Journal articles: 'GAD67 gene'

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SCHMIDLI, Robert S., Beverly E. FAULKNER-JONES, Leonard C. HARRISON, Roger F. L. JAMES, and Henry J. DeAIZPURUA. "Cytokine regulation of glutamate decarboxylase biosynthesis in isolated rat islets of Langerhans." Biochemical Journal 317, no. 3 (August 1, 1996): 713–19. http://dx.doi.org/10.1042/bj3170713.

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Insulin-dependent diabetes mellitus (IDDM) is an autoimmune disease in which cytokines are thought to play an important role in β-cell destruction and immune regulation. A major target of β-cell autoimmunity in IDDM is the enzyme glutamate decarboxylase (GAD). We hypothesized that cytokines in the insulitis lesion modulate the synthesis of GAD. This may, in turn, modify the rate of β-cell destruction. Accordingly we cultured rat islets in the presence and absence of cytokines, and measured synthesis of both isoforms of GAD, GAD65 and GAD67, by [35S]methionine incorporation and immunoprecipitation with a rabbit antiserum that recognizes both GAD65 and GAD67. Incubation of islets with interleukin (IL)-1β (1 ng/ml, 24 h), tumour necrosis factor α (TNF-α; 200 units/ml, 24 h) or interferon γ (IFN-γ; 500 units/ml, 72 h) significantly decreased the synthesis of both GAD65 and GAD67, but reduced neither total protein synthesis nor insulin accumulation in the medium or content. Incubation of islets for 24 h in IFN-α (1000 units/ml), TNF-β (50 ng/ml), IL 2 (1000 units/ml), IL-4 (100 ng/ml), IL-6 (10 ng/ml), IL-10 (20 ng/ml), IL-12 (10 ng/ml) or transforming growth factor β2 (TGF-β2; 5 ng/ml) did not significantly alter GAD65 or GAD67 synthesis. Inhibition of GAD65 and GAD67 protein synthesis by IL-1β, TNF-α or IFN-γ was reversed by co-incubation with the nitric oxide synthase inhibitor, NG-monomethyl arginine (NMMA). Expression of both GAD65 and GAD67 mRNA, measured by RNase protection assay, was also decreased by IL-1β and completely restored to baseline levels by NMMA. Thus the synthesis of both isoforms of islet GAD is selectively decreased in the presence of IL-1β, TNF-α or IFN-γ by a NO-mediated mechanism, probably at the level of cytokine gene transcription. As GAD autoimmunity has been previously shown to have a pathogenic role in an animal model of IDDM, its inhibition by cytokines might limit the immune response, thereby regulating the rate of β-cell destruction in IDDM.

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YANAGAWA, Yuchio, Takashi KOBAYASHI, Takashi KAMEI, Kenji ISHII, Michiharu NISHIJIMA, Akira TAKAKU, Takayasu KOBAYASHI, and Shinri TAMURA. "Structure and alternative promoters of the mouse glutamic acid decarboxylase 67 gene." Biochemical Journal 326, no. 2 (September 1, 1997): 573–78. http://dx.doi.org/10.1042/bj3260573.

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γ-Aminobutyric acid is synthesized by glutamic acid decarboxylase (GAD), which has two forms, GAD65 and GAD67. Genomic clones coding mouse GAD67 (mGAD67) have been isolated. The restriction map of the overlapping clones covers a region of more than 45 kb of genomic DNA. The mGAD67 gene contains 16 translated exons in addition to an exon which is preferentially expressed in foetal brain. The rapid amplification of 5′-cDNA ends showed that mGAD67 gene transcripts have two different 5′-untranslated regions. Analysis of the genomic clones encompassing the 5′-exons revealed that the two transcripts arose from a single gene by alternative splicing using two different donor sites and a common acceptor. The exons were found 1.5 and 0.6 kb upstream of exon 1. The corresponding promoter regions of these exons have a number of putative regulatory elements, including Sp1- and Krox-24-binding sites. Analysis of mGAD67 transcripts demonstrated that each of the 5′-untranslated exons was expressed in mouse brain. In contrast, exon 0A, but not exon 0B, was expressed in mouse testis and pancreas. These results suggest that these transcripts may be regulated under the control of independent promoters.

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Pedersen, Anette Amstrup, Helle Vestergaard Petersen, Nicoline Videbæk, Kresten Skak, and Birgitte Koch Michelsen. "PDX-1 mediates glucose responsiveness of GAD67, but not GAD65, gene transcription in islets of Langerhans." Biochemical and Biophysical Research Communications 295, no. 2 (July 2002): 243–48. http://dx.doi.org/10.1016/s0006-291x(02)00674-5.

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Ben David, Gil, Yam Amir, Kuldeep Tripathi, Lital Sharvit, Amir Benhos, Rachel Anunu, Gal Richter-Levin, and Gil Atzmon. "Exposure to Juvenile Stress Induces Epigenetic Alterations in the GABAergic System in Rats." Genes 14, no. 3 (February 23, 2023): 565. http://dx.doi.org/10.3390/genes14030565.

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Epigenetics is a gene–environment interaction mechanism, manifested mostly through changes in regulatory gene expression. Stress is an established environmental factor known to induce epigenetic changes. This study aimed to assess the long-term effect of stress as juveniles, or juvenile and adult stress, on alterations in glutamic acid decarboxylase genes (GAD65, GAD67). We assessed DNA methylation and RNA expression in four rat groups: (1) control group, (2) juvenile stress group sacrificed two days following stress exposure (JSe) (RNA only), (3) juvenile stress group sacrificed as adults (JS), and (4) juvenile and adult stress group (JS + AS). Three different areas of the brain were examined in each group: the dorsal dentate gyrus (dDG), the dorsal CA1 (dCA1), and the basolateral amygdala (BLA). A significantly low methylation level of GAD65 in the BLA was observed among the JS group, followed by almost complete recovery among the JS + AS group. However, in dDG, an opposite trend was captured, and higher GAD65 methylation was found in JS. In addition, RNA levels were found to be decreased in JS compared to JSe and JS + AS. These findings can point to a possible mechanism: while juvenile stress may enhance a better coping strategy with life challenges, additional stress in adulthood may trigger a contradictory response, either beneficial or harmful.

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Lariviere, K., L. MacEachern, V. Greco, G. Majchrzak, S. Chiu, G. Drouin, and V. L. Trudeau. "GAD65 and GAD67 Isoforms of the Glutamic Acid Decarboxylase Gene Originated Before the Divergence of Cartilaginous Fishes." Molecular Biology and Evolution 19, no. 12 (December 1, 2002): 2325–29. http://dx.doi.org/10.1093/oxfordjournals.molbev.a004057.

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Zhu, Xiya, Patricia J. Ward, and Arthur W. English. "Selective Requirement for Maintenance of Synaptic Contacts onto Motoneurons by Target-Derived trkB Receptors." Neural Plasticity 2016 (2016): 1–11. http://dx.doi.org/10.1155/2016/2371893.

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Synaptic contacts onto motoneurons were studied in mice in which the gene for the trkB neurotrophin receptor was knocked out selectively in a subset of spinal motoneurons. The extent of contacts by structures immunoreactive for either of two different vesicular glutamate transporters (VGLUT1 and VGLUT2), the vesicular GABA transporter, or glutamic acid decarboxylase 67 (GAD67) with the somata of motoneurons, was studied in wild type and trkB knockout cells in tamoxifen treated male and female SLICK-trkB−/−mice. Selective knockout of the trkB gene resulted in a marked reduction in contacts made by VGLUT2- and GAD67-immunoreactive structures in both sexes and a significant reduction in contacts containing only glycine in male mice. No reduction was found for glycinergic contacts in female mice or for VGLUT1 immunoreactive contacts in either sex. Signaling through postsynaptic trkB receptors is considered to be an essential part of a cellular mechanism for maintaining the contacts of some, but not all, synaptic contacts onto motoneurons.

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Pöstyéni, Etelka, Andrea Kovács-Valasek, Péter Urbán, Lilla Czuni, György Sétáló, Csaba Fekete, and Robert Gabriel. "Profile of miR-23 Expression and Possible Role in Regulation of Glutamic Acid Decarboxylase during Postnatal Retinal Development." International Journal of Molecular Sciences 22, no. 13 (June 30, 2021): 7078. http://dx.doi.org/10.3390/ijms22137078.

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As neurotransmitter, GABA is fundamental for physiological processes in the developing retina. Its synthesis enzymes are present during retinal development, although the molecular regulatory mechanisms behind the changes in expression are not entirely understood. In this study, we revealed the expression patterns of glutamic acid decarboxylase 67(GAD67) and its coding gene (GAD1) and its potential miRNA-dependent regulation during the first three postnatal weeks in rat retina. To gain insight into the molecular mechanisms, miRNA-sequencing supported by RT-qPCR and in situ hybridization were carried out. GAD1 expression shows an increasing tendency, peaking at P15. From the in silico-predicted GAD1 targeting miRNAs, only miR-23 showed similar expression patterns, which is a known regulator of GAD1 expression. For further investigation, we made an in situ hybridization investigation where both GAD67 and miR-23 also showed lower expression before P7, with the intensity of expression gradually increasing until P21. Horizontal cells at P7, amacrine cells at P15 and P21, and some cells in the ganglion cell layer at several time points were double labelled with miR-23 and GAD67. Our results highlight the complexity of these regulatory networks and the possible role of miR-23 in the regulation of GABA synthesizing enzyme expression during postnatal retina development.

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Soghomonian, Jean-Jacques, and Nathalie Laprade. "Glutamate decarboxylase (GAD67 and GAD65) gene expression is increased in a subpopulation of neurons in the putamen of parkinsonian monkeys." Synapse 27, no. 2 (October 1997): 122–32. http://dx.doi.org/10.1002/(sici)1098-2396(199710)27:2<122::aid-syn3>3.0.co;2-g.

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Khalifa, D., H. Gabr, H. Fathy, H. Abdou, and M. Batrawy. "Cognitive Impairment and the correlation with genetic Expression of GAD67, Gad65 and GABA beta2 Using Human Induced Pluripotent Stem Cells." European Psychiatry 65, S1 (June 2022): S314. http://dx.doi.org/10.1192/j.eurpsy.2022.801.

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Introduction Alteration of GABergic neurotransmission is accused to be sharing in the cognitive impairment in schizophrenia. Exploring the relation between the neuronal expression of GABergic genes and cognitive impairment in living patients through modeling of schizophrenia is an important step to know more about the core of the pathophysiology of this disorder Objectives Altered genetic expression of GAD 67 may have an important role in the pathophysiology of cognitive impairment in schizophrenia Methods . Reprogramming of human fibroblasts into human induced pluripotent stem cells (hIPSc) then neuronal differentiation was performed in 20 patients presenting with schizophrenia and 20 matched controls. Real time Polymerase chain reaction was done for measurement of genetic expression of GAD 65, GAD 67 and GABA beta 2. The Digit Symbol task, block design, block design task and similarities tasks from the Wechsler Adult Intelligence Scale., Trail A and Trail B making tests in addition to Rey-Osterrieth Complex Figure Test (ROCF) were applied to measure cognitive functions . Results There were lower means of GAD65, GAD67 and GABA beta2genetic expression in the patients group with significant statistical difference between the 2 groups. The down regulation of GAD 67 in patients presenting with schizophrenia is positively correlated with impairment in executive functions. Conclusions GAD 67 gene expression had the most significant correlations with the cognitive assessment in both patients and controls. The presence of those statistically significant correlations in both groups points to the possible role of GAD 67 gene functioning in the pathophysiology of cognitive impairment in schizophrenia Disclosure No significant relationships.

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Gass, P., D. Inta, A. Luoni, and M. A. Riva. "Differential Effects of MGluR5 Receptor Blockade on Behavior, Schizophrenia-relevant Gene Expression and Neuronal Activation Patterns from Development to Aging Mice." European Psychiatry 41, S1 (April 2017): S165. http://dx.doi.org/10.1016/j.eurpsy.2017.01.2048.

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IntroductionThe glutamate system is implicated both in mood disorders and schizophrenia. Mice lacking metabotropic mGlu5 receptors (mGluR5 KO) display schizophrenia-like abnormalities. Additionally, mGluR5 antagonists represent promising alternative anxiolytics/antidepressants. However, the underlying age-specific molecular/cellular mechanisms are only partially understood.ObjectivesWe aimed at identifying molecular alterations associated with a genetically induced mGluR5 deletion, which results in a schizophrenia-like phenotype. Additionally, we investigated age-specific effects of mGluR5 antagonists on emotional behaviour and c-fos activation.MethodsFor analysis of mRNA and protein levels we performed Real-time RT-PCR and Western blot investigations of brains from mGluR5 KO and wild-type mice. Additionally we used classical behavioral tests for determining anxiety- and depression-like changes triggered by the mGluR5 antagonist 2-Methyl-6-(phenylethynyl)pyridine (MPEP). Finally, we used profiling of c-Fos expression, as marker of neuronal activity, induced by MPEP from postnatal day 16 (P16) to adulthood (P90).ResultsWe found reduced expression levels of reelin, GAD65, GAD67, parvalbumin, as well as NMDA and AMPA receptor subunits in mGluR5 KO mice, especially in the prefrontal cortex (PFC). We measured age-specific alterations in emotional behaviour of mGluR5 KO mice, with marked increase of anxiety during aging. There was a remarkably conserved activation of the paraventricular nucleus of the hypothalamus, implicated in stress regulation, by MPEP at all investigated ages, whereas the extended amygdala was specifically activated in adulthood only.ConclusionsOur animal data provide new insights into the potential role of mGluR5 in neurochemical and behavioural changes associated with schizophrenia and mood disorders during the lifespan.Disclosure of interestThe authors have not supplied their declaration of competing interest.

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Pedersen, Anette A., Nicoline Videbaek, Kresten Skak, Helle V. Petersen, and Birgitte K. Michelsen. "Characterization of the Rat Gad67 Gene Promoter Reveals Elements Important for Basal Transcription and Glucose Responsiveness." DNA Sequence 11, no. 6 (January 2001): 485–99. http://dx.doi.org/10.3109/10425170109041332.

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Straub, R. E., B. K. Lipska, M. F. Egan, T. E. Goldberg, J. H. Callicott, M. B. Mayhew, R. K. Vakkalanka, B. S. Kolachana, J. E. Kleinman, and D. R. Weinberger. "Allelic variation in GAD1 (GAD67) is associated with schizophrenia and influences cortical function and gene expression." Molecular Psychiatry 12, no. 9 (May 1, 2007): 854–69. http://dx.doi.org/10.1038/sj.mp.4001988.

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Neuray, Caroline, Reza Maroofian, Marcello Scala, Tipu Sultan, Gurpur S. Pai, Majid Mojarrad, Heba El Khashab, et al. "Early-infantile onset epilepsy and developmental delay caused by bi-allelic GAD1 variants." Brain 143, no. 8 (July 23, 2020): 2388–97. http://dx.doi.org/10.1093/brain/awaa178.

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Abstract Gamma-aminobutyric acid (GABA) and glutamate are the most abundant amino acid neurotransmitters in the brain. GABA, an inhibitory neurotransmitter, is synthesized by glutamic acid decarboxylase (GAD). Its predominant isoform GAD67, contributes up to ∼90% of base-level GABA in the CNS, and is encoded by the GAD1 gene. Disruption of GAD1 results in an imbalance of inhibitory and excitatory neurotransmitters, and as Gad1−/− mice die neonatally of severe cleft palate, it has not been possible to determine any potential neurological dysfunction. Furthermore, little is known about the consequence of GAD1 disruption in humans. Here we present six affected individuals from six unrelated families, carrying bi-allelic GAD1 variants, presenting with developmental and epileptic encephalopathy, characterized by early-infantile onset epilepsy and hypotonia with additional variable non-CNS manifestations such as skeletal abnormalities, dysmorphic features and cleft palate. Our findings highlight an important role for GAD1 in seizure induction, neuronal and extraneuronal development, and introduce GAD1 as a new gene associated with developmental and epileptic encephalopathy.

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Liu, Wanhong, Zhongchun Liu, Li Liu, Zheman Xiao, Xiongbin Cao, Zhijian Cao, Lu Xue, Lixia Miao, Xiaohua He, and Wenxin Li. "A novel human foamy virus mediated gene transfer of GAD67 reduces neuropathic pain following spinal cord injury." Neuroscience Letters 432, no. 1 (February 2008): 13–18. http://dx.doi.org/10.1016/j.neulet.2007.11.054.

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Romano, Emilia, Andrea Fuso, and Giovanni Laviola. "Nicotine Restores Wt-Like Levels of Reelin and GAD67 Gene Expression in Brain of Heterozygous Reeler Mice." Neurotoxicity Research 24, no. 2 (February 6, 2013): 205–15. http://dx.doi.org/10.1007/s12640-013-9378-3.

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Ogawa, Nobuhiro, Tomoya Terashima, Kazuhiro Oka, Lawrence Chan, and Hideto Kojima. "Gene therapy for neuropathic pain using dorsal root ganglion–targeted helper-dependent adenoviral vectors with GAD67 expression." PAIN Reports 3, no. 6 (2018): e695. http://dx.doi.org/10.1097/pr9.0000000000000695.

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Qiao, Li-na, Jun-ling Liu, Lian-hong Tan, Hai-long Yang, Xu Zhai, and Yong-sheng Yang. "Effect of Electroacupuncture on Thermal Pain Threshold and Expression of Calcitonin-Gene Related Peptide, Substance P and γ-Aminobutyric Acid in the Cervical Dorsal Root Ganglion of Rats with Incisional Neck Pain." Acupuncture in Medicine 35, no. 4 (August 2017): 276–83. http://dx.doi.org/10.1136/acupmed-2016-011177.

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Objective Acupuncture therapy effectively reduces post-surgical pain, but its mechanism of action remains unclear. The aim of this study was to investigate whether expression of γ-aminobutyric acid (GABA) and the neuropeptides substance P (SP) and calcitonin gene-related peptide (CGRP) in the primary sensory neurons of cervical dorsal root ganglia (DRG) are involved in electroacupuncture (EA)-induced analgesia in a rat model of incisional neck pain. Methods The pain model was established by making a longitudinal midline neck incision in 60 rats. Another 15 rats underwent sham surgery (normal group). Post-incision, 15 rats remained untreated (model group) and 45 rats underwent EA (frequency 2/100 Hz, intensity 1 mA) at bilateral LI18, LI4-PC6 or ST36-GB34 (n=15 each) for 30 min at 4 hours, 24 hours, and 48 hours post-surgery, followed by thermal pain threshold (PT) measurement. 30 min later, the rats were euthanased and cervical (C3-6) DRGs removed for measurement of immunoreactivity and mRNA expression of SP/CGRP and the GABAergic neuronal marker glutamic acid decarboxylase 67 (GAD67). Results Thermal PT was significantly lower in the model group versus the normal group and increased in the LI18 and LI4-PC6 groups but not the ST36-GB34 group compared with the model group. Additionally, EA at LI18 and LI4-PC6 markedly suppressed neck incision-induced upregulation of mRNA/protein expression of SP/CGRP, and upregulated mRNA/protein expression of GAD67 in the DRGs of C3-6 segments. Conclusions EA at LI18/LI4-PC6 increases PT in rats with incisional neck pain, which is likely related to downregulation of pronociceptive mediators SP/CGRP and upregulation of the inhibitory transmitter GABA in the primary sensory neurons of cervical DRGs.

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Ellefsen, Stian, Kåre-Olav Stensløkken, Cathrine E. Fagernes, Tom A. Kristensen, and Göran E. Nilsson. "Expression of genes involved in GABAergic neurotransmission in anoxic crucian carp brain (Carassius carassius)." Physiological Genomics 36, no. 2 (January 2009): 61–68. http://dx.doi.org/10.1152/physiolgenomics.90301.2008.

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The crucian carp, Carassius carassius, survives days to months without oxygen, depending on temperature. In the anoxic crucian carp brain, increased GABAergic inhibition, mediated by increased extracellular levels of GABA, has been shown to suppress electric activity and ATP consumption. To investigate an involvement of gene expression in this response, we utilized real-time RT-PCR to test the effect of 1 and 7 days anoxia (8°C) on the expression of 22 genes, including nine GABAA receptor subunits (α1–6, β2, δ, and γ2), three GABAB receptor subunits (GB1a-1b and GB2), three enzymes involved in GABA metabolism (GAD65 and GAD67, GABAT), four GABA transporters (GAT1, 2a-b and 3), two GABAA receptor-associated proteins (GABARAP 1 and 2), and the K+/Cl− cotransporter KCC2. While the expression of GABAA receptor subunits was dominated by α4-, α6-, and δ-subunits, all of which are located to extrasynaptic sites in mammalian brains and respond to elevations in extracellular levels of GABA by showing tonic activity patterns, the expression of GABA transporters was dominated by GAT2 (a and b) and GAT3, which also show extrasynaptic location in mammals. These expression patterns differ from those observed in mammals and may be a prerequisite for GABAergic inhibition of anoxic metabolic rate in crucian carp. Furthermore, while the expression of the majority of the genes was largely unaltered by anoxia, the expression of GAT2 and GAT3 decreased to 20%. This suggests impairment of GABA transport, which could be a mechanism behind the accumulation of extracellular GABA and the increased GABAergic inhibition.

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Doyon, C., V. L. Trudeau, B. M. Hibbert, L. A. Howes, and T. W. Moon. "mRNA analysis in flattened fauna: obtaining gene-sequence information from road-kill and game-hunting samples." Canadian Journal of Zoology 81, no. 4 (April 1, 2003): 692–98. http://dx.doi.org/10.1139/z03-048.

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Whether gene-sequence information could be obtained using mRNA from road-kill and hunting samples was investigated. Adipose tissue was used to clone cDNA fragments of the hormone leptin and brain tissue was used for the enzyme glutamic acid decarboxylase (GAD). Tissues collected from road-killed animals were used to clone leptin from RNA samples of raccoon (Procyon lotor) and woodchuck (Marmota monax). We were able to extract RNA and clone GAD67 from samples of masked shrew (Sorex cinereus), although the time of death was unknown. We collaborated with hunters who provided tissues from which we cloned leptin and GAD isoforms from beaver (Castor canadensis), red squirrel (Tamiasciurus hudsonicus), black bear (Ursus americanus), and moose (Alces alces americana). Molecular phylogenetic analyses confirmed that the sequences obtained did not result from contamination. A time-course experiment showed that even 24 h after the death of rats, sufficient mRNA remains to amplify leptin from adipose tissue. These results suggest that road-kill and hunting samples could be used as a valuable source of gene-sequence information.

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Laprade, Nathalie, and Jean-Jacques Soghomonian. "Gene expression of the GAD67 and GAD65 isoforms of glutamate decarboxylase is differentially altered in subpopulations of striatal neurons in adult rats lesioned with 6-OHDA as neonates." Synapse 33, no. 1 (July 1999): 36–48. http://dx.doi.org/10.1002/(sici)1098-2396(199907)33:1<36::aid-syn4>3.0.co;2-0.

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Jakobsen, Linda P., Mary A. Knudsen, James Lespinasse, Carmen García Ayuso, Carmen Ramos, Jean-Pierre Fryns, Merete Bugge, and Niels Tommerup. "The Genetic Basis of the Pierre Robin Sequence." Cleft Palate-Craniofacial Journal 43, no. 2 (March 2006): 155–59. http://dx.doi.org/10.1597/05-008.1.

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Objective The Pierre Robin Sequence (PRS) is subgroup of the cleft palate population. As with the etiology of cleft lip or palate, the etiology of PRS is generally unknown. Some factors are suggestive of a genetic basis for PRS. The purpose of this study was to compare genetic information on PRS available in the literature and in a cytogenetic database to facilitate focused genetic studies of PRS. Design After searching Medline for “pierre robin and genetics,” the Mendelian Cytogenetics Network database for “robin” and “pierre robin,” and two reviews from the Human Cytogenetics Database for “cleft palate” and “micrognathia,” a comparison of the data and a search in Online Mendelian Inheritance in Man (OMIM) Gene Map was performed to identify relevant candidate genes. Results The findings revealed consistency to a certain degree to loci 2q24.1-33.3, 4q32-qter, 11q21-23.1, and 17q21-24.3. A search in the OMIM Gene Map provided many candidate genes for PRS in these regions. The GAD67 on 2q31, the PVRL1 on 11q23-q24, and the SOX9 gene on 17q24.3-q25.1 are suggested to be of particular importance. Conclusion Candidate loci and a few potential candidate genes for PRS are proposed from the present study. This may enable researchers to focus their effort in the studies of PRS.

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Wettergren, Erika Elgstrand, Luis Quintino, and Cecilia Lundberg. "Gene therapy using synthetic microRNA directed against GAD67 has beneficial effect on motor behaviour in 6-OHDA lesioned rats." Journal of Gene Therapy Aspects 1, no. 1 (2014): 1. http://dx.doi.org/10.7243/2057-164x-1-1.

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Perreault, Melissa L., Jace Jones-Tabah, Brian F. O'Dowd, and Susan R. George. "A physiological role for the dopamine D5 receptor as a regulator of BDNF and Akt signalling in rodent prefrontal cortex." International Journal of Neuropsychopharmacology 16, no. 2 (July 25, 2012): 477–83. http://dx.doi.org/10.1017/s1461145712000685.

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Abstract The dopamine D5 receptor (D5R) exhibits a wide distribution in prefrontal cortex (PFC) but its role in this region has not yet been elucidated. In the present study, we identified a novel physiological function for the D5R as a regulator of brain-derived neurotrophic factor (BDNF) and Akt signalling in PFC. Specifically, acute activation of the D5R by the dopamine agonist SKF 83959 enhanced BDNF expression and signalling through its receptor, tropomyosin receptor kinase B (TrkB), in rats and in mice gene-deleted for the D1 receptor but not the D5R. These changes were concomitant with increased expression of GAD67, a protein whose down-regulation has been implicated in the aetiology of schizophrenia. Furthermore, D5R activation increased phosphorylation of Akt at the Ser473 site, consequently decreasing the activity of its substrate GSK-3β. These findings could have wide-reaching implications given evidence showing activation of these pathways in PFC has therapeutic effects in neuropsychiatric disorders such as drug addiction, schizophrenia and depression.

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Sekerková, Gabriela, Zoya Katarova, Ferenc Joó, Joachim R. Wolff, Simona Prodan, and Gábor Szabó. "Visualization of β-Galactosidase by Enzyme and Immunohistochemistry in the Olfactory Bulb of Transgenic Mice Carrying the LacZ Transgene." Journal of Histochemistry & Cytochemistry 45, no. 8 (August 1997): 1147–55. http://dx.doi.org/10.1177/002215549704500812.

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In the olfactory bulb (OB) of a transgenic mouse line that carries the bacterial LacZ gene under the control of the 5'-regulatory region of the GAD67 gene, expression of the β-galactosidase was confined almost exclusively to the non-GABAergic mitral and tufted cells. By light microscopy, enzyme histochemistry showed strong staining in the cell bodies and faint diffuse staining in the axons and dendrites. With immunohistochemistry for β-galactosidase the entire cytoplasm, including the axons and dendrites, was strongly stained. By electron microscopy, β-galactosidase enzyme histochemistry resulted in a submicroscopic reaction product that was diffusely distributed in the cytoplasm of neurons. In addition, large deposits of the reaction product were also seen attached to the cytoplasmic side of the membranes. In contrast, when the intracellular localization of β-galactosidase was determined by immunohistochemistry, homogeneous cytoplasmic staining was obtained that filled the entire cytoplasm including the terminal dendrites and fine axons. Therefore, synaptic contacts of the β-galactosidase-positive output neurons with other β-galactosidase-negative neuronal cells were readily recognized in the OB. As we demonstrated, transgenic mouse lines expressing the LacZ reporter gene in a well-defined neuronal subpopulation can be used to follow β-galactosidase-positive neurons and to directly identify their synaptic connections. (J Histochem Cytochem 45:1147–1155, 1997)

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Li, F., H. Chen, C. Z. Lei, G. Ren, J. Wang, Z. J. Li, and J. Q. Wang. "Novel SNPs of the bovine GAD1/gad67 gene and their association with growth traits in three native Chinese cattle breeds." Molecular Biology Reports 37, no. 1 (September 2, 2009): 501–5. http://dx.doi.org/10.1007/s11033-009-9699-8.

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Trudeau, V. L., D. Spanswick, E. J. Fraser, K. Larivière, D. Crump, S. Chiu, M. MacMillan, and R. W. Schulz. "The role of amino acid neurotransmitters in the regulation of pituitary gonadotropin release in fish." Biochemistry and Cell Biology 78, no. 3 (April 2, 2000): 241–59. http://dx.doi.org/10.1139/o99-075.

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Both glutamate and γ-aminobutyric acid (GABA) are involved in pituitary hormone release in fish. Glutamate serves 2 purposes, both as a neurotransmitter and as a precursor for GABA synthesis. Glutamate can be catabolized to GABA by the actions of 2 distinct but related enzymes, glutamate decarboxylase 65 (GAD65) and GAD67. They derive from 2 different genes that likely arose from an early gene duplication prior to the emergence of teleosts more than 400 million years ago. There is good evidence for the involvement of GABA in luteinizing hormone (LH) release in fish. The mechanism of GABA action to stimulate LH release appears to be a combination of effects on GnRH release, potentiation of gonadotropin hormone-releasing hormone (GnRH) action, and in some cases directly at the LH cell. These actions appear to be dependent on such factors as sex or sex steroid levels, and there may also be species differences. Nevertheless, the stimulatory effects of GABA on LH are present in at least 4 fish species. In contrast, convincing data for the inhibitory effects of GABA on LH release have only been observed in 1 fish species. The sites and mechanisms of action of amino acid neurotransmitters on LH release have yet to be fully characterized. Both N-methyl-D-aspartic acid (NMDA) and S-α-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid (AMPA) type glutamate receptors are likely to have important roles. We suggest that it is a receptor similar to the GABAA type which mediates the effects of GABA on LH release in fish, at least partially acting on the GnRH neuron, but likely directly acting at the gonadotroph as well. GABA may also be involved in regulating the release of other pituitary hormones in fish, namely follicle stimulating hormone (FSH = GTH-I), prolactin, and growth hormone. Based on the findings described in this review, a working model for the involvement of glutamate and GABA in the regulation of LH release in teleost fish is proposed. Key words: glutamate, GABA, luteinizing hormone, muscimol, patch clamp electrophysiology, reproduction, fish.

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Thomas, T., A. K. Voss, K. Chowdhury, and P. Gruss. "Querkopf, a MYST family histone acetyltransferase, is required for normal cerebral cortex development." Development 127, no. 12 (June 15, 2000): 2537–48. http://dx.doi.org/10.1242/dev.127.12.2537.

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In order to find, and mutate, novel genes required for regulation of neurogenesis in the cerebral cortex, we performed a genetic screen in mice. As the result of this screen, we created a new mouse mutant, querkopf. The querkopf mutation is due to an insertion into a MYST family histone acetyltransferase gene. Mice homozygous for the querkopf mutation have craniofacial abnormalities, fail to thrive in the postnatal period and have defects in central nervous system development. The defects in central nervous system development are particularly prominent in the cerebral cortex, which is disproportionally smaller than in wild-type mice. A large reduction in the size of the cortical plate was already apparent during embryogenesis. Homozygous mice show a lack of large pyramidal cells in layer V of the cortex, which is reflected in a reduction in the number of Otx1-positive neurons in this layer during postnatal development. Homozygous mice also show a reduction in the number of GAD67-positive interneurons throughout the cortex. Our results suggest that Querkopf is an essential component of a genetic cascade regulating cell differentiation in the cortex, probably acting in a multiprotein complex regulating chromatin structure during transcription.

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Sengul, Gulgun, Huazheng Liang, Teri M. Furlong, and George Paxinos. "Dorsal Horn of Mouse Lumbar Spinal Cord Imaged with CLARITY." BioMed Research International 2020 (August 14, 2020): 1–8. http://dx.doi.org/10.1155/2020/3689380.

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The organization of the mouse spinal dorsal horn has been delineated in 2D for the six Rexed laminae in our publication Atlas of the Spinal Cord: Mouse, Rat, Rhesus, Marmoset, and Human. In the present study, the tissue clearing technique CLARITY was used to observe the cyto- and chemoarchitecture of the mouse spinal cord in 3D, using a variety of immunohistochemical markers. We confirm prior observations regarding the location of glycine and serotonin immunoreactivities. Novel observations include the demonstration of numerous calcitonin gene-related peptide (CGRP) perikarya, as well as CGRP fibers and terminals in all laminae of the dorsal horn. We also observed sparse choline acetyltransferase (ChAT) immunoreactivity in small perikarya and fibers and terminals in all dorsal horn laminae, while gamma aminobutyric acid (GABA) and glutamate decarboxylase-67 (GAD67) immunoreactivities were found only in small perikarya and fibers. Finally, numerous serotonergic fibers were observed in all laminae of the dorsal horn. In conclusion, CLARITY confirmed the 2D immunohistochemical properties of the spinal cord. Furthermore, we observed novel anatomical characteristics of the spinal cord and demonstrated that CLARITY can be used on spinal cord tissue to examine many proteins of interest.

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Katarova, Zoya, Enrico Mugnaini, Gabriela Sekerková, Jeffrey R. Mann, Attila Aszódi, Zsuzsanna Bösze, Ralph Greenspan, and Gábor Szabó. "Regulation of cell-type specific expression oflacZby the 5′-flanking region of mouse GAD67 gene in the central nervous system of transgenic mice." European Journal of Neuroscience 10, no. 3 (March 1998): 989–99. http://dx.doi.org/10.1046/j.1460-9568.1998.00109.x.

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Cashion, A. B., M. J. Smith, and P. M. Wise. "Glutamic Acid Decarboxylase 67 (GAD67) Gene Expression in Discrete Regions of the Rostral Preoptic Area Change During the Oestrous Cycle and with Age." Journal of Neuroendocrinology 16, no. 8 (August 2004): 711–16. http://dx.doi.org/10.1111/j.1365-2826.2004.01225.x.

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Ishiyama, Tamura, Ito, Takei, Hoshi, Asano, Itoh, and Shirakawa. "Early Postnatal Treatment with Valproate Induces Gad1 Promoter Remodeling in the Brain and Reduces Apnea Episodes in Mecp2-Null Mice." International Journal of Molecular Sciences 20, no. 20 (October 18, 2019): 5177. http://dx.doi.org/10.3390/ijms20205177.

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The deletion of Mecp2, the gene encoding methyl-CpG-binding protein 2, causes severe breathing defects and developmental anomalies in mammals. In Mecp2-null mice, impaired GABAergic neurotransmission is demonstrated at the early stage of life. GABAergic dysfunction in neurons in the rostral ventrolateral medulla (RVLM) is considered as a primary cause of breathing abnormality in Mecp2-null mice, but its molecular mechanism is unclear. Here, we report that mRNA expression levels of Gad1, which encodes glutamate decarboxylase 67 (GAD67), in the RVLM of Mecp2-null (Mecp2-/y, B6.129P2(C)-Mecp2tm1.1Bird/J) mice is closely related to the methylation status of its promoter, and valproate (VPA) can upregulate transcription from Gad1 through epigenetic mechanisms. The administration of VPA (300 mg/kg/day) together with L-carnitine (30 mg/kg/day) from day 8 to day 14 after birth increased Gad1 mRNA expression in the RVLM and reduced apnea counts in Mecp2-/y mice on postnatal day 15. Cytosine methylation levels in the Gad1 promoter were higher in the RVLM of Mecp2-/y mice compared to wild-type mice born to C57BL/6J females, while VPA treatment decreased the methylation levels in Mecp2-/y mice. Chromatin immunoprecipitation assay revealed that the VPA treatment reduced the binding of methyl-CpG binding domain protein 1 (MBD1) to the Gad1 promoter in Mecp2-/y mice. These results suggest that VPA improves breathing of Mecp2-/y mice by reducing the Gad1 promoter methylation, which potentially leads to the enhancement of GABAergic neurotransmission in the RVLM.

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Bu, Ding-Fang, and Allan J. Tobin. "The Exon-Intron Organization of the Genes (GAD1 and GAD2) Encoding Two Human Glutamate Decarboxylases (GAD67 and GAD65) Suggests That They Derive from a Common Ancestral GAD." Genomics 21, no. 1 (May 1994): 222–28. http://dx.doi.org/10.1006/geno.1994.1246.

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Singh, Yajuvinder, Henri Leinonen, Feroze Fazaludeen, Merja Jaronen, Debbie Guest, Noel Buckley, Nadiya Byts, et al. "Loss of Cln5 leads to altered Gad1 expression and deficits in interneuron development in mice." Human Molecular Genetics 28, no. 19 (July 17, 2019): 3309–22. http://dx.doi.org/10.1093/hmg/ddz165.

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Abstract The Finnish-variant late infantile neuronal ceroid lipofuscinosis, also known as CLN5 disease, is caused by mutations in the CLN5 gene. Cln5 is strongly expressed in the developing brain and expression continues into adulthood. CLN5, a protein of unknown function, is implicated in neurodevelopment but detailed investigation is lacking. Using Cln5−/− embryos of various ages and cells harvested from Cln5−/− brains we investigated the hitherto unknown role of Cln5 in the developing brain. Loss of Cln5 results in neuronal differentiation deficits and delays in interneuron development during in utero period. Specifically, the radial thickness of dorsal telencephalon was significantly decreased in Cln5−/− mouse embryos at embryonic day 14.5 (E14.5), and expression of Tuj1, an important neuronal marker during development, was down-regulated. An interneuron marker calbindin and a mitosis marker p-H3 showed down-regulation in ganglionic eminences. Neurite outgrowth was compromised in primary cortical neuronal cultures derived from E16 Cln5−/− embryos compared with WT embryos. We show that the developmental deficits of interneurons may be linked to increased levels of the repressor element 1-silencing transcription factor, which we report to bind to glutamate decarboxylase (Gad1), which encodes GAD67, a rate-limiting enzyme in the production of gamma-aminobutyric acid (GABA). Indeed, adult Cln5−/− mice presented deficits in hippocampal parvalbumin-positive interneurons. Furthermore, adult Cln5−/− mice presented deficits in hippocampal parvalbumin-positive interneurons and showed age-independent cortical hyper excitability as measured by electroencephalogram and auditory-evoked potentials. This study highlights the importance of Cln5 in neurodevelopment and suggests that in contrast to earlier reports, CLN5 disease is likely to develop during embryonic stages.

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Rohmah, Rista Nikmatu, Soraya Widyasari, A. Aulanni’am, and F. Fatchiyah. "Cloning and Expression of hGAD65 Gene in E. Coli BL21." Indonesian Journal of Biotechnology 18, no. 1 (November 9, 2015): 52. http://dx.doi.org/10.22146/ijbiotech.7868.

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The aim of this study is to construct the hGAD65 gene and to identify the hGAD65 clone by using PCR & RFLP. The samples were derived from normal person & DM patient’s blood. Blood DNA was isolated by salting out method and then amplified by PCR with a pair of specific primer, GAD65-F-BamH1-807 & GAD65-R-Xho1-945. The PCR-product was cloned into vector pET-28a and the pET28a-hGAD65-clone was transformed into E.coli BL21 competent cells. The pET28a-hGAD65-clone was confirmed by PCR and RFLP by BamH1 & XhoI. The PCR product of pET28a-hGAD65-clone was one band of 159bp and has two bands 5.3 kb and 159 bp by RFLPwith both restriction enzymes. The GAD65 protein is expressed in 65kD of pET28a-hGAD65-clone. PET28a-hGAD65-clone was able to recognize by gold standard monoclonal antibody specifically. These results indicated that the hGAD65 gene inserted into pET28a properly and provided the GAD65 protein expression. Key words: hGAD65, PCR, pET-28a, RFLP

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Goudy, Kevin, Li Li, and Roland Tisch. "Expansion of GAD65–Specific Immunoregulatory Effector Cells by Biolistic-Mediated Gene Delivery Prevents Autoimmune Diabetes in NOD Mice (131.14)." Journal of Immunology 178, no. 1_Supplement (April 1, 2007): S240. http://dx.doi.org/10.4049/jimmunol.178.supp.131.14.

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Abstract Intramuscular (i.m.) vaccination with plasmid DNA (pDNA) encoding beta cell autoantigens such as glutamic acid decarboxylase 65 (GAD65) is an approach to suppress ongoing Type 1 diabetes (T1D) in NOD mice. However, protection is dependent on co-treatment with pDNAs encoding IL-4 and/or IL-10, and the subsequent induction of type 2 CD4+ T effectors. To enhance the therapeutic efficacy of pDNA vaccination, we explored epidermal delivery of pDNA via “gene gun”. Notably, reports have shown induction of a preferential type 2-like CD4+ T cell response when pDNA encoding antigen-only is delivered to the epidermis via gene gun. We hypothesized that biolistic delivery of pDNA would preferentially induce type 2 CD4+ T effectors and suppress established beta cell autoimmunity in NOD mice. Groups of 10 wk-old NOD female mice were treated four times with pDNA encoding GAD65-Ig (pGAD65) administered i.m. or delivered by gene gun on 1.6 uM gold particles. Whereas i.m. injection of pGAD65 resulted in preferential induction of GAD65-specific CD4+ Th1 cells and no protection against T1D, the majority of NOD mice treated with gene gun delivered pGAD65 remained diabetes-free and protection correlated with increased GAD65-specific IL-4 secreting CD4+ T cells. These results demonstrate that gene-gun delivered pDNA encoding beta cell autoantigen-only is an effective strategy to induce immunoregulatory CD4+ T cells and suppress T1D.

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Maziarz, M., M. Janer, J. C. Roach, W. Hagopian, J. P. Palmer, K. Deutsch, C. B. Sanjeevi, I. Kockum, N. Breslow, and Å. Lernmark. "The association between the PTPN22 1858C>T variant and type 1 diabetes depends on HLA risk and GAD65 autoantibodies." Genes & Immunity 11, no. 5 (May 6, 2010): 406–15. http://dx.doi.org/10.1038/gene.2010.12.

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&NA;. "GAD65 gene therapy exhibits promise in NOD mice." Inpharma Weekly &NA;, no. 1345 (July 2002): 8. http://dx.doi.org/10.2165/00128413-200213450-00015.

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Vit, Jean-Philippe, Peter T. Ohara, Christopher Sundberg, Blanca Rubi, Pierre Maechler, Chunyan Liu, Mariana Puntel, Pedro Lowenstein, Maria Castro, and Luc Jasmin. "Adenovector GAD65 Gene Delivery into the Rat Trigeminal Ganglion Produces Orofacial Analgesia." Molecular Pain 5 (January 2009): 1744–8069. http://dx.doi.org/10.1186/1744-8069-5-42.

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Kim, Daewook, Kyung-Ran Kim, Yejin Kwon, Minjung Kim, Min-Ju Kim, Yeomoon Sim, Hyelin Ji, et al. "AAV-Mediated Combination Gene Therapy for Neuropathic Pain: GAD65, GDNF, and IL-10." Molecular Therapy - Methods & Clinical Development 18 (September 2020): 473–83. http://dx.doi.org/10.1016/j.omtm.2020.06.018.

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Perrot-Sinal, Tara S., Aline M. Davis, and Margaret M. McCarthy. "Developmental sex differences in glutamic acid decarboxylase (GAD65) and the housekeeping gene, GAPDH." Brain Research 922, no. 2 (December 2001): 201–8. http://dx.doi.org/10.1016/s0006-8993(01)03167-5.

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Pernia, M., I. Díaz, A. C. Colmenárez-Raga, C. Rivadulla, J. Cudeiro, I. Plaza, and M. A. Merchán. "Cross-modal reaction of auditory and visual cortices after long-term bilateral hearing deprivation in the rat." Brain Structure and Function 225, no. 1 (November 28, 2019): 129–48. http://dx.doi.org/10.1007/s00429-019-01991-w.

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AbstractVisual cortex (VC) over-activation analysed by evoked responses has been demonstrated in congenital deafness and after long-term acquired hearing loss in humans. However, permanent hearing deprivation has not yet been explored in animal models. Thus, the present study aimed to examine functional and molecular changes underlying the visual and auditory cross-modal reaction. For such purpose, we analysed cortical visual evoked potentials (VEPs) and the gene expression (RT-qPCR) of a set of markers for neuronal activation (c-Fos) and activity-dependent homeostatic compensation (Arc/Arg3.1). To determine the state of excitation and inhibition, we performed RT-qPCR and quantitative immunocytochemistry for excitatory (receptor subunits GluA2/3) and inhibitory (GABAA-α1, GABAB-R2, GAD65/67 and parvalbumin-PV) markers. VC over-activation was demonstrated by a significant increase in VEPs wave N1 and by up-regulation of the activity-dependent early genes c-Fos and Arc/Arg3.1 (thus confirming, by RT-qPCR, our previously published immunocytochemical results). GluA2 gene and protein expression were significantly increased in the auditory cortex (AC), particularly in layers 2/3 pyramidal neurons, but inhibitory markers (GAD65/67 and PV-GABA interneurons) were also significantly upregulated in the AC, indicating a concurrent increase in inhibition. Therefore, after permanent hearing loss in the rat, the VC is not only over-activated but also potentially balanced by homeostatic regulation, while excitatory and inhibitory markers remain imbalanced in the AC, most likely resulting from changes in horizontal intermodal regulation.

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Morrison, Barclay, David F. Meaney, Susan S. Margulies, and Tracy K. McIntosh. "Dynamic Mechanical Stretch of Organotypic Brain Slice Cultures Induces Differential Genomic Expression: Relationship to Mechanical Parameters." Journal of Biomechanical Engineering 122, no. 3 (February 6, 2000): 224–30. http://dx.doi.org/10.1115/1.429650.

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Although the material properties of biological tissues are reasonably well established, recent studies have suggested that the biological response of brain tissue and its constituent cells may also be viscoelastic and sensitive to both the magnitude and rate of a mechanical stimulus. Given the potential involvement of changes in gene expression in the pathogenic sequelae after head trauma, we analyzed the expression of 22 genes related to cell death and survival and found that a number of these genes were differentially regulated after mechanical stretch of an organotypic brain slice culture. Twenty-four hours after stretch, the expression of BDNF, NGF, and TrkA was significantly increased, whereas that of bcl-2, CREB, and GAD65 was significantly decreased (MANOVA followed by ANOVA, p<0.05). Expression of CREB and GAD65 was negatively correlated with strain, whereas expression of APP695 was negatively correlated with strain rate (all p<0.05). This study demonstrates that a subset of genes involved in cell death and survival are differentially regulated after dynamic stretch in vitro and that the expression of specific genes is correlated with mechanical parameters of that stretch. [S0148-0731(00)00303-4]

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Kakinohana, Osamu, Michael P. Hefferan, Atsushi Miyanohara, Tetsuya Nejime, Silvia Marsala, Stefan Juhas, Jana Juhasova, et al. "Combinational Spinal GAD65 Gene Delivery and Systemic GABA-Mimetic Treatment for Modulation of Spasticity." PLoS ONE 7, no. 1 (January 23, 2012): e30561. http://dx.doi.org/10.1371/journal.pone.0030561.

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Salazar, Juan J., Andrea Satriano, José A. Matamoros, José A. Fernández-Albarral, Elena Salobrar-García, Inés López-Cuenca, Rosa de Hoz, et al. "Retinal Tissue Shows Glial Changes in a Dravet Syndrome Knock-in Mouse Model." International Journal of Molecular Sciences 24, no. 3 (February 1, 2023): 2727. http://dx.doi.org/10.3390/ijms24032727.

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Dravet syndrome (DS) is an epileptic encephalopathy caused by mutations in the Scn1a gene encoding the α1 subunit of the Nav1.1 sodium channel, which is associated with recurrent and generalized seizures, even leading to death. In experimental models of DS, histological alterations have been found in the brain; however, the retina is a projection of the brain and there are no studies that analyze the possible histological changes that may occur in the disease. This study analyzes the retinal histological changes in glial cells (microglia and astrocytes), retinal ganglion cells (RGCs) and GABAergic amacrine cells in an experimental model of DS (Syn-Cre/Scn1aWT/A1783V) compared to a control group at postnatal day (PND) 25. Retinal whole-mounts were labeled with anti-GFAP, anti-Iba-1, anti-Brn3a and anti-GAD65/67. Signs of microglial and astroglial activation, and the number of Brn3a+ and GAD65+67+ cells were quantified. We found retinal activation of astroglial and microglial cells but not death of RGCs and GABAergic amacrine cells. These changes are similar to those found at the level of the hippocampus in the same experimental model in PND25, indicating a relationship between brain and retinal changes in DS. This suggests that the retina could serve as a possible biomarker in DS.

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Brown, Amanda L., Trevor A. Day, Christopher V. Dayas, and Doug W. Smith. "Purity and Enrichment of Laser-Microdissected Midbrain Dopamine Neurons." BioMed Research International 2013 (2013): 1–8. http://dx.doi.org/10.1155/2013/747938.

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The ability to microdissect individual cells from the nervous system has enormous potential, as it can allow for the study of gene expression in phenotypically identified cells. However, if the resultant gene expression profiles are to be accurately ascribed, it is necessary to determine the extent of contamination by nontarget cells in the microdissected sample. Here, we show that midbrain dopamine neurons can be laser-microdissected to a high degree of enrichment and purity. The average enrichment for tyrosine hydroxylase (TH) gene expression in the microdissected sample relative to midbrain sections was approximately 200-fold. For the dopamine transporter (DAT) and the vesicular monoamine transporter type 2 (Vmat2), average enrichments were approximately 100- and 60-fold, respectively. Glutamic acid decarboxylase (Gad65) expression, a marker for GABAergic neurons, was several hundredfold lower than dopamine neuron-specific genes. Glial cell and glutamatergic neuron gene expression were not detected in microdissected samples. Additionally, SN and VTA dopamine neurons had significantly different expression levels of dopamine neuron-specific genes, which likely reflects functional differences between the two cell groups. This study demonstrates that it is possible to laser-microdissect dopamine neurons to a high degree of cell purity. Therefore gene expression profiles can be precisely attributed to the targeted microdissected cells.

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Hiromatsu, Y., T. Mukai, H. Kaku, I. Miyake, M. Ichimura, T. Fukutani, H. Nakayama, et al. "IL-18 gene polymorphism confers susceptibility to the development of anti-GAD65 antibody in Graves' disease." Diabetic Medicine 23, no. 2 (February 2006): 211–15. http://dx.doi.org/10.1111/j.1464-5491.2005.01734.x.

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Shao, Z., A. C. Puche, E. Kiyokage, G. Szabo, and M. T. Shipley. "Two GABAergic Intraglomerular Circuits Differentially Regulate Tonic and Phasic Presynaptic Inhibition of Olfactory Nerve Terminals." Journal of Neurophysiology 101, no. 4 (April 2009): 1988–2001. http://dx.doi.org/10.1152/jn.91116.2008.

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Olfactory nerve axons terminate in olfactory bulb glomeruli forming excitatory synapses onto the dendrites of mitral/tufted (M/T) and juxtaglomerular cells, including external tufted (ET) and periglomerular (PG) cells. PG cells are heterogeneous in neurochemical expression and synaptic organization. We used a line of mice expressing green fluorescent protein under the control of the glutamic acid decarboxylase 65-kDa gene (GAD65+) promoter to characterize a neurochemically identified subpopulation of PG cells by whole cell recording and subsequent morphological reconstruction. GAD65+ GABAergic PG cells form two functionally distinct populations: 33% are driven by monosynaptic olfactory nerve (ON) input (ON-driven PG cells), the remaining 67% receive their strongest drive from an ON→ET→PG circuit with no or weak monosynaptic ON input (ET-driven PG cells). In response to ON stimulation, ON-driven PG cells exhibit paired-pulse depression (PPD), which is partially reversed by GABAB receptor antagonists. The ON→ET→PG circuit exhibits phasic GABAB-R-independent PPD. ON input to both circuits is under tonic GABAB-R-dependent inhibition. We hypothesize that this tonic GABABR-dependent presynaptic inhibition of olfactory nerve terminals is due to autonomous bursting of ET cells in the ON→ET→PG circuit, which drives tonic spontaneous GABA release from ET-driven PG cells. Both circuits likely produce tonic and phasic postsynaptic inhibition of other intraglomerular targets. Thus olfactory bulb glomeruli contain at least two functionally distinct GABAergic circuits that may play different roles in olfactory coding.

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Laprade, Nathalie, and Jean-Jacques Soghomonian. "Glutamate decarboxylase (GAD65) gene expression is increased by dopamine receptor agonists in a subpopulation of rat striatal neurons." Molecular Brain Research 48, no. 2 (September 1997): 333–45. http://dx.doi.org/10.1016/s0169-328x(97)00112-5.

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Vcelakova, Jana, Radek Blatny, Zbynek Halbhuber, Michal Kolar, Ales Neuwirth, Lenka Petruzelkova, Tereza Ulmannova, et al. "The Effect of Diabetes-Associated Autoantigens on Cell Processes in Human PBMCs and Their Relevance to Autoimmune Diabetes Development." Journal of Diabetes Research 2013 (2013): 1–10. http://dx.doi.org/10.1155/2013/589451.

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Type 1 Diabetes (T1D) is considered to be a T-helper- (Th-) 1 autoimmune disease; however, T1D pathogenesis likely involves many factors, and sufficient tools for autoreactive T cell detection for the study of this disease are currently lacking. In this study, using gene expression microarrays, we analysed the effect of diabetes-associated autoantigens on peripheral blood mononuclear cells (PBMCs) with the purpose of identifying (pre)diabetes-associated cell processes. Twelve patients with recent onset T1D, 18 first-degree relatives of the TD1 patients (DRL; 9/18 autoantibody positive), and 13 healthy controls (DV) were tested. PBMCs from these individuals were stimulated with a cocktail of diabetes-associated autoantigens (proinsulin, IA-2, and GAD65-derived peptides). After 72 hours, gene expression was evaluated by high-density gene microarray. The greatest number of functional differences was observed between relatives and controls (69 pathways), from which 15% of the pathways belonged to “immune response-related” processes. In the T1D versus controls comparison, more pathways (24%) were classified as “immune response-related.” Important pathways that were identified using data from the T1D versus controls comparison were pathways involving antigen presentation by MHCII, the activation of Th17 and Th22 responses, and cytoskeleton rearrangement-related processes. Genes involved in Th17 and TGF-beta cascades may represent novel, promising (pre)diabetes biomarkers.

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Liu, Xinyuan, Song Zhang, Xia Li, Peilin Zheng, Fang Hu, and Zhiguang Zhou. "Vaccination with a co-expression DNA plasmid containing GAD65 fragment gene and IL-10 gene induces regulatory CD4+T cells that prevent experimental autoimmune diabetes." Diabetes/Metabolism Research and Reviews 32, no. 6 (March 8, 2016): 522–33. http://dx.doi.org/10.1002/dmrr.2780.

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Journal articles on the topic 'GAD67 gene'

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