ABSTRACT
The advance in the understanding of depressive disorders has been spectacular in all areas. However, the psychopathological analysis of his clinical features has remained stagnant since the advent of DSM-III. Kurt Schneider was concerned with particular care of their study and his contributions are still valid although much of his work remains unknown by the present world psychiatry. His main contributions concern the fields of methodology, conceptualization and description. He distinguishes different clinical entities: endogenous, basic, background, endoreactive, reactive, and existential depression and finally the depressive personality. Any progress on the psychopathology of depression requires a thoroughly deepening in his research.
El avance en el conocimiento de los trastornos depresivos ha sido espectacular en todaslas áreas. Sin embargo el análisis psicopatológico de sus cuadros ha permanecido estancado desde la aparición del DSM-III. Kurt Schneider se preocupó con especial cuidado de su estudio y sus contribuciones todavía están vigentes aunque en gran parte permanecen desconocidas. Sus principales aportes se dan en los campos de la metodología, conceptualización y descripción. Él distingue distintas entidades: depresión endógena, de base, de trasfondo, endorreactiva, reactiva, existencial y personalidad depresiva. Cualquier avance en la psicopatología de la depresión requiere por necesidad una profundización en sus investigaciones.
Subject(s)
Humans , Depression/history , Psychopathology , Depressive DisorderABSTRACT
OBJECTIVES: It has been demonstrated that nitric oxide (NO) serves as an inter- and intra-cellular messenger in the brain. NO has been implicated in the regulation of monoaminergic neurotransmission and the neuronal growth and synaptogenesis. Recently, NO has been suggested to be involved in the pathogenesis of depression. The aim of this study was to investigate the involvement of NO in the underlying mechanisms of biological vulnerability to depression. METHODS: The author measured locomotor activities and postnatal behavioral changes in the forced swimming test (FST) in rats that were exposed prenatally to N omega-nitro-L-arginine, a NO synthase (NOS) inhibitor. It was also investigated that paroxetine, a selective serotonin reuptake inhibitor, may affect the behavioral changes in the FST. RESULTS: Locomotor activities were significantly diminished, and the immobility times in the FST were significantly prolonged in the rats that were exposed prenatally to NOS inhibitor compared with controls. Pretreatment with paroxetine blocked the prolongation of the immobility times in the FST. CONCLUSION: The results indicate that postnatal behavioral changes due to prenatal exposure to NOS inhibitor in rats may suggest an animal model of endogenous depression, and that the glutamate-NMDA-NO pathway may be involved in the pathophysiology of depression. It is also indicated that the action of NO may, in part, be affected by serotonergic mechanism. This implicates that the glutamate-NMDA-NO pathway may lead to a novel approach to the treatment of depression.