Using two independent antibodies developed against monoacylglycerol lipase (MGL), the predominant enzyme inactivating 2-AG, immunostaining also revealed a laminar and punctate staining pattern. However, as observed previously in rodent hippocampus, MGL was enriched in axon terminals instead of postsynaptic structures at the ultrastructural level. Taken together, these findings demonstrate the post- and presynaptic segregation of primary enzymes responsible for synthesis and

elimination of 2-AG, respectively, in the human hippocampus. Thus, molecular architecture of the learn more endocannabinoid signaling machinery supports retrograde regulation of synaptic activity, and its similar blueprint in rodents and humans further indicates that 2-AG’s physiological role as a negative feed-back signal is an evolutionarily conserved feature of excitatory synapses. (C) 2011 IBRO. Published by Elsevier Ltd. All rights reserved.”
“Neuronal cell death induced by anaesthetics in the developing brain was evident in previous pre-clinical studies. However, the neuronal cell types involved in anaesthesia-induced neuronal

cell death remains elusive. The aim of this study was to investigate glutamatergic, GABAergic, cholinergic and dopaminergic neuronal cell apoptosis induced by anaesthetic exposure in specific brain regions in rats. Separate cohorts of 7-day-old Sprague Dawley (SD) rat pups GSK621 manufacturer were randomly assigned to two groups: Naive and anaesthetics alone (70% nitrous oxide and 0.75% isoflurane exposure for 6 h). The brains were sectioned

and the slices that contained the basal forebrain, substantia nigra, cornu ammonis area 1 (CA1) subarea of hippocampus or cingulate cortex were selected and subsequently subjected to double-labelled fluorescent immunohistochemistry for choline acetyltransferase, dopamine, vesicular glutamate transporter 1 (vGLUT1) or glutamic acid decarboxylase 67 (GAD67) together with caspase LGX818 ic50 3, respectively. Compared to the naive control, anaesthetic exposure significantly increased the number of caspase-3 positive cells in the CA1 subarea of hippocampus, cingulate cortex, and substantia nigra, but not in the basal forebrain. 54% and 14% of apoptotic cells in the CA1 subarea of hippocampus were GABAergic and glutamatergic neurons respectively. In the cingulate cortex, 30% and 37% of apoptotic cells were GABAergic and glutamatergic neurons respectively. In the substantia nigra, 22% of apoptotic cells were dopaminergic neurons. Our data suggests, anaesthetic exposure significantly increases neuroapoptosis of glutamatergic, GABAergic and dopaminergic neurons in the developing brain but not that of the cholinergic neurons in the basal forebrain. (C) 2011 IBRO. Published by Elsevier Ltd. All rights reserved.”
“The performance of a demanding exercise can result in motor performance deterioration and depression of primary motor cortex excitability.