1,720,970 research outputs found
Immunohistochemical evidence that MPTP-induced parkinsonism affects dopaminergic neurons in mouse enteric nervous system
No full textMorphological evidence that MPTP-induced parkinsonism affects mouse enteric nervous system
No full textProteasome and autophagy activation in acute neurodegeneration following not invasive focal cerebral ischemia
No full textEsomeprazole dose-dependently counteracts glutathione deficiency and mitochondrial dysfunction induced by indomethacin in the rat gastric mucosa
No full textIl Parkinsonismo indotto da MPTP induce alterazioni a livello del sistema nervoso periferico intestinale.
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Histomorphometric evidence that esomeprazole prevents indomethacin-induced gastric mucosal damage in rats: involvement of gastroprotective mechanisms
No full textHistomorphometric evidence that esomeprazole prevents indomethacin-induced gastric mucosal damage in rats: involvement of gastroprotective mechanisms
No full textMPTP- but not methamphetamine-induced parkinsonism extends to catecholamine neurons in the gut
No full textMethamphetamine (METH) produces nigrostriatal dopamine (DA) loss, partly resembling that which occurs in Parkinson's disease (PD). In PD there is also a marked alteration in the gut. Given the similarities between the central DA denervation produced by METH and PD, in the present study we evaluated the alterations in the gut following upon METH administration. To compare these effects with those occurring in PD, we also administered the parkinsonism-inducing neurotoxin MPTP. METH and MPTP were administered to mice, and after 7 days we investigated the immunostaining for tyrosine hydroxylase in nervous plexuses. These data indicate that METH did not alter the catecholamine-containing axons and autonomic neurons, while MPTP markedly reduced these components
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