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Riederer, Peter ; Lange, Klaus W. ; Kornhuber, J. ; Jellinger, K.

Glutamate receptor antagonism: neurotoxicity, anti-akinetic effects, and psychosis

Riederer, Peter, Lange, Klaus W., Kornhuber, J. und Jellinger, K. (1991) Glutamate receptor antagonism: neurotoxicity, anti-akinetic effects, and psychosis. Journal of neural transmission. Supplementum supl. 34, S. 203-210.

Veröffentlichungsdatum dieses Volltextes: 20 Jul 2012 11:45
Artikel
DOI zum Zitieren dieses Dokuments: 10.5283/epub.25440


Zusammenfassung

There is evidence to suggest that glutamate and other excitatory amino acids play an important role in the regulation of neuronal excitation. Glutamate receptor stimulation leads to a non-physiological increase of intracellular free Ca2+. Disturbed Ca2+ homeostasis and subsequent radical formation may be decisive factors in the pathogenesis of neurodegenerative diseases. Decreased glutamatergic ...

There is evidence to suggest that glutamate and other excitatory amino acids play an important role in the regulation of neuronal excitation. Glutamate receptor stimulation leads to a non-physiological increase of intracellular free Ca2+. Disturbed Ca2+ homeostasis and subsequent radical formation may be decisive factors in the pathogenesis of neurodegenerative diseases. Decreased glutamatergic activity appears to contribute to paranoid hallucinatory psychosis in schizophrenia and pharmacotoxic psychosis in Parkinson's disease. It has been suggested that a loss of glutamatergic function causes dopaminergic over-activity. Imbalances of glutamatergic and dopaminergic systems in different brain regions may result in anti-akinetic effects or the occurrence of psychosis. The simplified hypothesis of a glutamatergic-dopaminergic (im)-balance may lead to a better understanding of motor behaviour and psychosis.



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Details

DokumentenartArtikel
Titel eines Journals oder einer ZeitschriftJournal of neural transmission. Supplementum
Verlag:Springer (Wien)
Band:supl. 34
Seitenbereich:S. 203-210
Datum1991
Zusätzliche Informationen (Öffentlich)ISBN des Bandes 3-211-82261-5, Titel " Age-associated neurological diseases", hg. v. Deecke, L.
InstitutionenHumanwissenschaften > Institut für Psychologie > Lehrstuhl für Psychologie III (Biologische, Klinische und Rehabilitationspsychologie) - Prof. Dr. Klaus W. Lange
Identifikationsnummer
WertTyp
1687783PubMed-ID
Klassifikation
NotationArt
AnimalsMESH
Glutamates/toxicityMESH
Glutamic AcidMESH
HumansMESH
Models, NeurologicalMESH
Models, PsychologicalMESH
Nerve Degeneration/drug effectsMESH
Neurons/physiologyMESH
Neurotoxins/toxicityMESH
Psychotic Disorders/physiopathologyMESH
Receptors, GlutamateMESH
Receptors, Neurotransmitter/physiologyMESH
Schizophrenia/physiopathologyMESH
Dewey-Dezimal-Klassifikation100 Philosophie und Psychologie > 150 Psychologie
StatusVeröffentlicht
BegutachtetJa, diese Version wurde begutachtet
An der Universität Regensburg entstandenUnbekannt / Keine Angabe
URN der UB Regensburgurn:nbn:de:bvb:355-epub-254400
Dokumenten-ID25440

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