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These results thus identify a molecularly distinct, orexin-activated lateral hypothalamus submodule that governs physical activity in mice.
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Results suggest age-dependent decrease of GAD65/67 mRNAs but normal densities of certain GABAergic interneurons in the Shank3 transgenic mice.
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GABA is the major inhibitory neurotransmitter in the brain. We show that Dlx1/Dlx2 homeobox genes regulate GABA synthesis during forebrain development through direct activation of glutamic acid decarboxylase enzyme isoforms that convert glutamate to GABA.
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Treadmill running prevented partial sciatic nerve ligation-induced reductions in GAD65/67 production, and, thus, GABA levels may be retained in interneurons and neuropils in the superficial dorsal horn.
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Increased activity due to bicuculline preferentially up-regulated GAD65. This was reduced by AP5, a selective blocker of Ca2+-permeable ion channels and NMDA-Rs, and by U0126, KN93, and K252a, affecting BDNF pathways.
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Data show that miRNAs are involved in regulating the expression of the major type 1 diabetes (T1D) autoantigens IA-2, IA-2beta, and GAD65 enzyme.
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Results indicate the significant contribution of not only GAD65, GAD67 and VGAT-mediated GABAergic but also glycinergic transmissions to both palate and abdominal wall formations
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Analysis of GAD65/67 single and double knock-out embryos revealed that the two GADs play complementary (inhibitory) roles in GnRH migration ultimately modulating the speed and/or direction of GnRH migration.
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Results show that GAD65 is required for efficient GABAergic synaptic transmission and plasticity, and for maintaining extracellular GABA at a level needed for associative plasticity at cortical inputs in the lateral amygdala
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Menin regulates spinal glutamate-GABA balance through GAD65 contributing to neuropathic pain.
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Our data suggest a role of GAD65-mediated GABA synthesis in the encoding of circadian information to fear memory
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Autoimmunity to GAD65 may play a role in the development of Stiff person syndrome.
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Prenatal and postnatal maternal effects influence GAD65 and GAD67 gene expression depending on the age of the offspring.
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These findings indicate novel, differential roles for GluN2A, B and D receptors and for GAD65-mediated GABA in the regulation of individual topographies of orofacial movement
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SMAR1 and p53 act synergistically to up-regulate GAD65 expression upon Streptozotocin treatment.
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The mouse lateral striatum concentrates medium-sized projection neurons with high-level expression of GAD1, but not of GAD2, mRNA.
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Data show that chronic pain epigenetically suppresses Gad2 transcription through histone deacetylase-mediated histone hypoacetylation, resulting in impaired gamma-aminobutyric acid synaptic inhibition.
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These results suggest that modulation of the synaptic transmission from primary afferents to SG neurons by group III mGluR agonist is specific to the type of nociceptive primary afferents but not to the type of target neurons.
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Dissection of the intracellular pathway that underlies this process revealed that BDNF/TrkB signaling controls the transcription of GAD65
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GAD65 is crucial for maintenance of biosynthesis of synaptic GABA particularly by direct synthesis from astrocytic glutamine via glutamate.
