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Despite the increased knowledge about the biological basis of behavior, the exact neurobiological mechanisms involved in the pathophysiology of schizophrenia remain unknown. As a consequence of this situation, pharmacological interventions in schizophrenia are mostly based on empirical evidence, but not pathophysiological models. A model of schizophrenia that leads to some testable hypothesis about new potential therapeutic interventions is therefore presented. From a theoretical viewpoint, this model integrates recent neuropsychological and brain imaging findings in schizophrenia patients with new studies in the molecular, cellular and circuit underpinnings of normal brain development and synaptic plasticity. Thus, it is proposed that schizophrenia is a neurodevelopmental illness characterized by inappropriately modulated glutamatergic neurotransmission secondary to dysfunctional GABAergic interneurons in extended regions of the brain. Subtle unbalances in GABA/Glutamate neurotransmission may explain the cognitive, social and motor-coordination deficits reported in the pre-psychotic stages of schizophrenia. Psychotic episodes emerge later on as a result of increased glutamatergic neurotransmission triggered by the increased dopaminergic neurotransmission of adolescence and early adulthood. Excessive glutamatergic neurotransmission during the first psychotic episodes may explain the progressive reductions in gray and white matter reported in patients with schizophrenia in recent prospective studies. In support of this hypothesis, I will summarize data obtained in our own laboratory studying patients with schizophrenia, as well as in an animal model of intermittent exposure to phencyclidine. As a corollary of these ideas, GABA/ Glutamate modulating drugs, such acamprosate or lamotrigine, are proposed as potential treatments for the early stages of this disorder.

Modelos fisiopatológicos de la esquizofrenia; de dopamina a glutamato, de glutamato a GABA