Low plasma γ-aminobutyric acid levels in male patients with depression☆
References (49)
5-Hydroxytraptamine facilities GABA-induced depolarization in bullfrog primary afferent neurons
Neurosci Lett
(1988)- et al.
The relationship between GABA concentrations in brain and cerebrospinal fluid
Brain Res
(1979) - et al.
Brain GABAA/benzodiazapine binding sites and glutamic acid decarboxylase activity in depressed suicide victims
Brain Res
(1988) - et al.
Brain GABAB binding sites in depressed suicide victims
Psychiatry Res
(1988) - et al.
Therapeutic effects of GABAergic drugs in affective disorders. A preliminary report
Pharmacol Biochem Behav
(1983) - et al.
Measurement of γ-aminobutyric acid (GABA) in blood
Life Sci
(1978) - et al.
Rapid and sensitive ion-exchange fluorometric measurement of γ-aminobutyric acid in physiological fluids
Annal Biochem
(1980) - et al.
GABAB receptors and norepinephrine-stimulated cAMP production in rat brain cortex
Brain Res
(1984) - et al.
GABA concentrations in forebrain areas of suicide victims
Biol Psychiatry
(1988) - et al.
Adrenoreceptors and the pharmacology of affective illness: A unifying theory
Life Sci
(1987)
The potential use of GABA agonists in psychiatric disorders: Evidence from studies with progabide in animal models and clinical traits
Pharmacol Biochem Behav
γ-Aminobutyric acid enhancement of potassium-stimulated release of [3H]norepinephrine by multiple mechanisms in rat cortical slices
Biochem Pharmacol
Neurotransmitter abnormalities in senile dementia
J Neurol Sci
Plasma GABA in affective illness: A preliminary investigation
J Affect Disorder
Plasma GABA levels in psychiatric illness
J Affect Disorder
Cerebrospinal fluid GABA in normals and patients with affective disorders
Brain Res Bull
Pentobarbital augments serotonin-mediated inhibition of cerebellar Purkinje cells
Neurosci
Parallel changes in the sensitivity of γ-aminobutyric acid and noradrenergic receptors following chronic administration of antidepressant and GABAergic drugs
Neuropharmacology
Validation of a Hamilton subscale for endogenomorphic depression
J Affect Disorder
The occurrence of γ-aminobutyric acid in human tissues other than brain
J Biol Chem
Preliminary studies on CSF gamma-aminobutyric acid levels in psychiatric patients before and during treatment with different psychotropic drugs
Prog Neuropsychopharmacol Biol Psychiatry
Genetic factors in affective illness
J Psychiatr Res
Reduced plasma and CSF γ-aminobutyric acid in affective illness: Effect of lithium carbonate
Biol Psychiatry
Plasma and CSF GABA in affective illness
Br J Psychiatry
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Supported by the Department of Veterans Affairs and a Department of Veterans Affairs Research Career Development Award to Frederick Petty, Ph.D., M.D. Also supported by NIMH Research Grant MH37899, NIAAA Research Grant AA07234, MHCRC Center Grant (MH41115), and the John Schemmerhorn Fund.
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We thank Dinah Turner-Knight for excellent secretarial support in preparing the manuscript, Tery Phillips, David Dunnam, B.S., and Gayle Patterson, B.A. for technical assistance and Kenneth Z. Altshuler, M.D. Stanton Sharpe Professor and Chairman for administrative support.