Examination of the neuroendocrine basis for the social conflict-induced enhancement of immunity in mice.
Physiol Behav
; 48(5): 685-91, 1990 Nov.
Article
en En
| MEDLINE
| ID: mdl-2082368
ABSTRACT
Intruder DBA/2 and C57BL/6 mice, which display different neuroendocrine responses to social conflict, evidence a pronounced increase in splenocyte phagocytosis of opsonized zymosan particles as a consequence of social conflict-induced stress. Interruption of the hypothalamic-pituitary-adrenal axis prior to social conflict results in an abrogation of the stress-induced enhancement of phagocytosis in DBA/2, but not in C57BL/6, mice. Administration of the opiate antagonists naloxone and naltrexone resulted in a potentiation of the stress-induced enhancement of phagocytosis in both strains. Similarly, administration of the alkylating antagonist beta-chlornaltrexamine which irreversibly blocks opioid binding sites potentiated the immune-enhancing effects of social conflict stress. Mitogen-induced T and B lymphocyte proliferation was unaffected by any of the experimental procedures with the exception of beta-chlornaltrexamine which suppressed activity equally in stressed and nonstressed groups. These results demonstrate the necessity of employing inbred murine strains in the dissection of the neuroendocrine pathways which govern stress-induced modulation of the immune system.
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Base de datos:
MEDLINE
Asunto principal:
Sistema Hipófiso-Suprarrenal
/
Nivel de Alerta
/
Endorfinas
/
Conflicto Psicológico
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Agresión
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Conducta Agonística
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Sistema Hipotálamo-Hipofisario
Límite:
Animals
Idioma:
En
Revista:
Physiol Behav
Año:
1990
Tipo del documento:
Article