The functional significance of ammonia production in brain under physi
ological or pathological conditions is not clearly known. NH4+ stimula
tes Na+, K+ activated ATPase causing stabilization of neuronal membran
es of which gangliosides are major structural components. Moreover amm
onia is known to inhibit lysosomal enzymes which include enzymes degra
ding gangliosides. Gangliosides have been shown to stimulate neuritoge
nesis in neuronal cultures and prevent the damage of the neurons from
glutamate toxicity particularly in areas of brain ischemia. Hyperammon
emia without any behavioural changes was induced in experimental rats
by intraperitoneal administration of either a single dose (0.8 mmol/10
0 g wt.) or by six 'hourly' doses (0.6 mmol/100 g wt.) of ammonium ace
tate. An increase in the content of gangliosides along with a rise in
the content of GD(1A) and GD(1B). without any change in beta-galactosi
dase and N-acetylhexosaminidase was observed in cerebral cortex, cereb
ellum, and brain stem, following the administration of single dose of
ammonium acetate. Gangliosides, after extraction from the different br
ain regions, were estimated by the thiobarbituric acid method and expr
essed in terms of sialic acid. Individual gangliosides were separated
and estimated by thin layer chromatography using resorcinol as the sta
ining agent. These results suggest that ammonia production in the neur
onal pathways in brain either as a result of repeated stimulation unde
r physiological conditions or as a result of focal ischemia or injury,
may likewise cause an increase in the content of gangliosides which m
ay help in neuritic growth (physiological conditions facilitating syna
ptic plasticity) and may exert a protective effect on the neurons in t
he ischemic area against glutamate toxicity.