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pilocarpine/atrofi
Länken sparas på Urklipp
Sida 1 från 216 resultat
Effect of a gel containing pilocarpine on vaginal atrophy in castrated rats.
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OBJECTIVE
To evaluate the effect of Carbopol gel formulations containing pilocarpine on the morphology and morphometry of the vaginal epithelium of castrated rats.
METHODS
Thirty-one female Wistar-Hannover rats were randomly divided into four groups: the control Groups I (n=7, rats in persistent
Neuronal degeneration is observed in multiple regions outside the hippocampus after lithium pilocarpine-induced status epilepticus in the immature rat.
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Although hippocampal sclerosis is frequently identified as a possible epileptic focus in patients with temporal lobe epilepsy, neuronal loss has also been observed in additional structures, including areas outside the temporal lobe. The claim from several researchers using animal models of acquired
Up-regulation of D-serine might induce GABAergic neuronal degeneration in the cerebral cortex and hippocampus in the mouse pilocarpine model of epilepsy.
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Epilepsy is a serious neurological disorder with neuronal loss and spontaneous recurrent seizures, but the neurochemical basis remains largely unclear. We hypothesize that D-serine, a newly identified endogenous co-agonist of N-methyl-D-aspartate (NMDA) receptor, may trigger excitotoxicity and
Neuron activation, degeneration and death in the hippocampus of mice after pilocarpine induced status epilepticus.
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OBJECTIVE
To examine the occurrence of neuron activation, neurodegeneraion and cell death, and the correlation among them in the hippocampus after status epilepticus.
METHODS
CFV, Fluoro Jade B and c-Fos staining were done at multiple time points after pilocarpine induced status
Degeneration and proliferation of astrocytes in the mouse dentate gyrus after pilocarpine-induced status epilepticus.
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Astrocytes are relatively resistant to injury compared to neurons and oligodendrocytes. Here, we report transient region-specific loss of astrocytes in mice early after pilocarpine-induced status epilepticus (SE). In the dentate hilus, immunoreactivity for glial acidic fibrillary protein (GFAP) was
Persistence and atrophy of septal/diagonal band neurons expressing the p75 neurotrophin receptor in pilocarpine-induced chronic epilepsy in the rat.
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Systemic administration of pilocarpine, which results in status epilepticus followed by recurrent seizures in rats, is a widely used experimental model of chronic limbic epilepsy. Marked structural alterations have been documented in pilocarpine-induced epilepsy, and these include cell loss in the
Memantine decreases neuronal degeneration in young rats submitted to LiCl-pilocarpine-induced status epilepticus.
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Several works have demonstrated that status epilepticus (SE) induced-neurodegeneration appears to involve an overactivation of N-methyl-d-aspartate receptors and treatment with high-affinity NMDAR antagonists is neuroprotective against this brain damage. However, these compounds display undesirable
Neuronal degeneration and gliosis time-course in the mouse hippocampal formation after pilocarpine-induced status epilepticus.
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Temporal lobe epilepsy (TLE) is the most common type of human epilepsy and has been related with extensive loss of hippocampal pyramidal and dentate hilar neurons and gliosis. Many characteristics of TLE are reproduced in the pilocarpine model of epilepsy in mice. This study analyzed the neuronal
A Case of Atrophy of the Optic Nerves Treated by Hypodermic Injections of Nitrate of Pilocarpine.
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Doxycycline protects against pilocarpine-induced convulsions in rats, through its antioxidant effect and modulation of brain amino acids.
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This work evaluated doxycycline (2nd generation tetracycline) protection against pilocarpine-induced convulsions in rats. The animals were treated with doxycycline (Dox: 10 to100 mg/kg, i.p., 7days), 30min before the pilocarpine injection (P: 300mg/kg, i.p.) and observed for cholinergic signs,
Transient receptor potential melastatin 2 contributes to neuroinflammation and negatively regulates cognitive outcomes in a pilocarpine-induced mouse model of epilepsy
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Neuroinflammation contributes to the generation of epileptic seizures and is associate with neuropathology and comorbidities. Transient receptor potential melastatin 2 (TRPM2) expresses in various cell types in the brain. It plays a pathological role in a wide range of neuroinflammatory diseases,
Amygdala opioid receptors mediate the electroacupuncture-induced deterioration of sleep disruptions in epilepsy rats.
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BACKGROUND
Clinical and experimental evidence demonstrates that sleep and epilepsy reciprocally affect each other. Previous studies indicated that epilepsy alters sleep homeostasis; in contrast, sleep disturbance deteriorates epilepsy. If a therapy possesses both epilepsy suppression and sleep
Disseminated corticolimbic neuronal degeneration induced in rat brain by MK-801: potential relevance to Alzheimer's disease.
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Blockade of N-methyl-D-aspartate (NMDA) glutamate receptors by MK-801 induces neuronal degeneration in the posterior cingulate/retrosplenial cortex and other corticolimbic regions although damage in the latter has not been adequately characterized. This disseminated corticolimbic damage is of
The functional anatomy and pathology of lithium-pilocarpine and high-dose pilocarpine seizures.
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Subcutaneous treatment of rats with low doses of lithium and pilocarpine or a high dose of pilocarpine results in a severe seizure--brain damage syndrome. Rats thus treated were studied with multiple-depth electrodes, quantitative [14C]2-deoxyglucose autoradiography, and light and electron
A suspected case of drug-induced tubulointerstitial nephritis by pilocarpine hydrochloride.
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A 63-year-old man with pharyngeal cancer had been prescribed pilocarpine hydrochloride for xerostomia after concomitant chemoradiotherapy. After 6 months of taking pilocarpine hydrochloride, he was referred to our hospital due to gradually developing renal insufficiency. The patient underwent
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