The role of the synthetic enzyme GAD65 in the control of neuronal gamma-aminobutyric acid release.
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Hypercapnic ventilatory response in mice lacking the 65 kDa isoform of Glutamic Acid Decarboxylase (GAD65)Transcriptional control of Gad2Internal and External Feedback Circuits for Skilled Forelimb MovementPlasticity of rat central inhibitory synapses through GABA metabolismDevelopmental Trajectories of Auditory Cortex Synaptic Structures and Gap-Prepulse Inhibition of Acoustic Startle Between Early Adolescence and Young Adulthood in MiceCytosolic Accumulation of L-Proline Disrupts GABA-Ergic Transmission through GAD BlockadeNeuronal Ig/Caspr recognition promotes the formation of axoaxonic synapses in mouse spinal cord.Reduced glutamate decarboxylase 65 protein within primary auditory cortex inhibitory boutons in schizophrenia.Critical role of the 65-kDa isoform of glutamic acid decarboxylase in consolidation and generalization of Pavlovian fear memoryDefective GABAergic neurotransmission and pharmacological rescue of neuronal hyperexcitability in the amygdala in a mouse model of fragile X syndromeThe class 4 semaphorin Sema4D promotes the rapid assembly of GABAergic synapses in rodent hippocampusMetabolic distinction between vesicular and cytosolic GABA in cultured GABAergic neurons using 13C magnetic resonance spectroscopy.Modulation of GABAergic transmission in development and neurodevelopmental disorders: investigating physiology and pathology to gain therapeutic perspectives.Persistent pain facilitates response to morphine reward by downregulation of central amygdala GABAergic function.Genetic modulation of GABA levels in the anterior cingulate cortex by GAD1 and COMTTwo distinct mechanisms target GAD67 to vesicular pathways and presynaptic clustersRespective implications of glutamate decarboxylase antibodies in stiff person syndrome and cerebellar ataxia.Calpain cleavage of brain glutamic acid decarboxylase 65 is pathological and impairs GABA neurotransmission.Molecular mechanisms of neurotransmitter release.Water maze experience and prenatal choline supplementation differentially promote long-term hippocampal recovery from seizures in adulthood.Lower glutamic acid decarboxylase 65-kDa isoform messenger RNA and protein levels in the prefrontal cortex in schizoaffective disorder but not schizophreniaKnockout of GAD65 has major impact on synaptic GABA synthesized from astrocyte-derived glutamine.Consensus Paper: Neuroimmune Mechanisms of Cerebellar Ataxias.Glutamic acid decarboxylase 67 expression by a distinct population of mouse vestibular supporting cellsPresynaptic inhibition of spinal sensory feedback ensures smooth movement.NF-kappaB/Rel regulates inhibitory and excitatory neuronal function and synaptic plasticity.Tonic excitation or inhibition is set by GABA(A) conductance in hippocampal interneurons.Prenatal choline deficiency does not enhance hippocampal vulnerability after kainic acid-induced seizures in adulthood.Differential distribution of proteins regulating GABA synthesis and reuptake in axon boutons of subpopulations of cortical interneurons.Epigenetic suppression of GAD65 expression mediates persistent painCompartmentalization of GABA synthesis by GAD67 differs between pancreatic beta cells and neuronsGAD67 deficiency in parvalbumin interneurons produces deficits in inhibitory transmission and network disinhibition in mouse prefrontal cortex.SOX2 and SOX2-MYC Reprogramming Process of Fibroblasts to the Neural Stem Cells Compromised by Senescence.Acrylamide neurotoxicity on the cerebrum of weaning rats.Reversal of cocaine sensitization-induced behavioral sensitization normalizes GAD67 and GABAA receptor alpha2 subunit expression, and PKC zeta activity.GAD2 Alternative Transcripts in the Human Prefrontal Cortex, and in Schizophrenia and Affective Disorders.Functional Differentiation of Cholecystokinin-Containing Interneurons Destined for the Cerebral Cortex.Serum from a Patient with GAD65 Antibody-Associated Limbic Encephalitis Did Not Alter GABAergic Neurotransmission in Cultured Hippocampal Networks.MeCP2 regulates the timing of critical period plasticity that shapes functional connectivity in primary visual cortex.Activity-dependent regulation of inhibition via GAD67
P2860
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P2860
The role of the synthetic enzyme GAD65 in the control of neuronal gamma-aminobutyric acid release.
description
1999 nî lūn-bûn
@nan
1999年の論文
@ja
1999年論文
@yue
1999年論文
@zh-hant
1999年論文
@zh-hk
1999年論文
@zh-mo
1999年論文
@zh-tw
1999年论文
@wuu
1999年论文
@zh
1999年论文
@zh-cn
name
The role of the synthetic enzy ...... mma-aminobutyric acid release.
@ast
The role of the synthetic enzy ...... mma-aminobutyric acid release.
@en
type
label
The role of the synthetic enzy ...... mma-aminobutyric acid release.
@ast
The role of the synthetic enzy ...... mma-aminobutyric acid release.
@en
prefLabel
The role of the synthetic enzy ...... mma-aminobutyric acid release.
@ast
The role of the synthetic enzy ...... mma-aminobutyric acid release.
@en
P2093
P2860
P356
P1476
The role of the synthetic enzy ...... mma-aminobutyric acid release.
@en
P2093
P2860
P304
12911-12916
P356
10.1073/PNAS.96.22.12911
P407
P577
1999-10-01T00:00:00Z