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Formulation of the Glutamate Hypothesis

Method: Participants were male subjects (N=15) with chronic schizophrenia who were randomly assigned to receive 4 weeks of treatment with the study drug MK-0777, a benzodiazepine-like agent with selective activity at GABAA receptors containing α2 or α3 subunits, or a matched placebo in a double-blind fashion.

Effect of on glutamatergic function in patients with schizophrenia.

A review of the glutamate data in schizophrenia provides evidence consistent with the observation that alterations in glutamate function may play a role in this disease. Data from postmortem brain tissue, in particular, suggests that receptor systems may be altered. The characterization, cloning and expression of the NMDA receptor subunits provide an opportunity for future investigations in the study of potential defects in schizophrenia. Finally, the identification of novel drug target sites may open up new alternative strategies for the next generation of antipsychotics.

Niacin-respondent subset of schizophrenia – a therapeutic review.

Glutamatergic dysfunction in the brain has been implicated in the pathophysiology of schizophrenia.

Conclusions: These findings provide preliminary support for the hypothesis that enhanced GABA activity at α2 subunit containing GABAA receptors improves behavioral and electrophysiological measures of prefrontal function in individuals with schizophrenia.AB - Objective: Deficits in working memory and cognitive control in schizophrenia are associated with impairments in prefrontal cortical function, including altered gamma band oscillations.

Some of the research described in this review was supported by a National Institute of Mental Health Conte Center on the Neurobiology of Schizophrenia (MH P50-60450) and MH RO1-572901 and a Lieber Senior Investigator Award from the National Alliance for Research on Schizophrenia and Affective Disorder (NARSAD) to JTC.

High dose D-serine in the treatment of schizophrenia.

This would explain why schizophrenia symptoms often first appear during the teen years.

A new article in titled "" explains recent findings on "GABAergic microcircuits, which are thought to underlie cognitive impairments in schizophrenia." The research was and conducted by scientists at the University of Pittsburgh.

There is a growing body of evidence suggesting that alterations in neurotransmitter systems, possibly reflecting defects in early neurodevelopmental processes, may play an important role in the etiology of schizophrenia (, ). A current focus of research is on two major brain neurotransmitters, dopamine (DA) and glutamate, both of which may be altered in schizophrenia. Briefly, the dopamine hypothesis attributes hyperdopaminergic function as a possible cause of schizophrenia, whereas the glutamate hypothesis proposes a hypofunctional glutamate system. There is substantial evidence for both hypotheses, but some of the most impressive data are from observations that certain classes of drugs can produce schizophrenic-like symptoms in normals. Of all the compounds administered to man, the two classes of drugs that produce the symptoms most similar to those of schizophrenia are the dopamine agonists (e.g., amphetamine) and glutamate antagonists (e.g., PCP). In general, the glutamate antagonists produce somewhat more positive and negative symptoms than the DA agonists, which—when given acutely—fail to produce some of the core symptoms of schizophrenia, such as formal thought disorder and negative symptoms (). Consequently, a great deal of research emphasis is being placed on the role of glutamate in schizophrenia. Nonetheless, to date, the current antipsychotics do not have significant glutamatergic activity, although promising research at the NMDA receptor site (e.g., the glycine transport inhibitors [, ]) may provide new clues for the development of future antipsychotics.

Dopamine is thought to play an important role in the development of schizophrenia.
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01/01/1995 · Benzodiazepines and GABA hypothesis of ..

Method: Participants were male subjects (N=15) with chronic schizophrenia who were randomly assigned to receive 4 weeks of treatment with the study drug MK-0777, a benzodiazepine-like agent with selective activity at GABAA receptors containing α2 or α3 subunits, or a matched placebo in a double-blind fashion.

Benzodiazepines and GABA hypothesis of schizophrenia A

However, no conclusion can be made for medium- to long-term effects of EPA in schizophrenia, in particular on relapse prevention in the early course of psychotic disorders.

Glutamate hypothesis of schizophrenia - Wikipedia

The authors conducted a proof-of-concept clinical trial designed to test the hypothesis that a novel compound with relatively selective agonist activity at GABAA receptors containing α2 subunits would improve cognitive function and gamma band oscillations in individuals with schizophrenia.

Benzodiazepines and GABA hypothesis of schizophrenia

One of the major deficits in schizophrenia, documented by a number of investigators over the years, is the general inability of patients to filter incoming external sensory information efficiently (). Historically, sensory gating deficits are reported to affect primary auditory and visual sensory modalities (,). The acoustic startle response is one of the models for the study of filtering deficits in schizophrenics. In this paradigm, a small auditory stimulus is presented at 80–120 ms prior to a larger stimulus pulse, and eyeblink responses are recorded. In normal individuals, an inhibition of eyeblink responses follows the second intensified pulse of sound. In schizophrenics, however, the inhibitory response to the second auditory stimulus is significantly diminished, indicating a lack of inhibition (!popup(ch114). Studies using electrophysiological recordings of evoked potentials in animals demonstrated that drugs which antagonize glutamate (PCP, MK-801, and ketamine) reliably produce startle deficits in animals (), similar to the changes observed in gating studies of schizophrenic patients (e.g., ref. ).

Research Disproves Hypothesis of GABA …

The use of brain imaging technology to investigate the effects of PCP provides clues to the acute and chronic regional effects of the drug on brain metabolism. Data from receptor binding studies in animals show that limbic regions (especially the hippocampus) contain high concentrations of NMDA receptors (,). Although it may be supposed that PCP would reduce brain metabolism (especially in frontal brain regions to mimic the hypofrontality seen in schizophrenics) [,], studies in animals administered PCP and PCP-like compounds show that PCP increased regional glucose metabolism, specifically in hippocampal regions (,,,). Ketamine, a PCP-like compound, was similarly shown in five of six studies to increase glucose metabolism in hippocampal regions in animals (,,,,). However, schizophrenia is a chronic illness associated with hypothesized reductions in glutamate activity and hypofrontality (). A chronic PCP study by Gao et al. () in rats showed that glucose metabolism was decreased in limbic regions. Lahti et al. () administered ketamine (0.3 mg/kg, i.v.) to a group of schizophrenics stabilized on haloperidol and measured metabolic activity with HO and PET. In these patients, ketamine increased cerebral blood flow in the anterior cingulate cortex and in an area which extended inferiorly to the medial wall of the prefrontal cortex. In contrast, blood flow to the hippocampus and the primary visual cortex was decreased ().

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