Stress model focuses on the idea of an allostatic interaction between negative and positive reinforcement throughout stages of addiction. These opponent processes start at the initial drug intake and, in the long run, results in the hypofunctioning of dopaminergic neurotransmitters, such as D2 and dopamine, but increase in stress chemicals including corticotropin releasing factor (CRF)(Johnson et al, 2016). These changes were said to be the effort of the brain to counteract the hedonic effect of drug use (Solomon and Corbit, 1974) and eventually results in negative affect, which drives addictive behaviours in order to alleviate the aversive emotional state. Hedonic Homeostatic Dysregulation (HD) Model by Koob and le Moal divided the addiction
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According to Van de Bree and her coauthors, the development of incentive salience towards drug-related cue is an allostatic, single-processed interaction between stress and dopamine systems. Chronic stress results in a hypodopaminergic state of the brain, which prompts an effort to increase brain level of dopamine. In this effort, the dopaminergic system is sensitized to cues and results in drug seeking behavior. It was also mentioned that drug seeking aims at relieving aversive emotional states as well as rebalancing the dopamine level. This interrelationship between the two systems becomes increasingly more pathological over longer period of substance use. Furthermore, the authors brought forward the idea that premorbid vulnerability, either in form of genetics and/or early adverse environment, has impact on different stages throughout the addiction cycle, by sensitizing dopaminergic network before initial drug use, creating “extended reward” networks. This observation suggests that the interaction between stress and dopamine systems began even preceding the onset of addiction, and further proves that positive reinforcement model alone was not sufficient to explain …show more content…
It was studied that stress, in the form of foot shock, elevates the dopamine level in the nucleus accumbens and results in more amphetamine and cocaine self-administration (Goeders and Guerin, 1994), suggesting that stress chemicals, such as CRF, glucocorticoids(GCs) , and norepinephrine (NE), have the ability to directly modulate dopaminergic pathway and in turn, response to stress and cue (Johnson et al, 2016). In details, the increase in CRF released during stress and received by the VTA might enhance dopamine release in the VTA. CRF was also said to have a direct impact on nucleus accumbens through the activation of CREB and mechanisms through which the brain reacts to the hypodopaminergic state by drug seeking. In addition, the alternation of the NE pathway in dorsal and ventral striatum was associated with the increase in possibility of relapse when exposed to conditioned cue and stress. The authors did also acknowledge that the blockage of glucocorticoid receptor in the mesolimbic reward pathway results in a decrease in dopamine. To explain the increasing pathological interaction between stress and dopamine, it was asserted that long term drug use sensitizes the dopaminergic pathways to stress, giving stress even more influence in the regulation of dopamine level in the
According to Van de Bree and her coauthors, the development of incentive salience towards drug-related cue is an allostatic, single-processed interaction between stress and dopamine systems. Chronic stress results in a hypodopaminergic state of the brain, which prompts an effort to increase brain level of dopamine. In this effort, the dopaminergic system is sensitized to cues and results in drug seeking behavior. It was also mentioned that drug seeking aims at relieving aversive emotional states as well as rebalancing the dopamine level. This interrelationship between the two systems becomes increasingly more pathological over longer period of substance use. Furthermore, the authors brought forward the idea that premorbid vulnerability, either in form of genetics and/or early adverse environment, has impact on different stages throughout the addiction cycle, by sensitizing dopaminergic network before initial drug use, creating “extended reward” networks. This observation suggests that the interaction between stress and dopamine systems began even preceding the onset of addiction, and further proves that positive reinforcement model alone was not sufficient to explain …show more content…
It was studied that stress, in the form of foot shock, elevates the dopamine level in the nucleus accumbens and results in more amphetamine and cocaine self-administration (Goeders and Guerin, 1994), suggesting that stress chemicals, such as CRF, glucocorticoids(GCs) , and norepinephrine (NE), have the ability to directly modulate dopaminergic pathway and in turn, response to stress and cue (Johnson et al, 2016). In details, the increase in CRF released during stress and received by the VTA might enhance dopamine release in the VTA. CRF was also said to have a direct impact on nucleus accumbens through the activation of CREB and mechanisms through which the brain reacts to the hypodopaminergic state by drug seeking. In addition, the alternation of the NE pathway in dorsal and ventral striatum was associated with the increase in possibility of relapse when exposed to conditioned cue and stress. The authors did also acknowledge that the blockage of glucocorticoid receptor in the mesolimbic reward pathway results in a decrease in dopamine. To explain the increasing pathological interaction between stress and dopamine, it was asserted that long term drug use sensitizes the dopaminergic pathways to stress, giving stress even more influence in the regulation of dopamine level in the