Abstract

Introduction

Materials & Methods

Results

Discussion & Conclusion

References

Discussion
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Cytokines, such as IL-1beta and TNF-alpha, provoke behavioral alterations which are often accompanied by elevated plasma ACTH and corticosterone levels (Dantzer et al.,1996; Warren et al., 1997). Likewise, systemic IL-1 treatment augments monoamine turnover at both hypothalamic (Dunn, 1992; Shintani et al., 1993) and extrahypothalamic brain regions (Dunn 1988a; Linthorst et al., 1995; Merali et al., 1997 ). However, much less attention has focused on the central neurochemical effects of TNF-a This is surprising in light of the integral role played by TNF-a in the acute phase response (Beutler et al., 1985) and the well documented anorexic effects of the cytokine (Plata-Salaman et al., 1988; Uomoto et al., 1998).

In addition to their acute actions, cytokines induce effects of a more protracted nature. Indeed, several days after a single IL-1 treatment increased colocalization of arginine vasopression (AVP) and corticotropin releasing hormone (CRH) was observed in CRH terminals located in the external zone of the median eminence (Schmidt et al., 1995; Tilders et al., 1993). Moreover, upon reexposure to either IL-1 or to a footshock stressor (some days after initial cytokine treatment) circulating corticosterone levels were markedly elevated (i.e. sensitization) (Schmidt et al., 1995), presumably as a result of the co-secretion of the two ACTH secretagogues (CRH and AVP).

To our knowledge, the possible sensitizing actions of TNF-a on central monoamine turnover have not been explored. The purpose of the present investigation was to (1) examine the acute effects of TNF-a on consumption of a palatable chocolate milk solution, sickness behavior, plasma corticosterone levels and central monoamine activity and (2) determine if TNF-a promotes a sensitization effect with respect to these behavioral, hormonal and central neurochemical parameters.

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