â mg/kg)-induced increases in extracellular glutamate levels in the medial prefrontal cortex (mPFC) was examined in this study. Then the effect of repeated co-administration of LTG (30Â mg/kg) on repeated METH (2.5Â mg/kg)-induced apoptosis in this region of rats was investigated. Results show that LTG (30Â mg/kg) blocked the METH (2.5Â mg/kg)-induced glutamate increase in the mPFC. Repeated co-administration of LTG (30Â mg/kg) blocked the development of apoptosis induced by repeated administration of METH (2.5Â mg/kg) in the mPFC. The LTG blocks histological abnormalities induced by repeated administration of METH, which suggests a mechanism of LTG that protects against progressive pathophysiology in schizophrenia.
Research highlightsⶠApoptosis plays an important role in progressive cortical atrophy in schizophrenia. ⶠMethamphetamine (METH) induced apoptosis in the medial prefrontal cortex (mPFC). ⶠMETH increased extracellular glutamate levels in the mPFC. ⶠLamotrigine (LTG) prevented these changes induced by METH in the mPFC. ⶠLTG may prevent longitudinal pathophysiological development in schizophrenia.
Journal: Neuroscience Letters - Volume 490, Issue 3, 3 March 2011, Pages 161-164