acidic peptide/crise epiléptica

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[Polyamines and activity of acid peptide-hydrolases in hyperoxia].

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The content of spermidine and spermine polyamines in the rat brain under hyperoxic convulsions and four hours after convulsions decreases sharply. The intraperitoneal administration of polyamines before hyperbaric oxygenation decreased the rate of development of hyperoxic convulsions in rats. In the

Gene therapy mediated seizure suppression in Genetic Generalised Epilepsy: Neuropeptide Y overexpression in a rat model.

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Neuropeptide Y (NPY) is an important 36 amino acid peptide that is abundantly expressed in the mammalian CNS and is known to be an endogenous modulator of seizure activity, including in rat models of Genetic Generalised Epilepsy (GGE) with absence seizures. Studies have shown that viral-mediated

Ghrelin protects against cell death of hippocampal neurons in pilocarpine-induced seizures in rats.

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Ghrelin, a 28-amino-acid peptide, is mainly secreted by the stomach. Evidence has shown ghrelin to have neuroprotective effects. However, whether ghrelin protects hippocampal neurons against cell death in pilocarpine-induced seizures is unknown. We used Nissl staining to show that ghrelin attenuated

Adeno-associated virus-mediated expression and constitutive secretion of NPY or NPY13-36 suppresses seizure activity in vivo.

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Neuropeptide Y (NPY) is a 36-amino-acid peptide that attenuates seizure activity following direct infusion or adeno-associated virus (AAV)-mediated expression in the central nervous system. However, NPY activates all NPY receptor subtypes, potentially causing unwanted side effects. NPY13-36 is a

Secretoneurin: a market in rat hippocampal pathways.

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Secretoneurin is a 33-amino acid peptide, generated in brain by proteolytic processing of secretogranin II. The distribution of secretoneurin-like immunoreactivity and secretogranin II mRNA was investigated in the hippocampus of the rat. Secretogranin II mRNA was found in high concentrations

Epileptogenic activity of two peptides derived from diazepam binding inhibitor after intrahippocampal injection in rats.

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Peptides DBI 42-50 (DRPGLLDLK) and DBI 43-50 (RPGLLDLK) are synthetic fragments of an 18 amino acid peptide called octadecaneuropeptide (QATVGDVNTDRPGLLDLK), a brain derivative of diazepam-binding inhibitor (DBI). The two peptides were unilaterally injected into the dorsal hippocampus (granule cells

Neuropeptide Y and its receptors as potential therapeutic drug targets.

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Neuropeptide Y (NPY) is a 36-amino-acid peptide that exhibits a large number of physiological activities in the central and peripheral nervous systems. NPY mediates its effects through the activation of six G-protein-coupled receptor subtypes named Y(1), Y(2), Y(3), Y(4), Y(5), and y(6). Evidence

Activation of metabotropic glutamate receptors increases neuropeptide Y expression in the rat hippocampus. Immunohistochemical studies.

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Neuropeptide Y (NPY), a 36-amino acid peptide, is present in some hippocampal interneurons and nerve terminals and seems to modulate glutamatergic transmission in this structure. Earlier studies of some other authors showed an increase in NPY expression in the hippocampus during seizures and

Nonclinical Safety Profile of Etelcalcetide, a Novel Peptide Calcimimetic for the Treatment of Secondary Hyperparathyroidism.

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Etelcalcetide is a novel d-amino acid peptide that functions as an allosteric activator of the calcium-sensing receptor and is being developed as an intravenous calcimimetic for the treatment of secondary hyperparathyroidism in patients with chronic kidney disease on hemodialysis. To support

A novel BK channel-targeted peptide suppresses sound evoked activity in the mouse inferior colliculus.

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Large conductance calcium-activated (BK) channels are broadly expressed in neurons and muscle where they modulate cellular activity. Decades of research support an interest in pharmaceutical applications for modulating BK channel function. Here we report a novel BK channel-targeted peptide with

Reversal of fragile X phenotypes by manipulation of AβPP/Aβ levels in Fmr1KO mice.

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Fragile X syndrome (FXS) is the most common form of inherited intellectual disability and the leading known genetic cause of autism. Fragile X mental retardation protein (FMRP), which is absent or expressed at substantially reduced levels in FXS, binds to and controls the postsynaptic translation of

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