TY  - JOUR
PY  - 2018//
TI  - Cocaine self-administration is increased after frontal traumatic brain injury and associated with neuroinflammation
JO  - European journal of neuroscience
A1  - Vonder Haar, Cole
A1  - Ferland, Jacqueline-Marie N.
A1  - Kaur, Sukhbir
A1  - Riparip, Lara-Kirstie
A1  - Rosi, Susanna
A1  - Winstanley, Catharine A.
SP  - ePub
EP  - ePub
VL  - ePub
IS  - ePub
N2  - Traumatic brain injury (TBI) has been linked to the development of numerous psychiatric diseases, including substance use disorder. However, it can be difficult to ascertain from clinical data whether the TBI is cause or consequence of increased addiction vulnerability. Surprisingly few studies have taken advantage of animal models to investigate the causal nature of this relationship. In terms of a plausible neurobiological mechanism through which TBI could magnify the risk of substance dependence, numerous studies indicate that TBI can cause widespread disruption to monoaminergic signaling in striatal regions, and also increases neuroinflammation. In the current study, male Long-Evans rats received either a mild or severe TBI centered over the frontal cortex via controlled cortical impact, and were subsequently trained to self-administer cocaine over ten six-hour sessions. At the end of the study, markers of striatal dopaminergic function, and levels of inflammatory cytokine levels in the frontal lobes, were assessed via western blot and multiplex ELISA, respectively. There was significantly higher cocaine intake in a subset of animals with either mild or severe TBI. However, many animals within both TBI groups failed to acquire self-administration. Principal components analysis suggested that both dopaminergic and neuroinflammatory proteins were associated with overall cocaine intake, yet only an inflammatory component was associated with acquisition of self-administration, suggesting neuroinflammation may make a more substantial contribution to the likelihood of drug-taking. Should neuroinflammation play a causal role in mediating TBI-induced addiction risk, anti-inflammatory therapy may reduce the likelihood of substance abuse in TBI populations. This article is protected by copyright. All rights reserved.<br><br>This article is protected by copyright. All rights reserved.<p />  <p>Language: en</p>
LA  - en
SN  - 0953-816X
UR  - http://dx.doi.org/10.1111/ejn.14123
ID  - ref1
ER  -