Amino acid neurotransmitters and their receptors in the brain synaptosomes of acute hepatic failure rats.

Ammonia contents in the brain stem and prosencephalon markedly increased in a rat model of acute hepatic failure induced by partial hepatectomy following CCl4 intoxication. In hepatic failure rats, synaptosomal glutamic acid (excitatory amino acid neurotransmitter) contents decreased significantly in the prosencephalon, and GABA (inhibitory amino acid neurotransmitter) contents decreased significantly in the brain stem. The molar ratio of glutamic acid to glutamine significantly diminished in the brain stem. Glutamic acid decarboxylase activity in the synaptosomes and the binding of [3H]glutamic acid and [3H]GABA to synaptosomal membrane preparations were unchanged in acute hepatic failure rats. These results indicate than an insufficiency of both excitatory and inhibitory neurotransmitter amino acids is induced by high ammonia contents in the synaptosomes of the brain stem during acute hepatic failure.