Trimethyltin, an organic compound of tin, is a potent neurotoxicant of mechanism of action yet to be uncovered.The neuropathological findings that causes selective hippocampal damage with several unique features, highly reminiscent of Ammon's horn sclerosis as a final result, have rised the possibility that there is a link between trimethyltin neurotoxicity and other degenerative events for which an imbalance between neuronal inhibition/excitation has been proposed.However, there still exist a whole catalog of issues which await clarification.One of the greatest importance is how does trimethyltin reach the critical sites within the brain and what are they ? Available data concerning the long-term consequences related to trimethyltin neurotoxicity are also far from being completed.This review current data from in vitro and in vivo studies on neurotoxic effects of trimethyltin.Several hypotheses on mechanisms that may led to neuronal death induced by the toxin are presented.
Partial deafferentation of the hippocampus due to trymethyltin (TMT) intoxication has been reported to induce plastic rearrangements of neuronal elements but the factors that direct these responses are unknown. To assess the possible involvement of nerve growth factor (NGF) in the phenomenon we evaluated the presumable changes in the expression pattern of NGF immunoreactivity (NGF-IR) in rat hippocampus 21 days after administration of TMT (8 mg/kg, i.p.) when reactive changes are fully developed. Immunolabelling for TrkA known to mediate biological effects of NGF and for GFAP to identify astroglial cells as a one of presumed source of postinjury produced factors was carried out on adjacent sections to establish the relation between expression of these proteins. In control hippocampus NGF-IR and TrkA-IR were localized in neurons and/or nueropil. After exposure to TMT remarkable non-neuronal expression of both proteins was observed. The distribution pattern of NGF, TrkA and GFAP overlapped suggesting that reactive asrtocytes may not only produce NGF but also may become responsive to this neurotrophin. Zones of extensive NGF and TrkA astroglial expression corresponded to areas of axonal-dendritic rearrangements reported earlier. That data suggest that astroglia-derived trophic activity may be involved in neuronal plastic events associated with treatment with TMT.
Septal cholinergic neurones depend on trophic support by nerve growth factor (NGF) which can rescue them from injury-induced degeneration.Since NGF exerts its effects via p75NTR and TrkA receptors coexpressed in vast majority of these neurones and down-regulated without NGF treatment after injury.In this study we aimed to examine how does the lesion to the cholonergic tracts affect distribution of both type of receptor proteins in damaged fibres.Early changes (two and seven days) were examined immunocytochemically within the septum and supracallosal stria after unilateral lesion to the supracollosal area and cingulum transecting some septal cholinergic efferents.
JavaScript is turned off in your web browser. Turn it on to take full advantage of this site, then refresh the page.