Table 1.
Relationship | Possible mechanism | Species | Drug | References |
---|---|---|---|---|
A/D | VTA Cav1.3 channel mediated cocaine-related and depressive-like behavior through a NAc shell CP-AMPAR mechanism via GluA1 phosphorylation at S831 | C57BL/6 mice | Cocaine | Martinez-Rivera et al. (2017) |
D→A | Dopaminergic dysfunction in bulbectomized rats | OBX rats | CB1 receptor agonist WIN | Amchova et al. (2014) |
A/D | Dopaminergic transmission in the NAc via D1-like receptors | Rats | Morphine | Gao et al. (2012) |
A→D | DAT ↓ | Heroin-dependent subjects | Heroin | Liu et al. (2013) |
A/D | CHT heterozygosity → blunted DA elevations following systemic nicotine or cocaine administration. | CHT+/– mice, C57BL/6J mice | Cocaine nicotine | Dong et al. (2013) |
A | The expression profile of the HCN2 subunit in both glycosylated and non-glycosylated protein isoforms ↑ | Sprague–Dawley rats | Cocaine | Santos-Vera et al. (2013) |
D | Expression and function of the HCN2 in ChIs of NAc shell ↓ | p11 conditional knockout (cKO) mice and SDS mice | / | Cheng et al. (2019) |
A | Cocaine→p11 expression in the NAc↓, while p11 expression↑→cocaine conditioned place ↓ | p11 knockout mice | Cocaine | Arango-Lievano et al. (2014) |
D | The expression of p11↓→ depression | p11 knockout mice | / | Alexander et al. (2010) and Warner-Schmidt et al. (2012) |
A/D | Silencing of GSK3β in the NAc shell →excitability of TANs↓ | GSK3β knockdown rats | Cocaine | Crofton et al. (2017) |
A | mGluR5-mediated reduction in GluA2-containing AMPARs at NAc shell synapses | Adult male C57BL/6J mice | Cocaine | Benneyworth et al. (2019) |
A | mGluR5 antagonists → elevation of extracellular glutamate in the NAc↑ → therapeutic anti-cocaine effects | Rats | Cocaine | Li et al. (2018) |
D | mGluR5-mediated signaling in the NAc ↓ | mGluR5#x02212;/– mice | / | Shin et al. (2015) |
A/D | Blockade of the mGlu2/3 receptor in the NAc → the antidepressant-like effects | Sprague–Dawley rats | Methamphetamine | Iijima et al. (2013) |
A | mGluR2/3 ↓→ neural plasticity | Sprague–Dawley rats | Morphine | Qian et al. (2019) |
A | AMN082 → mGluR7(+) → the development and expression of cocaine and morphine sensitization, and the reciprocal cross-sensitization↓ | Male Swiss mice | Cocaine, Morphine | Jenda et al. (2015) |
D | AMN082 → mGluR7(+) → adenylate cyclase/protein kinase A activation ↓→the entry of Ca2+ through voltage-dependent Ca2+ channels ↓→ glutamate release ↓ | Male Sprague–Dawley rats | / | Wang et al. (2018) |
D → A | Activate the KOR→ inhibition of phasic dopamine signaling | Sprague–Dawley rats | The KOR agonist salvinorinA (salvA) | Ebner et al. (2010) |
D → A | Immediate dysphoric effect of the KOR agonist salvA coincides with sensitivity to cocaine reward net ↑. Delayed effect of salvA → basal hedonic state rebound ↑ coincides with sensitivity to cocaine reward net ↓ | Sprague–Dawley rats | Cocaine | Chartoff et al. (2016) |
A/D | Knockdown of Pdyn within the NAc → depression-like behavior and cocaine sensitization↓ | Wistar rats | Cocaine | Cohen et al. (2014) |
A → D | Morphine withdrawal → Prodynorphin mRNA and protein levels ↑ → depressive-like behaviors | Male C57BL/6J mice | Morphine | Zan et al. (2015) |
A/D | CREB activity ↑→ depression-like signs. Disruption of CREB activity → anti-depressant like effects and more sensitive to the rewarding effects of cocaine | Mice | Cocaine | Dinieri et al. (2009) |
D | ΔFosB induction in NAc is both a necessary and sufficient mechanism of resiliency and of antidepressant responses | Human/Mice | / | Vialou et al. (2010) |
A | Δ FosB is both necessary and sufficient for cocaine induction of CaMKIIα gene expression. Overexpression of Δ FosB in NAc increased behavioral responsiveness to cocaine is CaMKII dependent | Human/Rats | Cocaine | Robison et al. (2013) |
A/D indicates that it has a important role in both addiction (A) and depression (D), A → D indicates that addiction (A) induce depression (D), D → A indicates that depression (D) induce addiction (A).