Novel Neuroprotective Effect Of Therapeutic Lithium Carbonate Doses In Rat Brain Tissue During Different Treatment Intervals

Amino acids are either neurotransmitters or precursors for neurotransmitters. This study aims to investigate the effect of therapeutic dose of lithium carbonate 75 mgkg on brain free amino acids thought to contribute in psychotic disorders and declare its effect on phosphate buffer insoluble protein fraction in rat brain at different treatment periods. Phosphate buffer insoluble protein fraction was chosen being the more stable part of tissue protein. Four groups of rats 6each were recruited randomly assorted into a control group given saline acute study group given single dose left for 2 hours sub-acute study group given a dose each 3 days for 2 weeks and a chronic study group given a dose each 3 days for a month. Brain content of l free amino acids - aminobutyrate GABA aspartate glutamate glycine phenyl alanine tryptophan branched chain amino acids and proline was significantly decreased on acute sub-acute and chronic administration while hydroxyl and dibasic amino acids were increased. Concomitantly increased phosphate buffer-insoluble protein fraction after two hours of administration decreasing to normal level after a month of therapy. These actions indicate an anabolic and neuroprotective impact of lithium on brain tissue with amelioration of nitrogen balance activated amidation hydroxylation and peptidases. These pathways possibly published for the first time elucidating a novel therapeutic prospect of lithium in psychotic disorders. Increasing a more stable fraction of tissue protein phosphate-buffer insoluble is a novel contribution to lithium tissue stabilization in affective disorders.