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Biomedical subjects

C Nyakas

Publications and source records attributed to C Nyakas.

111 records · Page 7Linked to original sources
PubMedDate not supplied

Cholinergic fiber aberrations in nucleus basalis lesioned rat and Alzheimer's disease.

Innervation density and morphological aberrations of cholinergic fibers were studied with choline acetyltransferase (ChAT) immunocytochemistry and acetylcholinesterase (AChE) histochemistry in 30-35 month-old aged rats and rats with long-term bilateral lesions of the magnocellular basal nucleus (MBN). In addition, AChE histochemistry was performed on human cortical sections derived from autopsy brains of normal aged and Alzheimer's disease (AD) patients. A limited but variable number of morphological alterations were observed in ChAT-immunoreactive fibers in the cortex and the hippocampus of the aged control rats. The aged MBN-lesioned rats displayed a severely reduced number of cholinergic fibers in the denervated areas of the neocortex, whereas the surviving fibers showed a strongly increased number of aberrations. Fiber anomalies were also observed in the cortex of the aged human subjects and Alzheimer patients, the latter showing a higher incidence of such aberrations. Only a part of these distended profiles were seen in close association with senile plaques as detected in the AChE-stained material. These findings suggest that experimental MBN lesions combined with aging share with AD the induction of large quantities of fiber malformations. Implications of possible mechanisms in both conditions are discussed.

Acetylcholinesterase↗
PubMedDate not supplied

Long-term cholinergic denervation caused by early postnatal AF64A lesion prevents development of muscarinic receptors in rat hippocampus.

The effect of early postnatal (day 8) intracerebroventricular injections of the putative cholinotoxin ethylcholine aziridinium mustard (AF64A) on development of cholinergic innervation and postsynaptic muscarinic acetylcholine receptors in the rat hippocampus was examined. The cholinotoxin applied at this stage of development leads to a permanent denervation of cholinergic fibres in the hippocampus in adulthood demonstrated by (immuno)histochemical methods and biochemical assays. Muscarinic receptor expression in the principal neurons of dentate gyrus and cornu ammonis was strongly reduced as studied by immunostaining with antibodies against muscarinic receptor proteins and binding assays with the muscarinic antagonist quinuclidinyl benzilate. Cholinoceptive interneurons and somatostatinergic interneurons are not affected by the developmental cholinergic lesion. Immunoreactivity to protein kinase C type I as a marker for inositolphosphate-related cellular activation systems slightly decreased in the apical dendrites of the hippocampal principal neurons. These findings indicate that damage to ingrowing cholinergic terminals in the hippocampus in the early postnatal period is a critical hazard for development of the muscarinic receptor system in the hippocampal principal neurons. These results are discussed for their significance to the neural mechanisms that underlie perinatal brain damage and associated cognitive dysfunction.

Animals↗