Combining Stress and XXXX Based Models of Addiction.

@entity935 @entity988 @entity16 @entity75 @entity2915
UNASSIGNED: The literature on the two main models of @entity988 ( @entity935 -based positive reinforcement and stress-based negative reinforcement models) have made many important contributions to understanding this @entity75 . However, rarely has there been a comprehensive critique of the limitations of both models. This article seeks to resolve theoretical issues inherent to each model, as well as propose a more @entity16 which reconciles important elements of both. We suggest that there is not only direct interaction of dopaminergic and stress systems throughout the @entity988 cycle, from initial use, via the abusing stage, to the endpoint of @entity988 , but that this interaction is present prior to initial use. A combination of genetic factors and/or experiences of adversity may result in a stress-triggered sensitisation of dopaminergic networks which is present before the onset of substance use, which cannot be explained solely in terms of dopaminergic (positive) reinforcement. Rather these processes are best explained by an allostatic model which reconciles aspects of both models of @entity988 and shows how @entity935 /stress interactions become increasingly pathological in the @entity988 cycle. Our model suggests that chronic stress eventually creates baseline hypodopaminergic activity, but also prompts dopaminergic @entity2915 in cue reactivity. This is the neural marker of allostatic mechanisms observed at endpoint @entity988 . We propose a multi-circuit explanation of how this cumulative effect of stress increasingly impacts on dopaminergic networks of reward, affect, attention, memory and behavioural control. This revised model provides a useful frame of reference for further research and ultimately clinical practice.
