Biological psychiatry
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Biological psychiatry · Mar 2015
Chronic cannabinoid receptor 2 activation reverses paclitaxel neuropathy without tolerance or cannabinoid receptor 1-dependent withdrawal.
Mixed cannabinoid receptor 1 and 2 (CB1 and CB2) agonists such as Δ(9)-tetrahydrocannabinol (Δ(9)-THC) can produce tolerance, physical withdrawal, and unwanted CB1-mediated central nervous system side effects. Whether repeated systemic administration of a CB2-preferring agonist engages CB1 receptors or produces CB1-mediated side effects is unknown. ⋯ Our results highlight the potential of prolonged use of CB2 agonists for managing chemotherapy-induced allodynia with a favorable therapeutic ratio marked by sustained efficacy and absence of tolerance, physical withdrawal, or CB1-mediated side effects.
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Biological psychiatry · Mar 2015
ReviewAnticipatory reward processing in addicted populations: a focus on the monetary incentive delay task.
Advances in brain imaging techniques have allowed neurobiological research to temporally analyze signals coding for the anticipation of reward. In addicted populations, both hyporesponsiveness and hyperresponsiveness of brain regions (e.g., ventral striatum) implicated in drug effects and reward system processing have been reported during anticipation of generalized reward. We discuss the current state of knowledge of reward processing in addictive disorders from a widely used and validated task: the monetary incentive delay task. ⋯ Divergent results across abstinent, recreationally using, and addicted populations demonstrate complexities in interpreting findings. Future studies would benefit from focusing on characterizing how impulsivity and other addiction-related features relate to anticipatory striatal signaling over time. Additionally, identifying how anticipatory signals recover or adjust after protracted abstinence will be important in understanding recovery processes.
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Biological psychiatry · Feb 2015
ReviewDepression, neuroimaging and connectomics: a selective overview.
Depression is a multifactorial disorder with clinically heterogeneous features involving disturbances of mood and cognitive function. Noninvasive neuroimaging studies have provided rich evidence that these behavioral deficits in depression are associated with structural and functional abnormalities in specific regions and connections. Recent advances in brain connectomics through the use of graph theory highlight disrupted topological organization of large-scale functional and structural brain networks in depression, involving global topology (e.g., local clustering, shortest-path lengths, and global and local efficiencies), modular structure, and network hubs. ⋯ Here, we summarize the current findings and historical understanding of structural and functional connectomes in depression, focusing on graph analyses of depressive brain networks. We also consider methodological factors such as sample heterogeneity and poor test-retest reliability of recordings due to physiological, head motion, and imaging artifacts to discuss result inconsistencies among studies. We conclude with suggestions for future research directions on the emerging field of imaging connectomics in depression.