Transcriptional Profile of Exercise-Induced Protection Against Relapse to Cocaine Seeking in a Rat Model

Towers, Eleanor Blair; Shapiro, Daniel; Abel, Jean M.; Bakhti-Suroosh, Anousheh; Kupkova, Kristyna; Auble, David T.; Grant, Patrick A.; Lynch, Wendy J.

doi:10.1016/j.bpsgos.2023.01.007

Cited by 1 publication

(2 citation statements)

References 88 publications

(130 reference statements)

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“…Similarly, SLC9A3R1, a regulator of vesicle-mediated transport, also was down-regulated. These proteins have been previously highlighted in CUD research (65)(66)(67)(68)(69). The observed modulation in membrane Fig.…”

Section: Discussionmentioning

confidence: 65%

“…A detailed exploration of the transporter activity cluster revealed several proteins with known associations to cocaine withdrawal, including GRIN2A (glutamate receptor ionotropic, NMDA 2A), ANK2 (ankyrin-2), and cyclin-dependent kinase 5 (CDK5) (Fig. 5E) ( 65 – 68 ). The cluster delineating the regulation of transport in down-regulated membrane proteins during withdrawal also offered corroborative insights.…”

Section: Resultsmentioning

confidence: 99%

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Decoding cocaine-induced proteomic adaptations in the mouse nucleus accumbens

Mews,

Sosnick,

Gurung

et al. 2024

Sci. Signal.

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Cocaine use disorder (CUD) is a chronic neuropsychiatric condition that results from enduring cellular and molecular adaptations. Among substance use disorders, CUD is notable for its rising prevalence and the lack of approved pharmacotherapies. The nucleus accumbens (NAc), a region that is integral to the brain’s reward circuitry, plays a crucial role in the initiation and continuation of maladaptive behaviors that are intrinsic to CUD. Leveraging advancements in neuroproteomics, we undertook a proteomic analysis that spanned membrane, cytosolic, nuclear, and chromatin compartments of the NAc in a mouse model. The results unveiled immediate and sustained proteomic modifications after cocaine exposure and during prolonged withdrawal. We identified congruent protein regulatory patterns during initial cocaine exposure and reexposure after withdrawal, which contrasted with distinct patterns during withdrawal. Pronounced proteomic shifts within the membrane compartment indicated adaptive and long-lasting molecular responses prompted by cocaine withdrawal. In addition, we identified potential protein translocation events between soluble-nuclear and chromatin-bound compartments, thus providing insight into intracellular protein dynamics after cocaine exposure. Together, our findings illuminate the intricate proteomic landscape that is altered in the NAc by cocaine use and provide a dataset for future research toward potential therapeutics.

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