4 amino butyric acid/atrophy

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Supernormal ERG oscillatory potentials in transgenic rabbit with rhodopsin P347L mutation and retinal degeneration.

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OBJECTIVE To determine the properties of the retina of a rhodopsin P347L transgenic (Tg) rabbit model of retinal degeneration by electroretinography (ERG). METHODS Full-field ERGs were recorded in 12- to 48-week-old wild-type (WT) and Tg rabbits. The a-wave was analyzed by the a-wave fitting model

Time course of the effect of status epilepticus induced in the developing rat on γ-amino butyric acid and glutamate cerebellar concentration.

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BACKGROUND Status epilepticus (SE) is an epileptic condition that can cause cerebellar atrophy and loss of Purkinje cells in both humans and research animals. Cerebellum is a region rich in γ-aminobutyric acid (GABA) and glutamate, and some studies have shown that their concentrations may be altered

Patterns of thalamocortical degeneration after ablation of somatosensory cortex in monkeys.

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We examined the pattern of cytochrome oxidase (CO), Nissl staining, and gamma-amino butyric acid (GABA) immunoreactivity in the ventroposterior lateral nucleus (VPL) of the thalamus in monkeys that received no, total, or subtotal, ablation of the hand representations in postcentral somatosensory

Neurochemical architecture of the normal and degenerating rat retina.

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We used post-embedding immunocytochemistry to determine the cellular localization of glutamate, gamma-amino butyric acid (GABA), glycine, aspartate, glutamine, arginine, and taurine in the normal and degenerating rat retina. Müller's cell function was also evaluated by determining the uptake and

Gamma Amino Butyric Acid Attenuates Brain Oxidative Damage Associated with Insulin Alteration in Streptozotocin-Treated Rats.

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The aim of the current study was to evaluate the role of γ-amino butyric acid (GABA) in insulin disturbance and hyperglycemia associated with brain oxidative damage in streptozotocin-treated rats. Streptozotocin (STZ) was administered to male albino rats as a single intraperitoneal dose (60 mg/kg

Photoreceptor degeneration and loss of immunoreactive GABA in the Abyssinian cat retina.

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GABA (gamma-amino butyric acid) and its synthesizing enzyme, GAD (glutamate decarboxylase; EC 4.1.1.15) were localized in the retina of Abyssinian cats homozygous for a recessively inherited retinal degenerative disorder which in several respects is similar to the human disease, retinitis

Stiff-person syndrome (SPS) and anti-GAD-related CNS degenerations: protean additions to the autoimmune central neuropathies.

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Stiff Person Syndrome (SPS) is a rare autoimmune neurological disease attributable to autoantibodies to glutamic acid decarboxylase (anti-GAD) more usually associated with the islet beta cell destruction of autoimmune type 1 diabetes (T1D). SPS is characterized by interference in neurons with the

Isoflurane-induced neuronal degeneration: an evaluation in organotypic hippocampal slice cultures.

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Prolonged exposure of postnatal day (PND) 7 rat pups to anesthetics, which act via N-methyl-D-aspartate antagonism and/or gamma-amino butyric acid enhancement, causes neurodegeneration and persistent behavioral deficits. We studied these findings in vitro and determined whether the age of rat pups

Role of gamma-amino-butyric acid in the dorsal anterior cingulate in age-associated changes in cognition.

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GABAergic mechanisms have been shown to contribute to cognitive aging in animal models, but there is currently limited in vivo evidence to support this relationship in humans. It is also unclear whether aging is associated with changes in GABA levels measured with proton magnetic resonance

Distribution of glutamic acid decarboxylase mRNA in the forebrain of the rainbow trout as studied by in situ hybridization.

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By using degenerate primers designed from glutamate decarboxylase (GAD) sequences of mammals, Xenopus and Drosophila, a 270-bp cDNA fragment was cloned by reverse transcriptase-polymerase chain reaction (RT-PCR) from cerebellum total RNA of rainbow trout. This partial cDNA shows 90% identity with

Kainic acid affects both plexiform layers of chicken retina.

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Intraocular injections of kainic acid produce marked lesions of the chicken retina. Low doses (6-20 nmol/retina) appear to cause lesions of the inner part of the retina, primarily involving amacrine cells. At around 60 nmol/retina there is a qualitative change in the nature of the lesion, as the

Acidic amino acids evoke a smaller [Ca2+]i rise in GABAergic than non-GABAergic hippocampal neurons.

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Changes in intracellular calcium concentration ([Ca2+]i) in response to topical application of the glutamate agonists N-methyl-D-aspartate (NMDA), or amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid (AMPA) were measured in cultured rat hippocampal neurons loaded with Fluo-3 and visualized in a

Development and persistence of neuropathic pain through microglial activation and KCC2 decreasing after mouse tibial nerve injury.

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Gamma-amino butyric acid (GABA) is an inhibitory neurotransmitter in the mature brain, but is excitatory during development and after motor nerve injury. This difference in GABAergic action depends on the intracellular chloride ion concentration ([Cl^-]_i), primarily regulated by

MDMA (Ecstasy) controls in concert a group of genes involved in GABA neurotransmission.

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In several countries, 3,4-methylenedioxymethamphetamine (MDMA) is currently the most abundant psychoactive recreational drug. MDMA induces numerous neuropsychiatric behaviors, serotonergic neuron degeneration, programmed death of cultured cells, hyperthermia and occasional fatality. Using gene

[Macrocephaly and dystonic cerebral palsy in a child with type I glutaric aciduria].

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In a male infant with macrocephaly and dystonic cerebral palsy glutaric aciduria type I was detected by analysis of urine for organic acids. Glutaric aciduria type I is an inherited metabolic disorder of organic acids due to a defect of glutaryl-CoA-dehydrogenase in the intermediate metabolic step

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