GAD67: the link between the GABA-deficit hypothesis and the dopaminergic- and glutamatergic theories of psychosis

@article{Kalkman2003GAD67TL,
  title={GAD67: the link between the GABA-deficit hypothesis and the dopaminergic- and glutamatergic theories of psychosis},
  author={H. Kalkman and E. Loetscher},
  journal={Journal of Neural Transmission},
  year={2003},
  volume={110},
  pages={803-812}
}
  • H. Kalkman, E. Loetscher
  • Published 2003
  • Medicine
  • Journal of Neural Transmission
    • Summary. Decreases in the 67 kDa isoenzyme of brain glutamic acid decarboxylase (GAD67) expression have been consistently found in patients with bipolar disorder and schizophrenia. In animals GAD67 expression is diminished by chronic, but not acute stimulation of dopamine D2 receptors and by short-term blockade of NMDA receptors. In contrast, chronic treatment with D2 receptor antagonists enhances GAD67 expression. Thus, antipsychotic treatment cannot explain the reduction in GAD67 levels in… CONTINUE READING
    View on Springer
    ncbi.nlm.nih.gov
    50 Citations
    Background Citations
    20
    Methods Citations
    1
    Results Citations
    3
    50 Citations
    Citation Type

    Citation Type

    Molecular and cellular mechanisms of altered GAD1/GAD67 expression in schizophrenia and related disorders
    • 319
    Allelic variation in GAD1 (GAD67) is associated with schizophrenia and influences cortical function and gene expression
    • 253
    • PDF
    Altered Excitatory-Inhibitory Balance in the NMDA-Hypofunction Model of Schizophrenia
    • 206
    • PDF
    The role of anti-glutamic acid decarboxylase autoantibodies in mood disorders
    • 3
    Decreased GAD67 mRNA levels in cerebellar Purkinje cells in autism: pathophysiological implications
    • 237
    Reelin down-regulation in mice and psychosis endophenotypes
    • 83
    Molecular mechanisms underlying synergistic effects of SSRI–antipsychotic augmentation in treatment of negative symptoms in schizophrenia
    • 24
    Methamphetamine induces long-term changes in GABAA receptor alpha2 subunit and GAD67 expression.
    • 38
    Neurotransmitter receptor binding in the posterior cingulate cortex in schizophrenia and in the phencyclidine mouse model: an exploration of the NMDA hypofunction hypothesis of schizophrenia
    Glutamic acid decarboxylase 67 haplodeficiency in mice: consequences of postweaning social isolation on behavior and changes in brain neurochemical systems
    • 1

    References

    SHOWING 1-10 OF 55 REFERENCES
    Dopaminergic and glutamatergic blocking drugs differentially regulate glutamic acid decarboxylase mRNA in mouse brain.
    • 63
    Dopamine in schizophrenia: a review and reconceptualization.
    • 1,821
    Gene expression for glutamic acid decarboxylase is reduced without loss of neurons in prefrontal cortex of schizophrenics.
    • 932
    Differential hippocampal expression of glutamic acid decarboxylase 65 and 67 messenger RNA in bipolar disorder and schizophrenia.
    • 258
    • PDF
    A decrease of reelin expression as a putative vulnerability factor in schizophrenia.
    • 690
    • Highly Influential
    • PDF
    Brain SPECT imaging of amphetamine-induced dopamine release in euthymic bipolar disorder patients.
    • 169
    The GABAergic system in schizophrenia.
    • 129
    • PDF
    The Relationship between Dorsolateral Prefrontal Neuronal N-Acetylaspartate and Evoked Release of Striatal Dopamine in Schizophrenia
    • 157
    • PDF
    Dopaminergic regulation of glutamic acid decarboxylase mRNA expression and GABA release in the striatum: A review
    • N. Lindefors
    • Biology, Medicine
    • Progress in Neuro-Psychopharmacology and Biological Psychiatry
    • 1993
    • 87
    Traditional and new antipsychotic drugs differentially alter neurotransmission markers in basal ganglia‐thalamocortical neural pathways
    • 50