glutamate decarboxylase/atrofia

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Autoantibodies to glutamate decarboxylase in a patient with cerebellar cortical atrophy, peripheral neuropathy, and slow eye movements.

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OBJECTIVE To study the existence of autoimmunity against the cerebellum in patients with sporadic cortical cerebellar atrophy. METHODS The presence of autoantibodies against the cerebellum in the serum and cerebrospinal fluid samples that were obtained from patients with sporadic cortical cerebellar

Aging in the rat hippocampus is associated with widespread reductions in the number of glutamate decarboxylase-67 positive interneurons but not interneuron degeneration.

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Increased excitability of principal excitatory neurons is one of the hallmarks of aging in the hippocampus, signifying a diminution in the number and/or function of inhibitory interneurons with aging. To elucidate this, we performed comprehensive GABA-ergic interneuron cell counts in all layers of

[Autoantibody to glutamate decarboxylase in a patient with spinocerebellar degeneration and Sjögren syndrome].

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We report a 52-year-old woman with Sjögren syndrome from the age of 46, developed cerebellar ataxia, autonomic dysfunction and dysarthria at 50. She had no family history, and all known causes of cerebellar disease were excluded. Serum of the patient contained autoantibodies directed against

Brain glutamate decarboxylase in Parkinson's disease with particular reference to a premortem severity index.

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Glutamate decarboxylase (GAD) activity was estimated in various areas of the brain in 21 control and 26 parkinsonian subjects matched for age, postmortem delay and premortem state. Retrospective analysis of clinical data was used to define a premortem severity index (PMSI), scaled from 0 to 6, based

Recovery of vestibular function in young guinea pigs after streptomycin treatment. Glutamate decarboxylase activity and nystagmus response assessment.

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Fifty-day streptomycin (STP) treatment in guinea pigs causes specific vestibular hair cell (VHC) types I and II (HCI; HCII) degeneration, depletion of glutamate decarboxylase (GAD) and a gradual disappearance of postrotatory nystagmus response (PRNR), which is a sign of vestibular function

gamma-Aminobutyric acid system in developing and degenerating mouse retina.

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Freeze-dried sections (14 microns thick) of retinal layers were prepared from mice with retinal degeneration (C3H strain) and control mice (C57BL strain). The weighed sections (2-30 ng dry weight) were analyzed using our microassay methods. In the control retina, gamma-aminobutyric acid (GABA)

Protective effects of neurotrophin-4/5 and transforming growth factor-alpha on striatal neuronal phenotypic degeneration after excitotoxic lesioning with quinolinic acid.

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Lesioning of the mammalian striatum with the excitotoxin quinolinic acid results in a pattern of neuropathology that resembles that of post mortem Huntington's disease brain. Certain neurotrophic factors can rescue degenerating cells in a variety of lesion types, including those produced by

Intrastriatal infusion of nerve growth factor after quinolinic acid prevents reduction of cellular expression of choline acetyltransferase messenger RNA and trkA messenger RNA, but not glutamate decarboxylase messenger RNA.

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Excitotoxic striatal lesions induced by quinolinic acid, a model for Huntington's disease, were used to test for neuroprotective actions of nerve growth factor on striatal cholinergic and GABAergic neurons. Expressions of the trkA receptor for nerve growth factor, choline acetyltransferase and

Synaptic neurochemical alterations associated with neuronal degeneration in an inherited cerebellar ataxia of Gordon Setters.

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Canine Inherited Ataxia (CIA) is an autosomal recessive cerebellar disease of Gordon Setters associated with degeneration of Purkinje and granule cells. To define specific biochemical correlates of neuronal loss, synaptic neurochemical parameters were measured in three cerebellar regions (vermis,

Idebenone attenuates neuronal degeneration induced by intrastriatal injection of excitotoxins.

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Previous studies with the N18-RE-105 neuronal-like cell line and primary cortical cultures demonstrate that glutamate can produce a calcium-dependent, delayed form of neuronal degeneration that results from its competitive inhibition of cystine transport, which leads to cellular glutathione

Regional brain atrophy and reductions in glutamate release and uptake after intrastriatal kainic acid.

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1 Neurochemical changes and tissue weights were measured following intrastriatal injection of 2.5 microgram of kainic acid in 2 microliter of 0.9% w/v NaCl solution (saline) in the rat. 2 After kainic acid the striatum and neocortex on the injected side showed a progressive reduction in weight, the

Neuroprotective effects of MK-801 in vivo: selectivity and evidence for delayed degeneration mediated by NMDA receptor activation.

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The ability of the noncompetitive N-methyl-D-aspartate (NMDA) receptor antagonist MK-801 to prevent neuronal degeneration in the rat striatum and hippocampus caused by intracerebral injection of excitotoxins has been examined. Excitotoxic damage was assessed after 7 d, using histological and

A comparative analysis of the neuroprotective properties of competitive and uncompetitive N-methyl-D-aspartate receptor antagonists in vivo: implications for the process of excitotoxic degeneration and its therapy.

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Injection of the N-methyl-D-aspartate receptor agonist, quinolinic acid, into the rat striatum in vivo results in the degeneration of cholinergic and GABAergic neurons, as determined seven days later using the marker enzymes, choline acetyltransferase and glutamate decarboxylase, respectively. Such

Cloning and nucleotide sequence of the glutamate decarboxylase-encoding gene gadA from Aspergillus oryzae.

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We cloned a genomic DNA encoding the glutamate decarboxylase (GAD) from Aspergillus oryzae using a 200-bp DNA fragment as the probe. This DNA fragment was amplified by the reverse transcription polymerase chain reaction with mRNA of A. oryzae as the template and degenerate primers designed from the

Commissural afferents innervate glutamate decarboxylase immunoreactive non-pyramidal neurons in the guinea pig hippocampus.

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The innervation of GABAergic hippocampal neurons by commissural fibers was investigated in the guinea pig by a combined anterograde degeneration - immunocytochemical technique. Presumed GABAergic neurons were identified by immunocytochemistry for glutamate decarboxylase (GAD) and the commissural

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