Interleukin-2 decreases accumbal dopamine efflux and responding for rewarding lateral hypothalamic stimulation

@article{citeulike:2483849, abstract = {Systemic administration of interleukin-2 (IL-2) provoked marked alterations of responding for rewarding brain stimulation from the medial forebrain bundle (MFB). In particular, when animals were tested for ICSS immediately following IL-2 treatment only a modest disturbance of responding was evident. However, if animals were subsequently exposed to repeated daily ICSS sessions (24-168 h) in the drug-free state, rightward shifts in the rate intensity functions and significant increases in reward thresholds were apparent. These results were dependent upon the presence of IL-2 during the initial ICSS session. If animals were tested for ICSS 24 h after IL-2 administration, without an intervening test, performance was unaffected. Evaluation of nonreinforced behavior after IL-2 treatment revealed that ICSS remained under stimulus control and the cytokine did not provoke reward-unrelated performance deficits. Dopamine (DA) activity in the nucleus accumbens has been implicated in goal-directed responding to positively reinforcing stimuli and in the present investigation, using in vivo microdialysis, it was observed that IL-2 markedly reduced DA release from this region. It was suggested that the protracted consequences of IL-2 on ICSS likely do not involve motoric, soporific, attentional or cognitive changes, but may be attributable to its specific actions on motivational arousal, possibly engendered by the cytokine-induced diminution of accumbal DA efflux.}, author = {Anisman, Hymie and Kokkinidis, L. and Merali, Z. }, citeulike-article-id = {2483849}, doi = {10.1016/0006-8993(96)00460-X}, journal = {Brain Research}, keywords = {cytokines, dopamine, hypothalamus, immunology, neuromodulation}, month = {August}, number = {1-2}, pages = {1--11}, posted-at = {2008-03-07 12:29:52}, priority = {0}, title = {Interleukin-2 decreases accumbal dopamine efflux and responding for rewarding lateral hypothalamic stimulation}, url = {http://dx.doi.org/10.1016/0006-8993(96)00460-X}, volume = {731}, year = {1996} }

TY - JOUR ID - citeulike:2483849 L3 - citeulike-article-id:2483849 TI - Interleukin-2 decreases accumbal dopamine efflux and responding for rewarding lateral hypothalamic stimulation JF - Brain Research VL - 731 IS - 1-2 SP - 1 EP - 11 N2 - Systemic administration of interleukin-2 (IL-2) provoked marked alterations of responding for rewarding brain stimulation from the medial forebrain bundle (MFB). In particular, when animals were tested for ICSS immediately following IL-2 treatment only a modest disturbance of responding was evident. However, if animals were subsequently exposed to repeated daily ICSS sessions (24-168 h) in the drug-free state, rightward shifts in the rate intensity functions and significant increases in reward thresholds were apparent. These results were dependent upon the presence of IL-2 during the initial ICSS session. If animals were tested for ICSS 24 h after IL-2 administration, without an intervening test, performance was unaffected. Evaluation of nonreinforced behavior after IL-2 treatment revealed that ICSS remained under stimulus control and the cytokine did not provoke reward-unrelated performance deficits. Dopamine (DA) activity in the nucleus accumbens has been implicated in goal-directed responding to positively reinforcing stimuli and in the present investigation, using in vivo microdialysis, it was observed that IL-2 markedly reduced DA release from this region. It was suggested that the protracted consequences of IL-2 on ICSS likely do not involve motoric, soporific, attentional or cognitive changes, but may be attributable to its specific actions on motivational arousal, possibly engendered by the cytokine-induced diminution of accumbal DA efflux. KW - cytokines KW - dopamine KW - hypothalamus KW - immunology KW - neuromodulation AU - Anisman, Hymie AU - Kokkinidis, L AU - Merali, Z PY - 1996/08/26/ UR - http://dx.doi.org/10.1016/0006-8993(96)00460-X ER -