Effect of interleukin-6 and tumor necrosis factor-alpha on GABA release from mediobasal hypothalamus and posterior pituitary.
Neuroimmunomodulation
; 7(2): 77-83, 2000.
Article
em En
| MEDLINE
| ID: mdl-10686516
ABSTRACT
The release of cytokines during infection, inflammation and stress induces brain-mediated responses, including alterations of neuroendocrine functions. We examined the effect of interleukin-6 (IL-6) and tumor necrosis factor-alpha (TNF-alpha) on release of gamma-aminobutyric acid (GABA) from mediobasal hypothalamic (MBH) explants and posterior pituitaries (PP) of male rats. IL-6 (10 ng/ml) did not modify basal GABA release from MBH and PP, but significantly increased GABA release under depolarizing conditions (40 mM K(+)). This effect was abolished by incubation of the tissue with indomethacin, an inhibitor of cyclooxygenase activity, indicating that prostaglandins could mediate the stimulation of GABA release induced by IL-6. On the contrary, TNF-alpha (50 ng/ml) significantly decreased K(+)-evoked GABA release from both MBH and PP. This inhibitory effect was not modified by indomethacin. Neither IL-6 nor TNF-alpha affected nitric oxide synthesis, as measured by [(14)C]citrulline production. The current results indicate that IL-6 stimulates GABA release from both hypothalamus and posterior pituitary by a mechanism mediated by prostaglandins. On the contrary, TNF-alpha inhibits GABA release from both tissues. These results suggest the possibility that GABAergic activity in the hypothalamic-pituitary axis could be involved in neuroendocrine responses to cytokines.
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Base de dados:
MEDLINE
Assunto principal:
Neuro-Hipófise
/
Interleucina-6
/
Fator de Necrose Tumoral alfa
/
Ácido gama-Aminobutírico
/
Hipotálamo Médio
Limite:
Animals
Idioma:
En
Revista:
Neuroimmunomodulation
Assunto da revista:
ALERGIA E IMUNOLOGIA
/
NEUROLOGIA
Ano de publicação:
2000
Tipo de documento:
Article
País de afiliação:
Argentina