Early Biochemical Effects of GM1 Ganglioside Treatment in Lesioned Brain: Dependence on Degree of Fiber Degeneration
Several reports show that ganglioside treatment, and especially GM1 ganglioside, facilitates various forms of long-term recovery following lesions of the brain (Agnati et al., 1984; Kojima et al., 1984; Oderfeld-Nowak et al., 1984a; b; Toffano et al., 1983; Toffano et al., 1984a; b; Wójcik et al., 1982). Enhanced recovery has been hypothesized to be due mainly to increased sprouting processes. Recently, however, several laboratories have also reported beneficial effects of GM1 treatment upon the impaired functions in an acute phase of CNS injury, (Fass and Ramirez, 1984; Karpiak and Mahadik, 1984; Sabel et al., 1984), and this fact, considering the time period, can hardly be ascribed to facilitation of sprouting. Therefore, other phenomena are probably involved. In fact, several authors pointed out some early compensatory biochemical effects of GM1 treatment after brain lesions. An increase in choline uptake in the cerebral cortex after lesion in the nucleus basalis magnocellularis (Pedata et al., 1984), an increase in dopamine uptake in the striatum following partial hemitransection (Toffano et al., 1984b), an increase of the lowered activity of Na+, K+-ATPase associated with edema (Karpiak and Mahadik, 1984; Karpiak et al., 1986), restoration of striatal energy metabolism (Fuxe et al., 1986), were reported. Hypotheses concerning the effect of ganglioside on increasing of the impulse flow, and/or enhancing biosynthetic processes (Pedata et al., 1984; Toffano et al., 1984b), and effects on restabilization of membrane properties (Janigro et al., 1984; Karpiak and Mahadik, 1984; Karpiak et al., 1986) have been advanced. We are now reporting data which indicate yet another early biochemical facilitatory effect of GM 1, namely, on post-lesion recovery of the hippocampal cholinergic and serotoninergic parameters.
KeywordsCholine Uptake ChAT Activity Impulse Flow Ganglioside Treatment Fidia Research
central nervous system
nerve growth factor.
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