Involvement of CREM in CYP1A1 induction through ligand-independent activation pathway of aryl hydrocarbon receptor in HepG2 cells

Increased Hippocampal Neurogenesis and Accelerated Response to Antidepressants in Mice with Specific Deletion of CREB in the Hippocampus: Role of cAMP Response-Element Modulator τ

“…In this case, as with the CREB ␣⌬ mice, the increase in baseline levels of hippocampal neurogenesis may be "priming" the brain to respond to antidepressant treatment, allowing for an accelerated behavioral response. This is consistent with recent work demonstrating that lithium augmentation of traditional antidepressants leads to enhanced antidepressant response in the novelty-induced hypophagia procedure in treatment-resistant mice, and this behavioral response is correlated with increased neurogenesis in the hippocampus (O'Leary et al, 2013). Although the majority of work has focused on the hippocampus, neurogenesis and gliogenesis in other brain areas have also been implicated in antidepressant response (Kodama et al, 2004;Czéh et al, 2007;Ohira et al, 2013), and future work examining the role of CREB in these neuroplastic changes could provide further insight into novel treatment options.…”

“…In contrast, we did not see a generalized anxiety phenotype in other tests of anxiety-like behavior (elevated zero maze, marble burying), nor did we see an "antidepressant" phenotype in the forced swim or tail suspension tests. This is in sharp contrast to other models of global deletion of CREB, which demonstrate a more general increase in anxiety-like behavior as well as an antidepressant phenotype in these tasks (Conti et al, 2002;Gur et al, 2007;Mombereau et al, 2010). Although these differences between the CREB ␣⌬ mice and specific hippocampal CREB deletion could be due to developmental effects or the fact that here we did not completely ablate CREB expression in the hippocampus, it is more likely that these behavioral phenotypes are mediated by CREB in different brain regions.…”

“…However, in BALB/c7 mice, the behavioral effects of antidepressants do not appear to require hippocampal neurogenesis (Holick et al, 2008;Huang et al, 2008). If increased hippocampal neurogenesis or some other increase in hippocampal plasticity is necessary for the behavioral response to antidepressants, as many propose (Eisch et al, 2008;Snyder et al, 2011;Snyder and Cameron, 2012), it may be one cause for the lengthy time course of response, as only chronic, not acute, treatment with antidepressants causes increased hippocampal neurogenesis (Malberg et al, 2000). In this case, as with the CREB ␣⌬ mice, the increase in baseline levels of hippocampal neurogenesis may be "priming" the brain to respond to antidepressant treatment, allowing for an accelerated behavioral response.…”

“…Because CREB is thought to play a role in long-term changes in gene expression and plasticity that might result from chronic antidepressant treatment, we assessed the role of hippocampal CREB in a procedure sensitive to treatment with chronic, but not acute, antidepressants: the novelty-induced hypophagia procedure (Merali et al, 2003;Dulawa and Hen, 2005). In wild-type animals, latency to consume a highly palatable food is increased in a novel environment.…”

“…CREB ␣⌬ mice, in which the ␣ and ⌬ forms of CREB are constitutively deleted, show baseline increases in anxiety-like behavior, as well as antidepressant-like behavioral responses in the forced swim test (FST) and tail-suspension test (Conti et al, 2002;Gur et al, 2007;Mombereau et al, 2010). In the novelty-induced hypophagia procedure, in which chronic, but not acute, antidepressants are effective in wild-type animals, CREB ␣⌬ mice show an accelerated response to antidepressant treatment (Gur et al, 2007).…”