Blunted stress responses in delayed type hypersensitivity in mice lacking the neuronal isoform of nitric oxide synthase.
Nitric oxide (NO) is implicated in inflammation and hypothalamic-pituitary responses to immune stimuli; however, the specific role of NO from neurons during stress-induced immune responses remains unspecified. We measured antigen-specific delayed-type-hypersensitivity (DTH) responses in the skin of wild-type (WT) and neuronal nitric oxide synthase knockout (nNOS(-/-)) mice at baseline and after 2 h of restraint. Baseline corticosterone concentrations were higher in nNOS(-/-) than WT mice. However, stress-induced increases in corticosterone were dampened in nNOS(-/-) mice, and restraint suppressed DTH only in WT animals. Furthermore, WT mice lost more body mass after stress, and exhibited more anxiety-like behavior in the open field, than nNOS(-/-) mice. Neuronal NO appears to be involved in the neuroendocrine-immune response to stress, perhaps via glucocorticoid regulation.
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Related Subject Headings
- Stress, Physiological
- Restraint, Physical
- Nitric Oxide Synthase Type I
- Nitric Oxide Synthase
- Neurons
- Neurology & Neurosurgery
- Nerve Tissue Proteins
- Motor Activity
- Mice, Knockout
- Mice, Inbred C57BL
Citation
Published In
DOI
EISSN
ISSN
Publication Date
Volume
Issue
Start / End Page
Related Subject Headings
- Stress, Physiological
- Restraint, Physical
- Nitric Oxide Synthase Type I
- Nitric Oxide Synthase
- Neurons
- Neurology & Neurosurgery
- Nerve Tissue Proteins
- Motor Activity
- Mice, Knockout
- Mice, Inbred C57BL