Gamma-Aminobutyric Acid (GABA) in the CSF of Schizophrenic Patients Before and After Neuroleptic Treatment

Lichtshtein, David; Dobkin, J.; Ebstein, Richard P.; Biederman, Joseph; Rimón, Ranan; Belmaker, Robert H.

doi:10.1192/bjp.132.2.145

Cited by 63 publications

(16 citation statements)

References 13 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…An increase in CSF GABA levels has been found after 30 d treatment with sulpride and to be correlated with long-term neuroleptic treatment . However, Lichtshtein et al (1978) noted a small but significant decrease in CSF GABA levels after 2 months of neuroleptic treatment while Gattaz et al (1986) observed no change in free CSF GABA levels in schizophrenic patients after 3 months of haloperidol treatment. Lastly, Zander et al (1981) reported that stopping chronic anti-psychotic medication treatment produced no change in CSF GABA levels.…”

Section: Csf Studiesmentioning

confidence: 91%

The GABAergic system in schizophrenia

Blum

Mann

2002

Int. J. Neuropsychopharm.

121

View full text Add to dashboard Cite

A defect in neurotransmission involving γ-amino butyric acid (GABA) in schizophrenia was first proposed in the early 1970s. Since that time, a considerable effort has been made to find such a defect in components of the GABAergic system. After a brief introduction focusing on historical perspectives, this paper reviews postmortem and other biological studies examining the following components of the GABAergic system in schizophrenic subjects : the GABA biosynthetic enzyme, glutamate decarboxylase ; free GABA ; the GABA transporter ; the GABA A , GABA B and benzodiazepine receptors ; and the catabolic enzyme GABA transaminase. Additionally, post-mortem studies using morphology or calcium-binding protein to identify GABAergic neurons are also reviewed. Substantial evidence argues for a defect in the GABAergic system of the frontal cortex in schizophrenia which is limited to the parvalbumin-class of GABAergic interneurons.

show abstract

Section: Csf Studiesmentioning

confidence: 91%

The GABAergic system in schizophrenia

Blum

Mann

2002

Int. J. Neuropsychopharm.

121

View full text Add to dashboard Cite

show abstract

“…This is at variance with data reported in the literature. Lichtshtein et al (1978) found a small but significant decline in mean CSF GABA levels in 10 schizophrenic patients after 2 months of neuroleptic treatment, whereas Zimmer et al (1980) reported a significant increase of GABA in 13 schizophrenics after 30 days on sulpiride.…”

Section: Discussionmentioning

confidence: 91%

Cerebrospinal fluid concentrations of free GABA in schizophrenia: No changes after haloperidol treatment

Gattaz

Roberts

Beckmann

1986

J. Neural Transmission

View full text Add to dashboard Cite

The concentrations of free GABA were determined in the cerebrospinal fluid of 19 paranoid schizophrenic patients before and after 3 weeks on haloperidol treatment. No significant effect of the neuroleptic treatment on the CSF free GABA concentrations was detected. Furthermore, no correlations were found between changes in GABA concentrations and psychopathological improvement on the Brief Psychiatric Rating Scale. These negative findings are at variance with earlier reports of increased or decreased CSF GABA concentrations after neuroleptics and suggest that subtle changes of the amino acid concentrations in the brain might not be faithfully reflected in the concentrations of its free fraction in the cerebrospinal fluid.

show abstract

“…This suppressive effect of HAL on GABA is in agreement with several clinical and experimental studies. A CSF study in schizophrenic patients has demonstrated a significant decline of 12% in mean GABA levels in CSF after -2 months of neuroleptic (chlorpromazine, perphenazine or fluphenazine) treatment (Lichtshtein et al, 1978). From animal studies, Kim and Hassler (1975) reported that 1 h after a single injection of HAL (10 mg/kg) there was a significant decrease in GABA content in tissue homogenates of rat striatum (37%) and substantia nigra (19%), respectively.…”

Section: Effects Of Carbamazepinementioning

confidence: 98%

In vivo effects of carbamazepine and haloperidol on GABA neurotransmission and LH secretion

1995

View full text Add to dashboard Cite

The in vivo effects of carbamazepine (CBZ) and haloperidol (HAL) on the neuroendocrine pre-optico-pituitary feedback system were studied by local application of the drugs, in single and in combination mode, through a push-pull cannula into the pre-optic area and measurement of their local effects on γ-aminobutyric acid (GABA) and their distant effects on a subsequent biological response: the pituitary luteinizing hormone (LH) secretion. The perfusion flow rate was 20 μl cerebrospinal fluid (CSF)/min; the fraction period was 15 min. Perfusion with 8 μg CBZ/ml CSF caused a reduction in pre-optic pre-synaptic GABA release and, concomitantly, a suppression of plasma LH levels. Application of 100 ng HAL/ml CSF also caused a reduction in GABA release, but no significant change in plasma LH levels. During the combined perfusion, the effects of CBZ and HAL did not add up with regard to the pre-optic GABA release. These results suggest that both drugs interact with the GABA system, but they may involve two different mechanisms of action. Due to the known inhibitory role of pre-optic GABA in pituitary LH secretion, it can be inferred that, in contrast to HAL, CBZ increases post-synaptic GABAergic transmission.

show abstract

Gamma-Aminobutyric Acid (GABA) in the CSF of Schizophrenic Patients Before and After Neuroleptic Treatment

Cited by 63 publications

References 13 publications

The GABAergic system in schizophrenia

The GABAergic system in schizophrenia

Cerebrospinal fluid concentrations of free GABA in schizophrenia: No changes after haloperidol treatment

In vivo effects of carbamazepine and haloperidol on GABA neurotransmission and LH secretion

Contact Info

Product

Resources

About