Effects of aluminium exposure on brain glutamate and GABA systems: an experimental study in rats

It has been postulated that the neurotoxic effects of aluminium could be mediated through glutamate,an excitatory amino acid. Hence the effects of aluminium administration (at a dose of 4.2 mg/kg body weight daily as aluminium chloride,hexahydrate, intraperitoneally,for 4 weeks)on glutamate and g-amino butyrate (GABA),an inhibitory amino acid, and related enzyme activities in different regions of the brain were studied in albino rats. The glutamate level increased significantly in the cerebrum,thalamic area,midbrain-hippocampal region and cerebellum in response to in vivo aluminium exposure. The aluminium insult also caused significant increases in glutamate a-decarboxylase activity in all the brain regions. However,on aluminium insult,the GABA content was not significantly changed except in the thalamic area,where it was elevated. On the contrary,the GABA-T activities of all the regions were reduced significantly in all regions except the midbrain-hippocampal region. However,the succinic semi-aldehyde content of all brain regions increased,often significantly. The aluminium-induced modification of the enzyme activities may be either due to the direct impact of aluminium or due to aluminium-induced changes in the cellular environment. The aluminiuminduced differential regional accumulation of glutamate or other alterations in enzymes of the glutamate-GABA system may be one of the causes of aluminium-induced neurotoxicity