In 52% of the rat hippocampal

slices tested, bath application of donepezil increased the frequency of EPSCs. Further, find more exposure to donepezil increased both burst-like and large-amplitude EPSCs, and increased the proportion of short (20-100 ms) inter-event intervals. Donepezil’s effects were suppressed significantly in presence of 10 mu M mecamylamine or 10 nM methyllycaconitine. These results support the concept that AChE inhibition is able to recruit nAChR-dependent glutamate transmission in the hippocampus and such a mechanism can contribute to the acute neurotoxicological actions of soman. (c) 2013 Elsevier Inc. All rights reserved.”
“Ketamine has been used in humans to model cardinal symptoms of schizophrenia, including working memory impairments and behavioral disorganization. Translational studies with ketamine in nonhuman primates promise to extend the neurobiological understanding of this model.

By establishing the dose-dependent effects Hormones inhibitor of ketamine on spatial working memory and behavior, we sought to test and compare the capacity of antipsychotic and procognitive agents to reverse these symptoms.

Behavioral

observations were taken following administration of placebo/ketamine (0.1-1.7 mg/kg, intramuscularly) and animals were tested on the spatial delayed response task 15 min post-injection. Pretreatments with risperidone as well as full and partial D1 receptor

agonists were tested for their ability to reverse ketamine-induced impairments.

Ketamine (median 1.0 mg/kg) produced a profound cognitive impairment and behavioral sequelae reminiscent of positive and negative symptoms. Risperidone within the therapeutic dose range failed to antagonize behavioral or cognitive consequences of acute ketamine but A77636 (0.1 and 1 A mu g/kg) and SKF38393 (0.1 A mu g/kg-100 A mu g/kg) ameliorated the spatial working memory deficit. selleckchem This effect of A77636 was blocked by the D1 receptor antagonist, SCH39166 (1 and 10 A mu g/kg).

These findings establish a valuable ketamine platform relevant to the treatment of cognitive dysfunction in schizophrenia. The reversal of ketamine-induced working memory deficits by a D1 receptor agonist, but not a commonly prescribed atypical antipsychotic, provides behavioral evidence for significant D1/N-methyl-d-aspartate receptor interactions in prefrontal dysfunction and concurs with suggestions that D1 agonists may be useful in the treatment of cognitive impairments in schizophrenia.”
“The effect of lead (Pb) on spatial memory and hippocampal long-term potentiation (LTP) as a key risk factor has been widely recognized and the oxidative damage has been proposed as a possible mechanism of lead neurotoxicity. Selenium (Se) is a nutritionally essential trace element with known antioxidant potential.