Differential behavioral effects following microinjection of an NMDA antagonist into nucleus accumbens subregions

1994 ◽  
Vol 116 (1) ◽  
pp. 65-72 ◽  
Author(s):  
Carmen S. Maldonado-Irizarry ◽  
Ann E. Kelley
Keyword(s):  
Nucleus Accumbens ◽  
Nmda Antagonist ◽  
Behavioral Effects

scholarly journals Early-life adversity selectively impairs α2-GABAA receptor expression in the mouse nucleus accumbens and influences the behavioral effects of cocaine

2018 ◽  
Vol 141 ◽  
pp. 98-112 ◽  
Author(s):  
Scott J. Mitchell ◽  
Edward P. Maguire ◽  
Linda Cunningham ◽  
Benjamin G. Gunn ◽  
Matthias Linke ◽  
...  
Keyword(s):  
Nucleus Accumbens ◽  
Gabaa Receptor ◽  
Early Life ◽  
Receptor Expression ◽  
Behavioral Effects ◽  
Early Life Adversity

scholarly journals Chronic Chemogenetic Stimulation of the Nucleus Accumbens Produces Lasting Reductions in Binge Drinking and Ameliorates Alcohol-Related Morphological and Transcriptional Changes

2020 ◽  
Vol 10 (2) ◽  
pp. 109 ◽  
Author(s):  
Dar’ya Y. Pozhidayeva ◽  
Sean P. Farris ◽  
Calla M. Goeke ◽  
Evan J. Firsick ◽  
Kayla G. Townsley ◽  
...  
Keyword(s):  
Nucleus Accumbens ◽  
Binge Drinking ◽  
Neuronal Morphology ◽  
Behavioral Effects ◽  
Designer Drugs ◽  
Molecular Pathways ◽  
Epigenetic Mechanisms ◽  
Transcriptional Changes ◽  
Induced Changes ◽  
Stimulation Of

Binge drinking is a dangerous pattern of behavior. We tested whether chronically manipulating nucleus accumbens (NAc) activity (via clozapine-N-oxide (CNO) and Designer Receptors Exclusively Activated by Designer Drugs (DREADD)) could produce lasting effects on ethanol binge-like drinking in mice selectively bred to drink to intoxication. We found chronically increasing NAc activity (4 weeks, via CNO and the excitatory DREADD, hM3Dq) decreased binge-like drinking, but did not observe CNO-induced changes in drinking with the inhibitory DREADD, hM4Di. The CNO/hM3Dq-induced reduction in ethanol drinking persisted for at least one week, suggesting adaptive neuroplasticity via transcriptional and epigenetic mechanisms. Therefore, we defined this plasticity at the morphological and transcriptomic levels. We found that chronic binge drinking (6 weeks) altered neuronal morphology in the NAc, an effect that was ameliorated with CNO/hM3Dq. Moreover, we detected significant changes in expression of several plasticity-related genes with binge drinking that were ameliorated with CNO treatment (e.g., Hdac4). Lastly, we found that LMK235, an HDAC4/5 inhibitor, reduced binge-like drinking. Thus, we were able to target specific molecular pathways using pharmacology to mimic the behavioral effects of DREADDs.

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