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Background And Purpose: Currently, there is no effective drug to treat cocaine-use disorder, which affects millions of people worldwide. Benzodiazepines are potential therapeutic candidates, as microdialysis and voltammetry studies have shown that they can decrease dopamine concentrations in the nucleus accumbens of rodents and block the increase in dopamine levels and appetitive 50-kHz ultrasonic vocalizations (USVs) induced by amphetamine in rats.
Experimental Approach: Here, we tested whether administration of 2.5-mg·kg diazepam (i.p.) in adult male rats could block the effects of 20-mg·kg cocaine (i.p.) on electrically evoked phasic dopamine signals in the nucleus accumbens measured by fast-scan cyclic voltammetry, as well as 50-kHz USV and locomotor activity.
Key Results: Cocaine injection increased evoked dopamine signals up to threefold within 5 min, and the increase was significantly higher than baseline for at least 75 min. The injection of diazepam, 5 min after cocaine, attenuated the cocaine effect by nearly 50%, and this attenuation was maintained for at least 40 min. Behaviourally, cocaine increased the number of appetitive 50-kHz calls by about 12-fold. Diazepam significantly blocked this effect for the entire duration of the session. Also, cocaine-treated rats were more active than controls and diazepam significantly attenuated cocaine-induced locomotion, by up to 50%.
Conclusion And Implications: These results suggest that the neurochemical and psychostimulant effects of cocaine can be mitigated by diazepam.
Linked Articles: This article is part of a themed issue on Building Bridges in Neuropharmacology. To view the other articles in this section visit http://onlinelibrary.wiley.com/doi/10.1111/bph.v179.8/issuetoc.
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http://dx.doi.org/10.1111/bph.15658 | DOI Listing |
J Affect Disord
December 2024
School of Health and Wellbeing, University of Glasgow, Glasgow, UK; Division of Psychiatry, Centre for Clinical Brain Sciences, University of Edinburgh, Edinburgh, UK.
Whether depression and poor sleep interact or have statistically independent associations with brain structure and its change over time is not known. Within a subset of UK Biobank participants with neuroimaging and subjective and/or objective sleep data (n = 28,351), we examined associations between lifetime depression and sleep disruption and their interaction with structural neuroimaging measures, both cross-sectionally and longitudinally. Sleep variables were: self-reported insomnia and difficulty getting up; actigraphy-derived short sleep (<7 h); sustained inactivity bouts during daytime (SIBD); and sleep efficiency.
View Article and Find Full Text PDFInt J Neuropsychopharmacol
December 2024
National Clinical Research Center for Geriatric Disorders, Xiangya Hospital, Central South University, Changsha, China.
Background: Understanding drug addiction as a disorder of maladaptive learning, where drug-associated or environmental cues trigger drug cravings and seeking, is crucial for developing effective treatments. Actin polymerization, a biochemical process, plays a crucial role in drug-related memory formation, particularly evident in conditioned place preference (CPP) paradigms involving drugs like morphine and methamphetamine. However, the role of actin polymerization in the reconsolidation of heroin-associated memories remains understudied.
View Article and Find Full Text PDFPsychopharmacology (Berl)
December 2024
Bowles Center for Alcohol Studies, Department of Psychiatry, School of Medicine, The University of North Carolina at Chapel Hill, Chapel Hill, NC, 27599, USA.
Rationale: The positive reinforcing effects of alcohol (ethanol) drive repetitive use and contribute to alcohol use disorder (AUD). Ethanol alters the expression of glutamate AMPA receptor (AMPAR) subunits in reward-related brain regions, but the extent to which this effect regulates ethanol's reinforcing properties is unclear.
Objective: This study investigates whether ethanol self-administration changes AMPAR subunit expression and synaptic activity in the nucleus accumbens core (AcbC) to regulate ethanol's reinforcing effects in male C57BL/6 J mice.
bioRxiv
December 2024
Department of Molecular and Medical Pharmacology, Geffen School of Medicine, UCLA, Los Angeles, CA 90095.
To identify genes involved in regulating the behavioral and brain transcriptomic response to the potentially addictive drug cocaine, we performed genome-wide association studies (GWASs) for intravenous self-administration of cocaine or saline (as a control) over 10 days using a panel of inbred and recombinant inbred mice. A linear mixed model increased statistical power for these longitudinal data and identified 145 loci for responding when saline only was delivered, compared to 17 for the corresponding cocaine GWAS. Only one locus overlapped.
View Article and Find Full Text PDFAm J Geriatr Psychiatry
December 2024
Weill Cornell Institute of Geriatric Psychiatry (NS, LWV, ZM, GSA, FMG), Weill Cornell Medicine, White Plains, NY.
Background: The course of late-life depression is associated with functioning of multiple brain networks. Understanding the brain mechanisms associated with response to psychotherapy can inform treatment development and a personalized treatment approach. This study examined how activation of key regions of the salience network, default mode network and reward systems is associated with response to psychotherapies for late-life depression.
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