CSF Levels of γ-Aminobutyric Acid in Schizophrenia

Kammen, Daniël P. van

doi:10.1001/archpsyc.1982.04290010065012

Cited by 51 publications

(10 citation statements)

References 54 publications

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“…Other investigators later supported (Gold et al, 1980;Spokes et al, 1980), or were unable to confirm (Cross etal., 1979;Perry etal., 1989) this finding. Furthermore, levels of GABA in cerebrospinal fluid (CSF) have previously been reported to be low in unmedicated schizoaffective disorder subjects (Gold et al, 1980), and in schizophrenic patients (Gerner and Hare, 1981), but this finding was not confirmed by van Kammen et al (1982), Gerner et al (1984) or Perry etal. (1989), andMcCarthy etal.…”

Section: Introductionmentioning

confidence: 98%

Gamma-aminobutyrate aminotransferase activity in brains of schizophrenic patients

Sherif

Eriksson

Oreland

1992

J. Neural Transmission

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The activity of gamma-aminobutyrate aminotransferase (GABA-T) was estimated in twelve regions of brains from 22 control subjects and 6 cases with schizophrenia. In the controls, no significant correlation was found between the enzyme activity and age or postmortem interval (PMI) in any of the brain regions studied. In experiments on rat brains, the enzyme activity decreased about 20% during the first 2 hours of storage at room temperature and at 4 degrees C but remained steady thereafter. A similar initial decline in activity in the human brain material cannot be excluded. In the human brains, a slightly lower activity was found in the group below 75 years (n = 8) when compared with the group above 75 years (n = 8). A tendency to higher activities was found in female brains (n = 10) compared with male brains (n = 12). No significant difference in the enzyme activity was found between schizophrenic brains, in any of the regions studied, when compared to controls, matched for age, sex and PMI.

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Section: Introductionmentioning

confidence: 98%

Gamma-aminobutyrate aminotransferase activity in brains of schizophrenic patients

Sherif

Eriksson

Oreland

1992

J. Neural Transmission

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“…Only mean values are quoted in this paper, but the standard deviations suggested a wide spread of values that may eventually provide evidence for heterogeneity. The results of McCarthy et al were not confirmed by the latest paper on this subject (Van Kammen et al, 1982). These authors reported a tendency for CSF GABA levels to be low in young patients during the early stages of their illness, but with increasing length of hospitalization the levels tended to increase.…”

Section: Y-aminobutyric Acidmentioning

confidence: 84%

Schizophrenia: Some Current Neurochemical Approaches

Rodnight

1983

Journal of Neurochemistry

203

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T o many neurochemists the conundrum of schizophrenia constitutes the most fascinating and challenging of all applied problems in neuroscience research. The term schizophrenia encompasses a syndrome of psychotic illnesses that devastate the afflicted patient and his family over a lifetime. The complete disintegration of an intact personality in a physically healthy individual, usually in early adulthood and with no insight, makes the condition the most distressing of all the serious mental disorders. It is also among the most common, with a prevalence of nearly 1% in the population and an incidence of new cases of 1 per 10,000 per year (Hare, 1982).The idea that biochemical abnormalities underlie the aetiology and symptomatology of schizophrenia has waxed and waned over more than half a century. These fluctuations in fashion reflected the old nature and nuture controversy, which most workers now dismiss as irrelevant. The modern consensus accepts that the syndrome arises from the interaction, to varying degrees, of both biological and environmental factors; t o those active in the field therefore, it is an article of faith that aetiological factors of a biochemical nature will eventually be discovered. In the search for these factors, however, numerous problems of interpretation and research strategy arise. The more obvious include the extent to which observed abnormalities may be of aetiological significance, rather than state-dependent; the influence of iatrogenic factors such as drugs or of other uncontrolled environmental factors such as diet: the question of the criteria used by clinicians to diagnose schizophrenia (although this is now a less serious problem than it used to be); and the relevance of peripheral body fluid parameters to a condition that is clearly a disorder of the CNS. These problems have often been considered in detail (e.g., Kety, 1978;Rodnight, 1980) and must be constantly borne in mind when assessing the research discussed below.

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“…However, the change of GABA level in schizophrenia is not conclusive. A recent study showed elevated GABA levels in the anterior cingulated cortex of schizophrenic patients [19], although normal and reduced GABA levels have also been reported [14], [15], [16], [17], [18]. Moreover, Neuregulin 1, a susceptibility gene of schizophrenia, has been shown to increase the release of GABA [43].…”

Section: Discussionmentioning

confidence: 99%

“…However, due to the concurrent downregulation of GAD67, the overall change of GABA level in schizophrenia is quite controversial. Indeed, the literature on GABA measurements in schizophrenia is more discrepant, with reports of either normal [14], [15], reduced [16], [17], [18] or elevated GABA levels [19], [20]. Although it was supposed in several studies that the GAT1 downregulation may be a compensatory mechanism to the reduction of GABA synthesis [3], [21], the functional significance of GAT1 downregulation remains unknown.…”

Section: Introductionmentioning

confidence: 99%

GABA Transporter-1 Deficiency Confers Schizophrenia-Like Behavioral Phenotypes

Fang

Xiao

et al. 2013

PLoS ONE

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The mechanism underlying the pathogenesis of schizophrenia remains poorly understood. The hyper-dopamine and hypo-NMDA receptor hypotheses have been the most enduring ideas. Recently, emerging evidence implicates alterations of the major inhibitory system, GABAergic neurotransmission in the schizophrenic patients. However, the pathophysiological role of GABAergic system in schizophrenia still remains dubious. In this study, we took advantage of GABA transporter 1 (GAT1) knockout (KO) mouse, a unique animal model with elevated ambient GABA, to study the schizophrenia-related behavioral abnormalities. We found that GAT1 KO mice displayed multiple behavioral abnormalities related to schizophrenic positive, negative and cognitive symptoms. Moreover, GAT1 deficiency did not change the striatal dopamine levels, but significantly enhanced the tonic GABA currents in prefrontal cortex. The GABAA receptor antagonist picrotoxin could effectively ameliorate several behavioral defects of GAT1 KO mice. These results identified a novel function of GAT1, and indicated that the elevated ambient GABA contributed critically to the pathogenesis of schizophrenia. Furthermore, several commonly used antipsychotic drugs were effective in treating the locomotor hyperactivity in GAT1 KO mice, suggesting the utility of GAT1 KO mice as an alternative animal model for studying schizophrenia pathogenesis and developing new antipsychotic drugs.

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CSF Levels of γ-Aminobutyric Acid in Schizophrenia

Cited by 51 publications

References 54 publications

Gamma-aminobutyrate aminotransferase activity in brains of schizophrenic patients

Gamma-aminobutyrate aminotransferase activity in brains of schizophrenic patients

Schizophrenia: Some Current Neurochemical Approaches

GABA Transporter-1 Deficiency Confers Schizophrenia-Like Behavioral Phenotypes

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