Neither acute nor chronic exposure to a naturalistic (predator) stressor influences the interleukin-1 beta system, tumor necrosis factor-alpha, transforming growth factor-beta 1, and neuropeptide mRNAs in specific brain regions

Physical (neurogenic) stressors may influence immune functioning and interl eukin-1 beta (IL-1 beta) mRNA levels within several brain regions. The pres ent study assessed the effects of an acute or repeated naturalistic, psycho genic stressor (predator exposure) on brain cytokine and neuropeptide mRNAs . Acute predator (ferret) exposure induced stress-like behavioral effects, including elicitation of a startle response and reduced exploratory behavio rs; these responses diminished after 30 sessions. Moreover, acute and repea ted predator exposure, like acute restraint stress, increased plasma cortic osterone levels measured 5 min later, but not 2 h after stressor exposure. In contrast, none of the stressors used influenced IL-1 beta, IL-1 receptor antagonist, IL-1 receptor type I, IL-1 receptor accessory proteins I and I I, or tumor necrosis factor-alpha mRNA levels in the prefrontal cortex, amy gdala, hippocampus, or hypothalamus. Likewise, there were no stressor effec ts on transforming growth factor-beta 1, neuropeptide Y, glycoprotein 130, or leptin receptor mRNAs in brain regions. Thus, the naturalistic/psychogen ic stressor used does not affect any of the brain cytokine component mRNAs studied. It is suggested that this type of stressor activates homeostatic m echanisms (e.g., glucocorticoid release), which act to preclude brain cytok ine alterations that would otherwise favor neuroinflammatory/neuroimmunolog ical responses and the consequent increase of brain sensitivity to neurotox ic and neurodegenerative processes. (C) 2000 Elsevier Science Inc.