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Important elements in the use of opiate analgesics are tolerance, dependence and withdrawal. A crucial question relates to the neuroanatomical circuits mediating dependence and abstinence. This group’s research demonstrated that affective or “emotional” signs of opioid withdrawal such as dysphoria and anxiety-like behavior are evoked following acute or occasional intermittent morphine treatment. These findings suggest that neural circuits mediating reward and affect may be sensitive to rapid opioid neuroadaptation. Recently, this group identified limbic and basal forebrain reward circuitry (e.g. amygdala, nucleus accumbens, bed nucleus of the stria terminalis) that mediate affective components of opioid withdrawal. Opioids in these limbic and basal forebrain nuclei produce analgesia, and these regions interact directly with well-defined supraspinal pain modulatory circuitry. It is hypothesized that neuroadaptation within these brain regions is responsible for affective signs of acute opioid withdrawal, and may also contribute to withdrawal-associated hyperalgesic states. An ultimate goal is to understand biological mediators of vulnerability to opioid dependence and addiction, with the working hypothesis that individual variability in the expression of withdrawal signs following an initial exposure to opioids might be one factor that imparts increased vulnerability. Thus, acute opioid dependence may have special relevance to the switch from initial use of an opioid to compulsive use. Finally, the work is relevant to understanding how affect and mood influence perception of pain, and conversely how pain states influence/affect mood (e.g. depression in chronic pain patients). The trainees would explore the relationship between these supraspinal systems mediating affective withdrawal and hyperalgesic states to delineate functional pathways linking structures participating in the expression of individual signs of withdrawal.
References (selected 75 publications)
Paulus MP, Tapert SF, Schulteis G.The role of interoception and alliesthesia in addiction. Pharmacol Biochem Behav. 94:1-7, 2009
Schulteis G, Chiang D, Archer C. Relative potency of the opioid antagonists naloxone and 6-alpha-naloxol to precipitate withdrawal from acute morphine dependence varies with time post-antagonist. Pharmacol Biochem Behav.;92:157-63,2009.
Schulteis G, Archer C, Tapert SF, Frank LR. Intermittent binge alcohol exposure during the periadolescent period induces spatial working memory deficits in young adult rats.Alcohol. 42:459-67, 2008
Wallace MS, Schulteis G.Effect of chronic oral gabapentin on capsaicin-induced pain and hyperalgesia: a double-blind, placebo-controlled, crossover study. Clin J Pain.;24:544-9, 2008.
Leung AY, Kim SJ, Schulteis G, Yaksh T.The effect of acupuncture duration on analgesia and peripheral sensory thresholds. BMC Complement Altern Med. 1;8:18, 2008
Zhang, Z., & Schulteis, G. Withdrawal from acute morphine dependence is accompanied by increased anxiety-like behavior in the elevated plus maze. Pharmacology Biochemistry and Behavior, 89, 392-403, 2008
Criner, S., Liu, J., & Schulteis, G.. Rapid neuroadaptation in the nucleus accumbens and bed nucleus of the stria terminalis mediates suppression of operant responding during withdrawal from acute opioid dependence. Neuroscience, 144, 1436-1446.2007.
Schulteis G, Liu J. Brain reward deficits accompany withdrawal (hangover) from acute ethanol in rats Alcohol 39:21-28, 2006.
Schulteis G, Liu J, Amital N, Tzeng S. Context- and cue-conditioned potentiation of acute morphine dependence and withdrawal. Pharmacol Biochem Behav 82:82-89, 2005.