Effect of L-deprenyl treatment on electrical activity, Na+, K+ ATPase, and protein kinase C activities in hippocampal subfields (CA1 and CA3) of aged rat brain.

L-deprenyl is considered to protect against age-related cognitive deficits by improving long-term learning/memory in the aged brain. The CA1 and CA3 hippocampal areas are the sites at which initial learning and memory processes occur. Chronic deprenyl treatment significantly augmented the basal electrical firing rate (multiple-unit action potentials),and Na+, K+-ATPase and protein kinase C activities of both CA1 and CA3 indicating that the drug increased the excitability of CA1 and CA3. The increase, however, was much greater in CA1 than in CA3 suggesting that deprenyl can improve longer term learning in aged animals by its excitability-enhancing action in CA1. The drug also countered the ageing-related loss of hippocampal protein kinase C activity.

Na+ K(+)-ATPase activity in response to exogenous dehydroepiandrosterone administration in aging rat brain.

Influence of exogenously administered dehydroepiandrosterone (DHEA) on the activity of Na+ K+ ATPase was investigated in synaptosomal fraction from cerebral cortex, cerebellum, hippocampus and medulla regions of brain of 12 and 22 months old rats. DHEA was administered daily at the dose of 30 mg/kg/body wt, intraperitonially (ip) in both the age groups of rats for 1 month. Results showed that Na+ K+ ATPase activity, increased in DHEA treated rats in both the age groups. In terms of per cent increase, 22 months old animals showed significant increase in Na+ K+ ATPase activity in the synaptosomal fraction of all the four brain regions than in 12 months old DHEA-treated rats. This showed that exogenous DHEA modulated the activity of Na+ K+ ATPase and also protected the age-related loss of membrane integrity and functions. It was concluded that exogenous DHEA might be beneficial in terms of neuroprotection against age-related loss of Na+ K+ ATPase mediated brain functions like learning and memory.