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A Critique Of the Stress Model

Brain-Activity-of-Pot-Smokers-Score-Addicaid

 

Theoretical challenges to the negative reinforcement model

 

  1. The preoccupation-anticipation phase, seen as one of dopaminergic positive reinforcement, can be critiqued in terms of a “premorbid allostasis” – although clinical and epidemiological studies suggests a dose-dependent relationship between accumulated lifetime adversity and addiction risk (8, 37-40) and studies have shown altered stress systems appear to augment dopaminergic activity and potentiate reward systems in those children who have suffered maltreatment (8, 36), positive reinforcement is mainly viewed as dopaminergic although these pathways may be already “primed” by stress chemicals in the preoccupation-anticipation phase.
  2. No apparent role for positive reinforcement in relapse during the abusing or binge-intoxication phase of addiction – the wanting/abusing stage may not be exclusively dependent on escape from aversive states, but may also involve some “positive reinforcement”; so-called positive emotions as opposed to negative. As Berridge et al (41, 42) illustrated, stress augmented wanting can occur after an increase in corticotropin-releasing factor (CRF) and without negative affect (NA) as the result of positive feelings, a “happy stress”.
  3. In the binge-intoxication phase, stress enhances the effect of brain circuits involved in reward processing and in attentional and mnemonic bias for drug use reminders (21) by  dual neuroplastic (dopaminergic) and plastic (stress-based) mechanisms (22) – rather than stress augmenting this extended reward area; consistent perhaps with the allostatic introduction of “…experience, memories, anticipation…” (17) in reward function. The basolateral amygdala (BLA) may also play a  role here in drug-conditioned memories (43).
  4. No role for stress chemicals in prompting the habit behaviour of the dorsal striatum (DS)  – the Hedonic Homeostatic Dysregulation (HD) Model suggests relapse is also prompted via the compulsivity of the C-L-S loop without clear elucidation of how chronic stress can also act as a stimulus to prompt the automatic response of the DS (35).
  5. The role of memory systems is unspecified – in the HD model, craving and compulsion appear to be a mainly explicit memory-based processes, involving the amygdala, nucleus accumbens (NaC) , hippocampus, anterior cingulate cortex (ACC),  dorsolateral PFC (dlPFC) and DS (14), without much acknowledgement of the DS as an implicit memory network. The former structures specialize in managing action-outcome explicit memory, with the dorsal lateral striatum (DLS) processing implicit stimulus-response associations (44-46), with the dorsal medial striatum (DMS) playing an important part orchestrating the switching between these memories through a “hippocampal-to-striatal pathway” passing through the ACC (47). ACC hypo-functioning, the result of stress dysregulation, may aid transition between explicit and implicit memory networks (48).
  6. The recruitment of more compulsive regions not clearly elucidated in HD with regards to memory systems (or in associative structures becoming automatic or habitual) – although Koob and Volkow (22) mention different memory systems, the mechanisms whereby addiction hijacks different memory systems is not clearly specified. Basolateral amgydala (BLA) modulation of dorsal striatal over hippocampal memory may “switch” explicit to implicit memory, action outcome to habitual (35). This may also reflect an emotionally-distressed expression of “must do!” behaviour; “I can’t cope!”/“to hell with it!” compulsive responding to emotional distress, as responding to internal stress becomes habitualised and increasingly under automatic striatal control, akin to a compulsive “emotional arousal habit bias” (49).  This is an escalation of the emotional dysregulation Koob has discussed throughout his work and a transition to a more automatic relapse trigger e.g. prompted by inter-personal relationships.
  7. The role for orbitofrontal cortex (OFC)  dysfunction in recruiting the compulsive brain region of the DS – recruitment of compulsive OFC/amgydaloid/DS circuitry the consequence of OFC dysfunction is implicated in both positive and negative reinforcement models. Compulsive behaviour of the DS may, however, involve a hippocampal dysfunction caused by stress dysregulation, in addition to OFC (and possibly ventromedial PFC (VM PFC) dysfunction (50)) in a pathway to amgydaloid (BLA) hyperactivity and modulation of implicit DS-implicit memory over hippocampal-explicit memory.

 

References

  1. Sinha R (2008): Chronic stress, drug abuse, and vulnerability to addiction. Annals of the New York Academy of Sciences 1141: 105–130.
  2. Franken IH (2003): Drug craving and addiction: integrating psychological and neuropsychopharmacological approaches. Progress in Neuro-Psychopharmacology and Biological Psychiatry 27: 563-579.
  1. Duncan E, Boshoven W, Harenski K, Fiallos A, Tracy H, Jovanovic T, et al. (2007): An fMRI study of the interaction of stress and cocaine cues on cocaine craving in cocaine-dependent men. The American Journal on Addictions 16: 174–182.
  2. Koob GF, Volkow N D (2010): Neurocircuitry of addiction. Neuropsychopharmacology 35: 217-238.
  1. Pruessner JC, Champagne F, Meaney MJ, Dagher A (2004): Dopamine release in response to a psychological stress in humans and its relationship to early life maternal care: a positron emission tomography study using [11C] raclopride.The Journal of Neuroscience 24: 2825-2831.
  1. Rogosch FA, Oshri A, Cicchetti, D (2010): From child maltreatment to adolescent cannabis abuse and dependence: A developmental cascade model. Development and psychopathology 22: 883-897.
  2. Lo CC, Cheng TC (2007): The impact of childhood maltreatment on young adults’ substance abuse.The American Journal of Drug and Alcohol Abuse33: 139-146.
  3. Fowler T, Lifford K, Shelton K, Rice F, Thapar A, Neale MC, Van Den Bree M (2007): Exploring the relationship between genetic and environmental influences on initiation and progression of substance use. Addiction 102: 413-422.
  4. Meaney MJ, Brake W, Gratton A (2002): Environmental regulation of the development of mesolimbic dopamine systems: a neurobiological mechanism for vulnerability to drug abuse? Psychoneuroendocrinology 27: 127-138.
  5. Berridge KC, Ho CY, Richard JM, DiFeliceantonio AG (2010): The tempted brain eats: pleasure and desire circuits in obesity and eating disorders. Brain Research 1350: 43-64.
  6. Peciña S, Schulkin J, Berridge KC (2006): Nucleus accumbens corticotropin-releasing factor increases cue-triggered motivation for sucrose reward: paradoxical positive incentive effects in stress? BMC Biology 4: 8.
  7. Wiener SI (1996): Spatial, behavioral and sensory correlates of hippocampal CA1 complex spike cell activity: Implications for information processing functions. Progress in Neurobiology 49: 335–361.
  8. Mizumori SJ, Yeshenko O, Gill KM,  Davis DM (2004): Parallel processing across neural systems: Implications for a multiple memory system hypothesis. Neurobiology of Learning and Memory 82: 278–298.
  9. Devan BD, McDonald RJ, White NM (1999): Effects of medial and lateral caudate–putamen lesions on place- and cue-guided behaviors in the water maze: Relation to thigmotaxis. Behavioural Brain Research 100: 5–14.
  10. Devan BD, Hong NS, McDonald RJ (2011): Parallel associative processing in the dorsal striatum: Segregation of stimulus–response and cognitive control subregions. Neurobiology of Learning and Memory 96: 95-120.
  11. Li CSR, Sinha R (2008): Inhibitory control and emotional stress regulation: neuroimaging evidence for frontal–limbic dysfunction in psycho-stimulant addiction. Neuroscience & Biobehavioral Reviews 32: 581-597.
  12. Goodman J, Leong KC, Packard MG (2012): Emotional modulation of multiple memory systems: implications for the neurobiology of post-traumatic stress disorder. Reviews in the Neurosciences 23: 627-43.
  13. Joëls, M (2008): Functional actions of corticosteroids in the hippocampus. European Journal of Pharmacology 583: 312-321.
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