| Addiction Biology Volume 24, Issue 5 Pages: 847-1118 September 2019 |
ISSUE INFORMATION
PRECLINICAL STUDIES
Pages: 849-859 | First Published: 19 June 2018
Pages: 860-873 | First Published: 11 June 2018
We investigated the effect of endogenous brain‐derived neurotrophic factor (BDNF) secretion on cocaine seeking in the NAcore and discovered that BDNF‐induced tropomyosin receptor kinase B (TrkB) signaling during cued‐reinstatement promoted within session extinction and decreased cocaine seeking. We were able to pharmacologically recreate the inhibition of cocaine seeking by acutely microinfusing BDNF in the NAcore before cue‐induced reinstatement. This effect was specific to cocaine seeking and did not alter inactive lever pressing, spontaneous or cocaine‐induced locomotion, or sucrose seeking.
Pages: 874-885 | First Published: 27 June 2018
Kratom has received considerable attention due to the potential for abuse and the potential to reduce opiate intake. We investigated whether the kratom alkaloids, mitragynine (MG) and 7‐hydroxymitragynine (7‐HMG) would substitute for morphine and engender and maintain responding. We conclude that MG does not have abuse potential and reduces morphine intake, desired characteristics of candidate pharmacotherapies for opiate addiction and withdrawal, whereas 7‐HMG has a high abuse potential and may also increase the intake of other opiates.
Pages: 886-897 | First Published: 09 July 2018
Galanin receptor‐3 has been linked to alcohol use disorders as well as alcohol seeking in rodent models. Antagonism of this receptor via the selective antagonist, SNAP 37889, has previously been shown to reduce alcohol consumption in rodents. In the current study, we show that galanin receptor‐3 knockout mice have an increased preference for ethanol as observed by a two‐bottle free choice continuous access paradigm. A battery of behavioral tests revealed intact cognitive and locomotor function.
Pages: 898-907 | First Published: 04 September 2018
Pages: 908-920 | First Published: 18 July 2018
Reinstatement of alcohol place preference activates mammalian target of rapamycin complex 1 (mTORC1) in the nucleus accumbens of mice, which in turn initiates the translation of the synaptic protein collapsin response mediator protein‐2 (CRMP‐2). Inhibition of mTORC1 or CRMP‐2 by using the Food and Drug Administration‐approved drugs rapamycin and lacosamide attenuates alcohol‐priming‐induced reinstatement of conditioned place preference. Our results reveal that mTORC1 and its downstream target CRMP‐2 contribute to mechanisms underlying reinstatement of alcohol reward seeking.
Pages: 921-934 | First Published: 11 October 2018
Disorders associated with cannabis use are often accompanied by sleep disturbances. Starting from the hypothesis that microglial cells could be implicated in addictions through acting on circadian rhythm, impact of CBD and THC on the expression of clock genes has been studied in microglial cells. This work highlighted that CBD but not THC regulates core clock genes in these cells, which is in accordance with international literature suggesting a CBD‐stimulating effect at low concentration.
Pages: 935-945 | First Published: 08 August 2018
Pages: 946-957 | First Published: 09 August 2018
Per2‐overexpressed mice showed decreased locomotor sensitization and rewarding effects of methamphetamine (METH) compared to wildtype mice, whereas the opposite was observed in Per2 knockout mice. Additionally, these transgenic mice exhibited altered expression levels of dopamine‐related genes after repeated METH administration. Taken together, Per2 expression levels may influence the addictive effects of METH through the dopaminergic system in the striatum of mice.
Pages: 958-968 | First Published: 14 August 2018
Social stress and drug availability are directly linked to relapse in patients with substance use disorder. We developed a rat model of social stress‐potentiated methamphetamine (METH) seeking where rats experiencing both a social stressor and low dose METH prior to reinstatement lever press at a higher rate than rats exposed to social stress or METH alone. We link the basolateral amygdala to this effect and present this model as a tool for further mechanistic dissection and therapeutic discovery.
Pages: 969-980 | First Published: 14 August 2018
Young adult mice exposed to enriched environment (EE) significantly recover recognition memory (novel object recognition test‐NORT), spatial memory (novel object location test‐NOLT), coordination skills (rotarod) and balance (beam walking test) impaired after adolescent ethanol (EtOH) intake. The results indicate that EE exerts positive effects on the long‐term cognitive and motor deficits as a result of EtOH consumption during adolescence.
Pages: 981-993 | First Published: 17 October 2018
Pages: 994-1007 | First Published: 21 September 2018
Intranasal noninvasive administration of human mesenchymal stem cell exosomes markedly inhibits (80–85 percent) chronic ethanol intake by alcohol‐preferring rats and fully reversed ethanol‐induced oxidative stress and neuroinflammation. Exosomes also inhibited (50–60 percent) relapse binge‐drinking following chronic ethanol intake, deprivation and ethanol reaccess.
Pages: 1008-1018 | First Published: 25 June 2019
In a longitudinal study using the SNI model of neuropathic pain in mice, we show the co‐occurrence of chronic pain and several alcohol‐related behaviors and phenomena. This work sheds light onto the variables determining sex‐dependent co‐occurrence of chronic pain and alcohol use and proposes that a lower sensitivity to the intoxicating effects of alcohol together with the ability of alcohol to reduce the negative affective component of pain may explain the higher co‐occurrence of AUD in male chronic pain patients.
TRANSLATIONAL STUDY
Pages: 1019-1033 | First Published: 12 September 2018
There was a negative correlation between plasma BDNF and cognition deficit in alcohol patients. Hippocampal Bdnf levels and recognition memory negatively correlated in alcohol‐exposed rats during adolescence, an effect that was associated with a neurogenic regulator ERK2 deactivation. Early alcohol‐induced cognitive decline is related to BDNF signaling deficits.
CLINICAL STUDIES
Pages: 1034-1043 | First Published: 08 August 2018
Self‐efficacy is a strong predictor of outcomes in the addictions literature but has been questioned as either being a cause or reflection of behaviour change. Using path analyses, we demonstrate a bidirectional and reciprocal relationship between smoking cessation self‐efficacy and smoking behaviour during the treatment phase of a randomized control trial. Changes for both self‐efficacy and smoking affected subsequent scores, with scores on both measures associated with cessation outcomes at week 10.
Pages: 1044-1055 | First Published: 17 October 2018
Aging (50–60 years old) regular cocaine smokers had pronounced problems in daily social function relative to demographically matched controls, assessed by both their own and their peers' reports. They had stronger amygdala responses to social threat versus control stimuli, with no other differences in social processing or cognition. Aging cocaine users appear to have marked, generalized difficulties in ‘real‐world’ interpersonal function but largely intact social processing on laboratory‐based measures when compared with appropriately matched controls and tested under well‐controlled conditions.
Pages: 1056-1065 | First Published: 04 October 2018
Using established DNA methylation sites, cg05575921 and cg03636183, from blood samples as a criterion standard for smoking behavior, we compared three candidate electronic medical record (EMR) smoking metrics based on longitudinal EMR text notes: most recent, modal, and trajectories using data from the Veterans Aging Cohort Study Biomarker Cohort (VACS‐BC). Among 728 individuals in the VACS‐BC, both DNA methylation sites were associated with all three EMR summary metrics, and the strongest association with both methylation sites was observed for trajectories.
HUMAN NEUROIMAGING STUDIES
Pages: 1066-1076 | First Published: 09 July 2018
Ghrelin has been shown to be involved in the pathophysiology of alcohol dependence, affecting alcohol self‐administration and craving. Alcohol‐induced brain response in a network of brain clusters, including the right and left ventral striata, showed a significant positive association with acylated ghrelin plasma concentration, which was significantly associated with craving. Mediation analyses showed that the association between acylated ghrelin plasma concentration and alcohol craving is mediated by a cue‐induced brain response in the ventral striatum.
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