Two human glutamate decarboxylases, 65-kDa GAD and 67-kDa GAD, are each encoded by a single gene.

Bu, Dingfang; Erlander, Mark G.; Hitz, B. C.; Tillakaratne, Niranjala J.K.; Kaufman, D. L.; Wagner-McPherson, Caryn; Evans, Glen A.; Tobin, A. J.

doi:10.1073/pnas.89.6.2115

Cited by 465 publications

(330 citation statements)

References 47 publications

(60 reference statements)

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“…67-kDa glu tamate decarboxylase (GAD67, also known as GAD1) and 65-kDa glutamate decarboxylase (GAD65, also GAD2) [11] . GAD65 is mainly distributed in synaptic terminals, whereas GAD67 is found in cell bodies, dendrites, and terminals [12] .…”

Section: Molecular Marker Classifi Cationmentioning

confidence: 99%

Dysfunction of hippocampal interneurons in epilepsy

Liu

et al. 2014

Neurosci. Bull.

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Gamma-amino-butyric acid (GABA)-containing interneurons are crucial to both development and function of the brain. Down-regulation of GABAergic inhibition may result in the generation of epileptiform activity. Loss, axonal sprouting, and dysfunction of interneurons are regarded as mechanisms involved in epileptogenesis. Recent evidence suggests that network connectivity and the properties of interneurons are responsible for excitatory-inhibitory neuronal circuits. The balance between excitation and inhibition in CA1 neuronal circuitry is considerably altered during epileptic changes. This review discusses interneuron diversity, the causes of interneuron dysfunction in epilepsy, and the possibility of using GABAergic neuronal progenitors for the treatment of epilepsy.

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Section: Molecular Marker Classifi Cationmentioning

confidence: 99%

Dysfunction of hippocampal interneurons in epilepsy

Liu

et al. 2014

Neurosci. Bull.

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“…(Jackson et al, 1990), Feline Gad67 (Kobayashi et al, 1987) and Human Gad65 (Bu et al, 1992). The asterisk identifies the conserved tyrosine, residue 347, that is altered to histidine in the black 1 mutant.…”

Section: S R T H R H -P R F T G V E R a D S V T W N P H K 321 Fel Gamentioning

confidence: 99%

The Drosophila black enigma: The molecular and behavioural characterization of the black1 mutant allele

Phillips

Smart

Strauß³

et al. 2005

Gene

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The cuticular melanization phenotype of black flies is rescued by h-alanine, but h-alanine production, by aspartate decarboxylation, was reported to be normal in assays of black mutants, and although black/Dgad2 is expressed in the lamina, the first optic ganglion, no electroretinogram (ERG) or other visual defect has been demonstrated in black flies. The purpose of this study was to investigate the black gene, and protein, in black 1 mutants of Drosophila melanogaster in order to resolve the apparent paradox of the black phenotype. Using black 1 mutant flies we show that (1) aspartate decarboxylase activity is significantly reduced in adults and at puparium formation, consistent with defects in cuticular and non-cuticular processes, (2) that the black 1 mutation is a frameshift, and black 1 flies are nulls for the black/ DGAD2 protein, and (3) that behavioural experiments using Buridan's paradigm, demonstrate that black responds abnormally to visual cues. No ERG, or target recognition defects can be demonstrated suggesting a problem with higher order visual functions in black mutants. D

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“…Desinramine (0.3 ILM) was added to the incubation medium to The goal ofthe present st;dy was to investigate pdssible changes in GAD67 mRNA levels in the striatum and pallidum of primates rendered parkinsonians with single or repeated injections of MPTP. The mRNA levels were measured in different regions of the striatum and in the pallidum by radioactive in situ hybridization histochemistry with probes synthesized from the human or feline GAD67 cDNAs (Erlander et al, 1991;Bu et al, 1992).…”

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Increased glutamate decarboxylase mRNA levels in the striatum and pallidum of MPTP-treated primates

et al. 1994

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The mRNA levels encoding for the enzyme glutamate decarboxylase (GAD67) were measured by computerized image analysis after in situ hybridization histochemistry and radioautography in the striatum and pallidum of normal squirrel monkeys (Saimiri sciureus), or after treatment with the neurotoxin 1-methyl-4-phenyl-1,2,3,6- tetrahydropyridine (MPTP). All MPTP-injected monkeys exhibited profound motor deficits including akinesia. The dopaminergic innervation, as visualized and quantified on x-ray films after 3H-mazindol binding on tissue sections, was uniformly lost throughout the striatum of MPTP- treated monkeys. Brain sections processed with a probe synthesized from a feline or human GAD67 cDNA exhibited intense radioautographic labeling throughout the striatum. When measured on x-ray films, the intensity of GAD67 mRNA labeling was increased in the striatum of MPTP- treated versus control monkeys. Increased labeling reached statistical significance in the dorsolateral sector of the rostral putamen and throughout the putamen and the caudate at the caudal, postcommissural, level. Analysis of emulsion radioautographs demonstrated that the increase in GAD67 mRNA labeling in MPTP-treated monkeys occurred in individual neurons of the striatum. In the external and internal segments of the pallidum, numerous neurons labeled with the GAD67 cRNA probe were visualized on emulsion radioautographs. The intensity of GAD67 mRNA labeling in single neurons of both pallidal segments was increased in MPTP-treated versus control monkeys. Construction of the histograms of frequency distribution of labeling indicated that this increase occurred in a majority of labeled neurons. The present study demonstrates that GAD67 mRNA levels are significantly altered in the striatum and pallidum of parkinsonian monkeys. The preferential increase of GAD67 mRNA labeling in the dorsolateral putamen, which receives afferents from the sensorimotor cortex, provides further evidence of the involvement of GABAergic transmission in the expression of the motor deficits elicited after MPTP. In addition, increased GAD67 mRNA levels in the internal segment of the pallidum support the hypothesis of an increased activity of GABAergic neurons in the output structures of the basal ganglia in parkinsonism.

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Two human glutamate decarboxylases, 65-kDa GAD and 67-kDa GAD, are each encoded by a single gene.

Abstract: We report the isolation and sequencing of cDNAs encoding two human glutamate decarboxylases (GADs;

Cited by 465 publications

References 47 publications

Dysfunction of hippocampal interneurons in epilepsy

Dysfunction of hippocampal interneurons in epilepsy

The Drosophila black enigma: The molecular and behavioural characterization of the black1 mutant allele

Increased glutamate decarboxylase mRNA levels in the striatum and pallidum of MPTP-treated primates

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