N-acetyl cysteine treatment rescues cognitive deficits induced by mitochondrial dysfunction in G72/G30 transgenic mice.

Genetic studies have implicated the evolutionary novel, anthropoid primate-specific gene locus G72/G30 in psychiatric diseases. This gene encodes the protein LG72 that has been discussed to function as a putative activator of the peroxisomal enzyme D-amino-acid-oxidase (DAO) and as a mitochondrial protein. We recently generated 'humanized' bacterial artificial chromosome transgenic mice (G72Tg) expressing G72 transcripts in cells throughout the brain.

Analysis of pThr286-CaMKII and CaMKII immunohistochemistry in the hippocampus of patients with temporal lobe epilepsy.

Ca2+/calmodulin-dependent protein kinase II (CaMKII) phosphorylates a variety of neuronal proteins, thereby, coordinating responses to changes of intracellular Ca2+ concentrations. Autophosphorylation at threonine286 generates an autonomously active form of CaMKII (pThr286-CaMKII), thus prolonging responses to transient increases in Ca2+. Our previous studies in hippocampi of temporal lobe epilepsy (TLE) patients revealed a significant up-regulation of CaMKII in dentate granule cells (DGCs) of specimens with Ammon's horn sclerosis (AHS).

Hippocampal synaptic metaplasticity requires inhibitory autophosphorylation of Ca2+/calmodulin-dependent kinase II.

Virtually all CNS synapses display the potential for activity-dependent long-term potentiation (LTP) and/or long-term depression (LTD). Intriguingly, the potential to exhibit LTP or LTD at many central synapses itself is powerfully modulated by previous synaptic activity. This higher-order form of plasticity has been termed metaplasticity.