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Abstract

The purpose of this study was to determine if social vs nonsocial cues (peer vs light/ tone) can serve as discriminative stimuli to reinstate cocaine seeking. In addition, to assess a potential mechanism, an oxytocin (OT) promoter-linked hM3Dq DREADD was infused into the paraventricular nucleus of the hypothalamus to determine whether peer-induced cocaine seeking is decreased by activation of OT neurons. Male rats underwent twice-daily self-administration sessions, once with cocaine in the presence of one peer (S+) and once with saline in the presence of a different peer (S-). Another experiment used similar procedures, except the discriminative stimuli were nonsocial (constant vs flashing light/tone), with one stimulus paired with cocaine (S+) and the other paired with saline (S-). A third experiment injected male and female rats with OTp-hM3Dq DREADD or control virus into PVN and tested them for peer-induced reinstatement of cocaine seeking following clozapine (0.1 mg/ kg). Although acquisition of cocaine self-administration was similar in rats trained with either peer or light/tone discriminative stimuli, the latency to first response was reduced by the peer S+, but not by the light/tone S+. In addition, the effect of the conditioned stimulus was overshadowed by the peer S+ but not by the light/tone S+. Clozapine blocked the effect of the peer S+ in rats receiving the OTp-hM3Dq DREADD virus, but not in rats receiving the control virus. These results demonstrate that a social peer can serve as potent trigger for drug seeking and that OT in PVN modulates peer-induced reinstatement of cocaine seeking.

Document Type

Article

Publication Date

2022

Notes/Citation Information

© 2022 Society for the Study of Addiction

Digital Object Identifier (DOI)

https://doi.org/10.1111/adb.13217

Funding Information

Deutsche Forschungsgemeinschaft, Grant/ Award Numbers: GR 3619/13-1, GR 3619/15-1, GR 3619/16-1; National Institute on Drug Abuse, Grant/Award Numbers: R21 DA041755, T32 DA16176; SFB Consortium, Grant/Award Number: 1158-2

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