Natural and Drug Rewards Act on Common Neural Plasticity Mechanisms with ΔFosB as a Key Mediator
“…When comparing the expression profiles of the immediate early gene (IEG) early growth response protein 1 (EGR1) - alias Zif268, KROX24, NGFI-A - after the acquisition and expression of CPP for either cocaine or social interaction, both conditioning stimuli lead to increased expression of EGR1 in the nucleus accumbens core and shell, which are central regions of the reward pathway as well as in other associated brain regions [8]. These results strongly support the idea that both natural and drug rewards are processed in similar brain regions [9,10,11,12,13]. …”
Section: Introductionmentioning
“…When comparing the expression profiles of the immediate early gene (IEG) early growth response protein 1 (EGR1) - alias Zif268, KROX24, NGFI-A - after the acquisition and expression of CPP for either cocaine or social interaction, both conditioning stimuli lead to increased expression of EGR1 in the nucleus accumbens core and shell, which are central regions of the reward pathway as well as in other associated brain regions [8]. These results strongly support the idea that both natural and drug rewards are processed in similar brain regions [9,10,11,12,13]. …”
Section: Introductionmentioning
“…As these addictive drugs and natural rewards can induce expression of ΔFosB (i.e., they cause the brain to produce more of it), thus, long-term acquisition of these natural rewards can lead to similar pathological state of addiction. Therefore, ΔFosB is considered as one of the most significant factors found to be involved in both addiction of amphetamine and compulsive sex addictions induced by amphetamine [76,77]. These sex addictions are linked with a dopamine dysregulation syndrome (DDS) which arises in some patients who are taking dopaminergic drugs [78].…”
Section: Amphetamine Addiction and Dependencementioning
“…Drugs of abuse also produce regulation of genes related to LTP in NAc, including Fos B, c-fos, NR2B and NR4A, CamKII, and dynorphin (Carlezon et al 1998;Hyman et al 2006;Lee et al 2006;Brown et al 2011;Malvaez et al 2011;Damez-Werno et al 2012;Pitchers et al 2013;Robison et al 2013;Rogge et al 2013). That regulation involves a variety of mechanisms, including activation of CREB and epigenetic changes in histone acetylation and methylation (Carlezon et al 1998;Brown et al 2011;Malvaez et al 2011;Maze et al 2011;Damez-Werno et al 2012;Sun et al 2012;Taniguchi et al 2012;Rogge et al 2013).…”
Section: Drugs Of Abuse Hijack the Normal Reward Processmentioning
“…That regulation involves a variety of mechanisms, including activation of CREB and epigenetic changes in histone acetylation and methylation (Carlezon et al 1998;Brown et al 2011;Malvaez et al 2011;Maze et al 2011;Damez-Werno et al 2012;Sun et al 2012;Taniguchi et al 2012;Rogge et al 2013). In addition, drugs of abuse produce synaptic growth and structural changes related to L-LTP in NAc, including increases in dendritic branching, spine density, and spine size (Lee et al 2006;Ren et al 2010;Dobi et al 2011;Shen et al 2011;Dietz et al 2012;Dumitriu et al 2012;Gipson et al 2013a,b;Pitchers et al 2013;Robison et al 2013), as well as increases in pre-and postsynaptic proteins (Subramaniam et al 2001;Gipson et al 2013b). The drugs produce the same types of structural changes in PFC as well Kolb 1997, 1999;Robinson et al 2001;Hamilton et al 2010;Gourley et al 2012).…”
Section: Drugs Of Abuse Hijack the Normal Reward Processmentioning