Aims: Implication of modified N-methyl-D-aspartate receptors (NMDAR) in synaptic plasticity and learning was investigated in normal and pathological conditions.
Study design: We studied the efficiency of synaptic plasticity, the development of the long-term potentiation/depression (LTP/LTD) in olfactory cortex slices, treated with antisense or sense oligodeoxynucleotides (aODNs and sODNs) to the GluN1 subunit of NMDAR.
Main outcome: aODNs induced the LTD development in slices after high-frequency tetanization. Contrariwise, in sliced treated with sODNs the enhanced LTP developed. Under conditions of severe anoxia (10 min), treatment of slices with aODNs and sODNs contributed to the preservation of synaptic activity which has been blocked in the control untreated slices. In practical implications such directed up- and down regulation of NMDAR might be useful in the readjustment of brain activity by the controlling balance of excitation/inhibition.
Sleep is considered as a complex process in human beings and is least understood mechanism. Role of sleep in synaptic plasticity remains a debatable topic till date. Sleep is influenced by genetic background of the individual. EEG done in human sleep showed strong influence of genetic factors. A handful of familial analyses involving specific gene loci and twin studies has been done in this regard. In this review article focused discussion on genetic contribution to sleep phenotypes, twin and familial linkage studies and effect of genetic variation on sleep will be covered
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