choline acetyltransferase/atrofie

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Recovery of acetylcholine release and choline acetyltransferase activity after freezing-induced degeneration of rat soleus muscle.

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In order to study the effect of synaptic contact on the amounts of choline acetyltransferase (ChAT) and acetylcholine (ACh) in the nerve terminals and on their ability to release ACh, a freeze-thaw procedure was developed as a means to induce long lasting degeneration of rat soleus muscle. It was

Brain choline acetyltransferase reduction in dominantly inherited olivopontocerebellar atrophy.

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We measured the activity of choline acetyltransferase, the cholinergic marker enzyme, in the brains of 17 patients from five established pedigrees with dominantly inherited olivopontocerebellar atrophy (OPCA). OPCA is a group of cerebellar ataxia disorders in which serious intellectual impairment is

Acetylcholinesterase-transgenic mice display embryonic modulations in spinal cord choline acetyltransferase and neurexin Ibeta gene expression followed by late-onset neuromotor deterioration.

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To explore the possibility that overproduction of neuronal acetylcholinesterase (AChE) confers changes in both cholinergic and morphogenic intercellular interactions, we studied developmental responses to neuronal AChE overexpression in motoneurons and neuromuscular junctions of AChE-transgenic

Progesterone modulates brain-derived neurotrophic factor and choline acetyltransferase in degenerating Wobbler motoneurons.

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Progesterone (PROG) shows neuroprotective effects in nervous system diseases. The Wobbler mouse, a model of motoneuron degeneration, suffers a mutation of the Vsp154 gene on chromosome 11 leading to motoneuron vacuolation and astrocytosis of the spinal cord. Previous work has demonstrated beneficial

Effects of cholesterol and its 24S-OH and 25-OH oxysterols on choline acetyltransferase-positive neurons in brain slices.

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In Alzheimer's disease (AD) neurons expressing the enzyme choline acetyltransferase (ChAT) degenerate and a loss of cholinergic activity directly correlates with cognitive decline. Recent studies have suggested that cholesterol plays a role in AD. The aim of the present study was to explore if

Cholinergic degeneration is associated with increased plaque deposition and cognitive impairment in APPswe/PS1dE9 mice.

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Cholinergic dysfunction and deposition of plaques containing amyloid β-peptides (Aβ) are two of the characteristics of Alzheimer's disease. Here, we combine APPswe/PS1dE9 (APP/PS1) mice with the cholinergic immunotoxin mu p75-saporin (SAP) to integrate partial basal forebrain cholinergic

Acetyl-L-carnitine restores choline acetyltransferase activity in the hippocampus of rats with partial unilateral fimbria-fornix transection.

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Transection of the fimbria-fornix bundle in adult rats results in degeneration of the septohippocampal cholinergic pathway, reminiscent of that occurring in aging as well as Alzheimer disease. We report here a study of the effect of a treatment with acetyl-L-carnitine (ALCAR) in three-month-old

Acetyl-L-carnitine treatment increases choline acetyltransferase activity and NGF levels in the CNS of adult rats following total fimbria-fornix transection.

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Transection of the fimbria-fornix in adult rats is a useful model for producing impairments of cholinergic activity in the hippocampus (HIPP) and atrophy of the medial septum cholinergic perikarya, similar to those observed during senescence, that are possibly due to the lack of nerve growth factor

Behavioral and degeneration changes in the basal forebrain systems of aged rats: a quantitative study in the region of the basal forebrain after levo-acetyl-carnitine treatments assessed by Abercrombie estimation.

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One group of six male control rats [21 months old] and one group of six male rats of the same age, singularly stored in a cage, and treated with acetyl-l-carnitine-HCl (ALCAR: 60 mg/kg/day/p.o.) for six months were tested in the spatial learning/memory Morris maze-water task and for atrophy and cell

The expression of calcitonin gene-related Peptide and acetylcholine in the vestibular-related nucleus population of wild-type mice and retinal degeneration fast mice after rotary stimulation.

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Due to the lack of an appropriate animal model, few studies have addressed the integration of visual and vestibular information in the visual system. Using a mouse model with a visual defect (retinal degeneration fast, rdf), we have verified that the prepositus hypoglossal nucleus (PrH) and the Kooy

Recombinant human nerve growth factor prevents retrograde degeneration of axotomized basal forebrain cholinergic neurons in the rat.

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Cholinergic neurons in the basal forebrain magnocellular complex (BFMC) respond to nerve growth factor (NGF) during development and in adult life, and it has been suggested that the administration of NGF might ameliorate some of the abnormalities that occur in neurological disorders associated with

Implants of polymer-encapsulated human NGF-secreting cells in the nonhuman primate: rescue and sprouting of degenerating cholinergic basal forebrain neurons.

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Baby hamster kidney (BHK) cells were genetically modified to secrete high levels of human nerve growth factor (BHK-hNGF). Following polymer encapsulation, these cells were implanted into the lateral ventricle of four cynomolgus monkeys immediately following a unilateral transection/aspiration of the

Hippocampal and midline thalamic fibers and terminals in relation to the choline acetyltransferase-immunoreactive neurons in nucleus accumbens of the rat: a light and electron microscopic study.

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The synaptic interactions between terminals of allocorticostriatal and thalamostriatal fibers and the cholinergic neurons in the nucleus accumbens were investigated using degeneration and dual labelling immunocytochemistry in Wistar rats. The presumptive cholinergic neurons were labelled with

Parenterally administered GM1 ganglioside prevents retrograde degeneration of cholinergic cells of the rat basal forebrain.

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The effect of daily intraperitoneal injections of GM1 ganglioside on retrograde degeneration in the basal forebrain has been examined, using a monoclonal antibody directed against choline acetyltransferase to identify the cholinergic neurones. Rats underwent extensive damage of the cerebral cortex

GABA/glycine signaling during degeneration and regeneration of mouse hypoglossal nerves.

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In the adult central nervous system (CNS), GABA and glycine (Gly) are predominant inhibitory neurotransmitters, negatively regulating glutamatergic transmission. In the immature CNS, on the other hand, they act as trophic factors, mediating morphogenesis. In the present study, to investigate their

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