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    • Finally we expected that the cannabis only group

    2018-11-07

    Finally, we expected that the cannabis-only group would show increased reward responding in the NAcc compared to the tobacco-only and control groups. However, no differences emerged between the cannabis-only group and any of the other groups. Importantly, cannabis use is becoming increasingly normative in adolescent populations, particularly among socioeconomically disadvantaged youth like the high-risk youth in this sample (Redonnet et al., 2012). Thus, examining the relationship between cannabis use and developing bradykinin receptor antagonist structure and function is especially timely. This is an area of great current debate (e.g., Batalla et al., 2013; Vaidya et al., 2012; Weiland et al., 2015; Filbey et al., 2014; Gilman et al., 2014), and it is not clear whether and/or to what extent cannabis use is associated with MID response in adolescents.
    Conflict of interest
    Acknowledgements This material is based upon work supported by the National Science Foundation Graduate Research Fellowship Program under Grant No. DGE 1144083 awarded to Hollis Karoly. This research was also supported by 1R01NR013332-01 (MPIs: Feldstein Ewing and Bryan). The authors acknowledge Dr. Francesca Filbey for providing the version of the MID task used in this project, as well as for descriptions of task procedures/parameters, and to Dr. James Bjork for his consultation on task design.
    Introduction With more than 25% of high school seniors reporting recent use and 6.5% of 12th graders being daily users (Johnston et al., 2014), marijuana (MJ) is the most frequently used illicit substance among adolescents. Across all age groups over 70% of new drug initiates start with using MJ at an average age of 18 years (SAMHSA, 2014). Indeed, the scope of MJ use prevalence is of great public interest, as MJ use in early adolescence is associated with increased risk of greater substance use, legal problems, disrupting education, injuries/medical problems, developing psychopathology, cognitive changes and chronic psychosocial struggles (CASA, 2011; Fergusson and Horwood, 1997; Fergusson et al., 1996; Patton et al., 2002). Taken together, rates of MJ use are suggestive of an epidemic based in adolescence, which is concerning not just due to societal cost, but also due to the potential to offset sensitive brain development during this period. Despite its prevalence, the impact of MJ use on adolescent brain development is not fully known. Important neuromaturational processes during adolescence through young adulthood are believed to bring about improved higher-order cognition by refining neural systems locally and globally through white and gray matter development (Casey et al., 2005; Giedd, 2008; Paus, 2005). In general, gray matter reductions and cortical thinning coincide with increased white matter volume and organization through adolescence and young adulthood, suggestive of synaptic pruning and axonal myelination (Giorgio et al., 2010; Gogtay et al., 2004; Hasan et al., 2007; Lebel et al., 2010; Shaw et al., 2008). The endogenous cannabinoid (CB) system is also immature during adolescence (Anavi-Goffer and Mulder, 2009; Verdurand et al., 2011). In an animal model (Verdurand et al., 2011) imaged CB1 receptor binding using PET and found relatively lower activation of CB1 receptors in adolescent rats compared to adult rats in brain areas including those in the frontal cortex, temporal lobe (hippocampus and amygdala) and sub-cortical regions including striatal regions, thalamus, hypothalamus, superior colliculus. Thus, adolescence represents a developmental period with vulnerability to structural and functional changes due to exogenous MJ exposure. Adolescent MJ use has the potential to cause structural and functional changes in the brain by altering cannabinoid signaling. One possible mechanism would be blunt neurotoxic influence. For example, delta9-tetrahydrocannabinol (THC), the primary psychoactive component in MJ that binds CB1 receptors, is reported to cause cell shrinkage and damage DNA strands in THC-treated neuron cultures (Chan et al., 1998). This may be the mechanism by which smaller volumes have been observed in individuals exposed to cannabis during adolescence (Battistella et al., 2014). However, it is more likely that MJ exerts its influence on brain development indirectly. The cannabinoid system plays a role in modulating other neurotransmitters, including gamma-aminobutyric acid (GABA), glutamate and monoamines (Lopez-Moreno et al., 2008). Specifically, activation of CB1 receptors is associated with down-regulating inhibitory GABAergic transmission in cortical interneurons during adolescence (Caballero and Tseng, 2012; Cass et al., 2014). In addition, CB signaling inhibits microglia function (Walter et al., 2003). These two points are important because cortical pruning processes involve glial-mediated synaptic elimination and altering the excitatory/inhibitory balance is liable to disrupt the selective tagging and preserving synapses (Selemon, 2013). The impact of this indirect influence on the developing brain may be in the observations of abnormal connectivity in those who began MJ use in adolescence (Jacobus et al., 2009). Evidence from human neuroimaging studies lends greater support to MJ-related disruptions to brain development.