Research reportDifferential regulation of mRNA levels encoding for the two isoforms of glutamate decarboxylase (GAD65 and GAD67) by dopamine receptors in the rat striatum
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No effect of riluzole and memantine on learning deficit following quinpirole sensitization - An animal model of obsessive-compulsive disorder
2019, Physiology and BehaviorCitation Excerpt :One possible explanation of the present findings lays in the glutamatergic effect of QNP on different brain structures. While QNP was found to increase levels of glutamate in substantia nigra [1] and striatum [28], it was also shown to decrease glutamate concentration in nucleus accumbens (NAc) [12,27]. Lesion of NAc has been found to result in stereotypical behavior [10].
Gamma aminobutyric acidergic and neuronal structural markers in the nucleus accumbens core underlie Trait-like impulsive behavior
2014, Biological PsychiatryCitation Excerpt :Moreover, a reduction in DA D1 receptors in the left NAcbC may have been responsible for the observed reduction in GAD65/67 in this region. In support of this hypothesis, previous research has shown that intrastriatal administration of D1 receptor agonists increases GAD65 expression in striatal neurons (50,51) and facilitates GABA release in the substantia nigra pars reticulata (52). Our results indicate a strong inverse relationship between GAD65/67 and behavioral impulsivity (Figure 3).
GABA concentration in schizophrenia patients and the effects of antipsychotic medication: A proton magnetic resonance spectroscopy study
2010, Schizophrenia ResearchCitation Excerpt :Our study has demonstrated that the in vivo GABA concentrations of the ACC and the ltBG did not differ significantly between medicated chronic schizophrenia patients and healthy control subjects. Animal studies have reported that typical antipsychotics increased the expression of GAD67 and GAD67 mRNA in the basal ganglia (Chen and Weiss, 1993; Johnson et al., 1994; Jolkkonen et al., 1994; Delfs et al., 1995a,b; Laprade and Soghomonian, 1995; Sakai et al., 2001), but that administration of atypical antipsychotic drugs did not (Delfs et al., 1995a; Sakai et al., 2001). Our observation of significantly higher GABA concentrations in the TYP group compared to the ATY group is therefore compatible with the findings of these animal studies.