Glutamaterge Neurotransmission bei Schizophrenien

 

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Zusammenfassung:

Glutamat ist der wichtigste erregende Neurotransmitter im zentralen Nervensystem. Es gibt Hinweise darauf, dass seine Aktivität bei schizophrenen Patienten vermindert, an anderen Stellen vermehrt ist. In den letzten Jahren wurden mit epidemiologischen, genetischen, histopathologischen und bildgebenden Untersuchungen deutliche Fortschritte in der Aufklärung der Krankheitsursachen erreicht und es wurden zunehmend integrative Modelle zur Pathogenese und Pathophysiologie schizophrener Psychosen entwickelt. Wenngleich auch verschiedene Vulnerabilitätsfaktoren und Stressoren zur Manifestation von schizophrenen Psychosen führen können, bildet die Glutamathypothese mit dem Modell eines kortiko-striato-thalamo-kortikalen Regelkreises weiterhin eine interessante Grundlage und bietet auch künftig zahlreiche Forschungsansätze, insbesondere in der weiteren Aufklärung der Affektion von Glutamatrezeptoren (z. B. NMDA-Rezeptoren), der glutamatergen Transmission sowie deren pharmakologische Beeinflussbarkeit.

Glutamatergic Neurotransmission in Schizophrenics:

Glutamate is the most abundant amino acid in the brain, where it plays an important role as a well-established major excitatory neurotransmitter in the central nervous system. It has been suggested that reduced glutamate neurotransmission may be involved in the pathophysiology of schizophrenia. The glutamate hypothesis of schizophrenia postulates alterations in the glutamatergic system as an important neurobiochemical event in the pathophysiology of this group of psychotic disorders. An altered glutamate release from synaptosomes including a hypofunction of different glutamate receptors (i.e. NMDA receptors) from different brain areas have previously been reported. Furthermore, partial agonists at the glycine co-agonist site of the NMDA receptor might be a new approach in the treatment of schizophrenic symptoms but further studies are necessary to clarify the role and efficacy of these substances in schizophrenia. Changes in the glutamatergic cortico-striatal connections in schizophrenia could precipitate a potential perceptive overstimulation of the neocortex from thalamic input and an inhibiting influence of the striatum on the thalamus would modulate the information input of the cortex, thereby possibly counteracting the disturbed information processing which is relatively characteristic for schizophrenic psychoses.

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Dr. Stefan Bleich

Klinik und Poliklinik für Psychiatrie und Psychotherapie
Georg-August-Universität

Von-Siebold-Str. 5

37075 Göttingen

Email: E-mail: stefan.bleich@t-online.de