The distinctive nature of adolescent behaviors, such as alteration in anxiety, sensitivity to stress and perception of reward and aversion quite possibly contribute, in part, to adolescent personality characteristics associate with increased risk for drug abuse. Moreover, early exposure to drugs of abuse correlates with the increased probability of developing a drug addiction and other psychiatric disorders during adulthood. These factors are probably the result of the susceptibility to disruption of the normal ontogenesis of the emotional/ motivational system and of brain sensitization processes (i.e. long-lasting plasticity) by neurochemical adaptations resulting from the administration of drugs of abuse. The opioid system has been suggested to have a fundamental role in the neurochemical adaptation leading to drug addiction to opiates as well as other drugs of abuse. Additionally, the opioid system is known to be involved in shaping emotional state, e. g., hedonic tone, anxiety and stress, reward and aversion. Thus, the opioid system could have a direct (drug of abuse induced neurochemical adaptations) and indirect (contribution to the altered emotional response) effect on both drug abuse during adolescence and on the long-term consequences of early drug exposure. There is histological literature indicating that the opioid system, including brain regions and receptor systems mediating opioid and emotional processing are not fully mature until mid to late adolescence. However, there is a very limited literature targeting the functionality of the opioid system during this period. Therefore, the purpose of this project is to broaden our understanding of the opioid system during adolescence with respect to function and ontogenesis, and to build a foundation for future studies seeking to uncover the molecular mechanisms underlying such ontogenesis and functionality.
The specific aims of this study are to determine the contribution of age (adolescent vs. adult), gender, and social condition (representing emotional status) to the activation of cellular signaling molecules (such as kinases and immediate early genes) by acute and repeated morphine exposure. ? ? ?
| Hodgson, Stephen R; Hofford, Rebecca S; Roberts, Kris W et al. (2010) Sex differences in affective response to opioid withdrawal during adolescence. J Psychopharmacol 24:1411-7 |
| Hodgson, S R; Hofford, R S; Buckman, S G et al. (2010) Morphine-induced stereotyped thigmotaxis could appear as enhanced fear and anxiety in some behavioural tests. J Psychopharmacol 24:875-80 |
| Hodgson, Stephen R; Hofford, Rebecca S; Roberts, Kris W et al. (2010) Socially induced morphine pseudosensitization in adolescent mice. Behav Pharmacol 21:112-20 |
| Hodgson, Stephen R; Hofford, Rebecca S; Wellman, Paul J et al. (2009) Different affective response to opioid withdrawal in adolescent and adult mice. Life Sci 84:52-60 |
| Buckman, Sam G; Hodgson, Stephen R; Hofford, Rebecca S et al. (2009) Increased elevated plus maze open-arm time in mice during spontaneous morphine withdrawal. Behav Brain Res 197:454-6 |
| Hofford, Rebecca S; Hodgson, Stephen R; Roberts, Kris W et al. (2009) Extracellular signal-regulated kinase activation in the amygdala mediates elevated plus maze behavior during opioid withdrawal. Behav Pharmacol 20:576-83 |
| Hodgson, Stephen R; Hofford, Rebecca S; Norris, Chris J et al. (2008) Increased elevated plus maze open-arm time in mice during naloxone-precipitated morphine withdrawal. Behav Pharmacol 19:805-11 |
