`Up-regulation of histone acetylation induced by social defeat mediates the conditioned rewarding effects of cocaine

Social defeat stress: Mechanisms underlying the increase in rewarding effects of drugs of abuse

“…On the contrary, inhibition of HAT activity with the HAT inhibitor curcuma longa, or through viral‐mediated transfer and overexpression of specific HDACs in the NAc, markedly inhibits the increase in cocaine‐induced CPP in defeated animals (Hui, Wang, & Li, ; Renthal et al., ). These results confirm that the alterations in histone acetylation induced by SD correlate with the increase in the conditioned rewarding effects of cocaine (Montagud‐Romero, Montesinos et al., ).…”

“…Interestingly, the increase in histone H3 in the hippocampus acetylation induced by SD can be reverted by physical exercise (Patki et al., ). Contrasting results have been reported regarding H4 acetylation after SD, with no changes (Hollis et al., ; Tsankova et al., ) and increases both being reported in defeated mice (Erburu et al., ; Montagud‐Romero, Montesinos et al., ). Epigenetic mechanisms also seem to play a role in resilience to the effects of SD because susceptible rats display higher levels of histone H3 (K9,14,18) and total H3 and H4(K5,12,16) acetylation (Hollis et al., ; Kenworthy et al., ; Tsankova et al., ).…”

“…Other epigenetic changes induced by SD described in the literature include a three methylation in H3(K4; H3(K4)me3), which is closely associated with transcriptional initiation. In one study, an increase was detected in the hippocampus 3 weeks after the last defeat experience (Montagud‐Romero, Montesinos et al., ). In another, an increment of H3K9me2/me3 in the NAc and of the promoter of the BDNF IV gene in the mPFC were produced by SD, and were associated with a repression of transcription (Pathak, Maitra, Chakravarty, & Kumar, ; Xu et al., ).…”

“…For example, short‐ and long‐term reductions in the histone deacetylase (HDAC) levels (specifically HDAC 2), in the NAc and hippocampus have been observed in defeated mice. On the contrary, increases in histone acetyltransferase (HAT) activity have been described in the same structure (Covington et al., ; Martin et al., ; Montagud‐Romero, Montesinos et al., ). In addition, a downregulation of HDAC6 (in raphe neurons and in the hippocampus) and HDAC5 (in NAc and PFC) has been reported a few weeks after the last SD, changes that were reverted by the HDAC inhibitor imipramine (Espallergues et al., ; Fuchikami et al., ; Martin et al., ; Renthal et al., ).…”

“…These drugs also reverse social avoidance when administered to the amygdala and PFC (Covington, Maze, Vialou, & Nestler, ; Covington et al., ). Inhibition of HDAC with valproic acid not only increases the effects induced by SD (McCann et al., ), but also the conditioning rewarding effects of cocaine because HDAC inhibitors increase associative learning (Montagud‐Romero, Montesinos et al., ; Ploense et al., ). On the contrary, inhibition of HAT activity with the HAT inhibitor curcuma longa, or through viral‐mediated transfer and overexpression of specific HDACs in the NAc, markedly inhibits the increase in cocaine‐induced CPP in defeated animals (Hui, Wang, & Li, ; Renthal et al., ).…”