ABSTRACT
Over the past three decades, evidence pointing to bi-directional communication between the nervous system and the immune system has been clearly established. Several lines of research support this contention, including the following evidence: (1) lesions in thecentral nervous system (CNS) lead to
altered immune responses (Katayama et al., 1987;Felten et al., 1991); (2) immune responses can be classically conditioned (Ader and Cohen,1975, 2001), involving a CNS learning paradigm; (3) primary and secondary lymphoidorgans are innervated with noradrenergic (NA) sympathetic nerve fibres and otherpeptidergic nerve fibres (Felten and Felten, 1991; Bellinger et al., 2001); (4) cells of theimmune system possess receptors for a host of hormones and neurotransmitters, includingreceptors for catecholamines, ACTH, opioid peptides, substance P, and vasoactive intestinal peptide (VIP), to name a few (Plaut, 1987; Carr and Blalock, 1991; Madden et al.,1995); (5) functions of these same immune system cells that possess receptors are alteredby the appropriate hormones and neurotransmitters (see Madden and Felten, 1995); and (6)cytokines produced in the periphery can affect the brain, producing illness behaviour andactivation of neuroendocrine and autonomic stress-related circuits (Hori et al., 2001; Maier et al., 200l; Rivier, 2001).
