Altered corticolimbic control of the nucleus accumbens by chronic Δ⁹-Tetrahydrocannabinol Exposure

@article{HWANG2019,

title = {Altered corticolimbic control of the nucleus accumbens by chronic Δ9-THC-Tetrahydrocannabinol Exposure},

author = {Eun-Kyung Hwang and Carl R Lupica},

url = {http://www.sciencedirect.com/science/article/pii/S0006322319315598},

doi = {10.1016/j.biopsych.2019.07.024},

issn = {0006-3223},

year  = {2019},

date = {2019-08-06},

journal = {Biological Psychiatry},

abstract = {Background 

Decriminalization, legalization and expansion of medical cannabis has led to an increase in its use and availability of high-potency strains. Cannabis potency is determined by the concentration of Δ9-tetrahydrocannabinol (Δ9-THC), a psychoactive constituent that activates CB1 and CB2 cannabinoid receptors (CB1R, CB2R), and use of high-potency cannabis is associated with cannabis use disorder (CUD) and increased susceptibility to psychiatric illness. The nucleus accumbens (NAc) is part of a brain reward circuit affected by Δ9-THC through modulation of glutamate afferents arising from corticolimbic brain areas implicated in drug addiction and psychiatric disorders. Moreover, brain imaging studies show alterations in corticolimbic and NAc properties in human cannabis users. 

Methods 

Using in vitro electrophysiology and optogenetics, we examine how Δ9-THC alters corticolimbic input to the NAc in rats. 

Results 

We find that chronic Δ9-THC weakens prefrontal cortex glutamate input to the NAc shell (NAcs) and strengthens input from basolateral amygdala and ventral hippocampus. Further, whereas chronic Δ9-THC had no effect on net strength of glutamatergic input to NAcs arising from midbrain DA neurons, it alters fundamental properties of these synapses. 

Conclusions 

Chronic Δ9-THC shifts control of the NAcs from cortical to limbic input likely contributing to cognitive and psychiatric dysfunction associated with cannabis use.},

keywords = {},

pubstate = {published},

tppubtype = {article}

}