Behavioral effects of orally administered glycine in socially housed monkeys chronically treated with phencyclidine

Linn, Gary; O'Keeffe, Robert T.; Lifshitz, Kenneth; Schroeder, Charles E.; Javitt, Daniel C.

doi:10.1007/s00213-007-0771-6

Cited by 26 publications

(16 citation statements)

References 77 publications

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“…For example, schizophrenia-like auditory hallucinations are not observed during acute ketamine administration. In monkeys, such phenomena are observed during subchronic, but not acute ketamine administration, 47 suggesting that they may reflect secondary consequences of persistent NMDAR dysfunction. Psychotic symptoms, including hallucinations, are also observed in autoimmune disorders associated with anti-NMDA antibodies.…”

Section: Brain Adaptations To Chronic Nmdar Functionmentioning

confidence: 99%

Has an Angel Shown the Way? Etiological and Therapeutic Implications of the PCP/NMDA Model of Schizophrenia

Javitt

Zukin²,

Heresco-Levy

et al. 2012

Schizophrenia Bulletin

275

203

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Section: Brain Adaptations To Chronic Nmdar Functionmentioning

confidence: 99%

Has an Angel Shown the Way? Etiological and Therapeutic Implications of the PCP/NMDA Model of Schizophrenia

Javitt

Zukin²,

Heresco-Levy

et al. 2012

Schizophrenia Bulletin

275

203

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“…Direct agonists have included treatment with the naturally occurring amino acids glycine and D-serine, which serve as endogenous modulators of NMDA receptors in vivo, as well the antituberculosis drug D-cycloserine, which fortuitously cross-reacts with the NMDA/glycine site (see [134] for a review). These agents have proven effective in several preclinical models, including reversal of PCP effects in both rodents (135, 137) and primates (137). …”

Section: Nmda-based Treatmentsmentioning

confidence: 99%

Thinking Glutamatergically: Changing Concepts of Schizophrenia Based Upon Changing Neurochemical Models

Kantrowitz¹,

Javitt²

2010

Clinical Schizophrenia & Related Psychoses

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Clinical concepts of mental illness have always been modulated by underlying theoretical considerations. For the past fifty years, schizophrenia has been considered primarily a disease of dopaminergic neurotransmission. Although this conceptualization has helped greatly in explaining the clinical effects of psychostimulants and guiding the clinical use of both typical and atypical antipsychotics, it has nevertheless shaded how we look at the disorder from both a pathophysiological and therapeutic perspective. For example, most explanatory research in schizophrenia has focused on dopamine-rich regions of the brain, with little investigation of regions of the brain that are relatively dopamine poor. Starting approximately twenty years ago, an alternative formulation of schizophrenia was proposed based upon actions of the “dissociative anesthetic” class of psychotomimetic agents, including phencyclidine (PCP), ketamine and various designer drugs. These compounds induce psychosis by blocking neurotransmission at N-methyl-D-aspartate (NMDA)-type glutamate receptors, suggesting an alternative model for pathogenesis in schizophrenia. As opposed to dopamine, the glutamatergic system is widely distributed throughout the brain and plays a prominent role in sensory processing as well as in subsequent stages of cortical analysis. Glutamatergic theories of schizophrenia, thus, predict that cortical dysfunction will be regionally diffuse but process specific. In addition, NMDA receptors incorporate binding sites for specific endogenous brain compounds, including the amino acids glycine and D-serine and the redox modulator glutathione, and interact closely with dopaminergic, cholinergic and γ-aminobutyric acid (GABA)-ergic systems. Glutamatergic theories, thus, open new potential approaches for treatment of schizophrenia, most of which are only now entering clinical evaluation.

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“…Following chronic administration, more prolonged schizophrenia-like symptoms may emerge. 16 Given the widespread distribution of transmitters such as glutamate, GABA, and nicotine and of receptors such as NMDA, the critical issue in schizophrenia may not be what brain regions are involved but rather what specific processes are impaired within each region. Patients with schizophrenia as a group are neither blind nor deaf.…”

Section: Etiological Models Of Schizophreniamentioning

confidence: 99%

Sensory Processing in Schizophrenia: Neither Simple nor Intact

Javitt

2009

Schizophrenia Bulletin

274

186

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This special issue focuses on the theme of sensory processing dysfunction in schizophrenia. For more than 50 years, from approximately the time of Bleuler until the early 1960s, sensory function was considered one of the few preserved functions in schizophrenia (Javitt 1 ). Fortunately, the last several decades have brought a renewed and accelerating interest in this topic. The articles included in the issue range from those addressing fundamental bases of sensory dysfunction (Brenner, Yoon, and Turetsky) to those that examine how elementary deficits in sensory processing affect the sensory experience of individuals with schizophrenia (Butler, Kantrowitz, and Coleman) to the question of how sensory-based treatments may lead to improvement in remediation strategies (Adcock). Although addressing only a small portion of the current complex and burgeoning literature on sensory impairments across modalities, the present articles provide a cross-section of the issues currently under investigation. These studies also underscore the severe challenges that individuals with schizophrenia face when trying to decode the complex world around them.

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Behavioral effects of orally administered glycine in socially housed monkeys chronically treated with phencyclidine

Cited by 26 publications

References 77 publications

Has an Angel Shown the Way? Etiological and Therapeutic Implications of the PCP/NMDA Model of Schizophrenia

Has an Angel Shown the Way? Etiological and Therapeutic Implications of the PCP/NMDA Model of Schizophrenia

Thinking Glutamatergically: Changing Concepts of Schizophrenia Based Upon Changing Neurochemical Models

Sensory Processing in Schizophrenia: Neither Simple nor Intact

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