FUNCTIONAL-RELATIONSHIP BETWEEN AMMONIA AND GANGLIOSIDES IN BRAIN

Citation
P. Modi et al., FUNCTIONAL-RELATIONSHIP BETWEEN AMMONIA AND GANGLIOSIDES IN BRAIN, Neurochemical research, 19(3), 1994, pp. 353-358
Citations number
37
Categorie Soggetti
Biology,Neurosciences
Journal title
ISSN journal
03643190
Volume
19
Issue
3
Year of publication
1994
Pages
353 - 358
Database
ISI
SICI code
0364-3190(1994)19:3<353:FBAAGI>2.0.ZU;2-H
Abstract
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.