may be related to the observation that activation of cytokine signaling (e.g., by lipopolysaccharide) produces a ‘sickness’ behavior that includes decreases in reward function (measured by intracranial self-stimulation) (Borowski et al., 1998; Henry et al., 2008) similar to that observed in alcoholism. A possible neurochemical mechanism for neuroimmune regulation of drinking behavior is activation of glutamatergic transmission as Crews et al. (2006) proposed that cytokines can induce a hyperglutamatergic state and Spanagel et al. (2005) proposed that a hyperglutamate state drives drinking behavior. Reversal of the dysregulation of glutamatergic and reward function produced by alcohol and other drugs by neuroimmune signals may provide new opportunities for pharmacotherapy of alcoholism and other addictions.
