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Traumatic stress reactivity promotes excessive alcohol drinking and alters the balance of prefrontal cortex-amygdala activity.

Edwards S, Baynes BB, Carmichael CY, Zamora-Martinez ER, Barrus M, Koob GF, Gilpin NW - Transl Psychiatry (2013)

Bottom Line: The aim of these studies was to examine the effects of traumatic stress (and stress reactivity) on alcohol-related behaviors and neuronal activation patterns.Furthermore, activity of upstream regions was differentially predictive of downstream regional activity in the Avoiders versus Non-Avoiders.An animal model for assessing the effect of traumatic stress on alcohol drinking reveals individual differences in neuronal activation patterns associated with re-exposure to traumatic stress-related stimuli, and may provide insight into the neural mechanisms underlying excessive alcohol consumption in humans with PTSD.

View Article: PubMed Central - PubMed

Affiliation: Committee on the Neurobiology of Addictive Disorders, The Scripps Research Institute, La Jolla, CA, USA.

ABSTRACT
Post-traumatic stress disorder (PTSD) and alcoholism are highly comorbid in humans and have partially overlapping symptomatic profiles. The aim of these studies was to examine the effects of traumatic stress (and stress reactivity) on alcohol-related behaviors and neuronal activation patterns. Male Wistar rats were trained to respond for alcohol, were exposed to predator odor (bobcat urine) paired with context and were tested for short- and long-term avoidance of the predator odor-paired context, alcohol self-administration and compulsivity of alcohol responding. Rats were re-exposed to the odor-paired context for western blot analysis of ERK phosphorylation in subregions of the medial prefrontal cortex (mPFC) and the amygdala. Rats that avoided the predator-paired chamber (Avoiders) exhibited persistent avoidance up to 6 weeks post conditioning. Avoiders exhibited increases in operant alcohol responding over weeks, as well as more compulsive-like responding for alcohol adulterated with quinine. Following re-exposure to the predator odor-paired context, Avoiders and Non-Avoiders exhibited unique patterns of neuronal activation in subregions of the mPFC and the amygdala, which were correlated with changes in avoidance and alcohol drinking. Furthermore, activity of upstream regions was differentially predictive of downstream regional activity in the Avoiders versus Non-Avoiders. An animal model for assessing the effect of traumatic stress on alcohol drinking reveals individual differences in neuronal activation patterns associated with re-exposure to traumatic stress-related stimuli, and may provide insight into the neural mechanisms underlying excessive alcohol consumption in humans with PTSD.

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Related in: MedlinePlus

Relationship between alterations in individual levels of alcohol drinking (19 days post conditioning) and odor-paired-context-induced ERK phosphorylation in the dorsomedial prefrontal cortex (dmPFC) and basolateral amygdala (BLA). Elevations in drinking after odor exposure significantly correlated with context-induced reductions in ERK phosphorylation (pERK) levels in both the dmPFC (a, r2=0.25, P<0.05) and BLA (b, r2=0.24, P<0.05) of Avoiders, but not of Non-Avoiders or Controls.
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fig4: Relationship between alterations in individual levels of alcohol drinking (19 days post conditioning) and odor-paired-context-induced ERK phosphorylation in the dorsomedial prefrontal cortex (dmPFC) and basolateral amygdala (BLA). Elevations in drinking after odor exposure significantly correlated with context-induced reductions in ERK phosphorylation (pERK) levels in both the dmPFC (a, r2=0.25, P<0.05) and BLA (b, r2=0.24, P<0.05) of Avoiders, but not of Non-Avoiders or Controls.

Mentions: Finally, we examined individual relationships between alterations in ethanol drinking behavior and biochemical reactivity to the stress-paired context. Elevations in ethanol self-administration after predator odor exposure were significantly and negatively correlated with context-induced pERK levels in both the dmPFC (r2=0.25, P<0.05) and BLA (r2=0.24, P<0.05) in Avoiders (Figure 4). In contrast, weak positive correlations (r2=0.13–0.15) were observed between post-odor drinking and ERK phosphorylation in these two regions in Non-Avoiders.


Traumatic stress reactivity promotes excessive alcohol drinking and alters the balance of prefrontal cortex-amygdala activity.

Edwards S, Baynes BB, Carmichael CY, Zamora-Martinez ER, Barrus M, Koob GF, Gilpin NW - Transl Psychiatry (2013)

Relationship between alterations in individual levels of alcohol drinking (19 days post conditioning) and odor-paired-context-induced ERK phosphorylation in the dorsomedial prefrontal cortex (dmPFC) and basolateral amygdala (BLA). Elevations in drinking after odor exposure significantly correlated with context-induced reductions in ERK phosphorylation (pERK) levels in both the dmPFC (a, r2=0.25, P<0.05) and BLA (b, r2=0.24, P<0.05) of Avoiders, but not of Non-Avoiders or Controls.
© Copyright Policy - open-access
Related In: Results  -  Collection

License
Show All Figures
getmorefigures.php?uid=PMC3756295&req=5

fig4: Relationship between alterations in individual levels of alcohol drinking (19 days post conditioning) and odor-paired-context-induced ERK phosphorylation in the dorsomedial prefrontal cortex (dmPFC) and basolateral amygdala (BLA). Elevations in drinking after odor exposure significantly correlated with context-induced reductions in ERK phosphorylation (pERK) levels in both the dmPFC (a, r2=0.25, P<0.05) and BLA (b, r2=0.24, P<0.05) of Avoiders, but not of Non-Avoiders or Controls.
Mentions: Finally, we examined individual relationships between alterations in ethanol drinking behavior and biochemical reactivity to the stress-paired context. Elevations in ethanol self-administration after predator odor exposure were significantly and negatively correlated with context-induced pERK levels in both the dmPFC (r2=0.25, P<0.05) and BLA (r2=0.24, P<0.05) in Avoiders (Figure 4). In contrast, weak positive correlations (r2=0.13–0.15) were observed between post-odor drinking and ERK phosphorylation in these two regions in Non-Avoiders.

Bottom Line: The aim of these studies was to examine the effects of traumatic stress (and stress reactivity) on alcohol-related behaviors and neuronal activation patterns.Furthermore, activity of upstream regions was differentially predictive of downstream regional activity in the Avoiders versus Non-Avoiders.An animal model for assessing the effect of traumatic stress on alcohol drinking reveals individual differences in neuronal activation patterns associated with re-exposure to traumatic stress-related stimuli, and may provide insight into the neural mechanisms underlying excessive alcohol consumption in humans with PTSD.

View Article: PubMed Central - PubMed

Affiliation: Committee on the Neurobiology of Addictive Disorders, The Scripps Research Institute, La Jolla, CA, USA.

ABSTRACT
Post-traumatic stress disorder (PTSD) and alcoholism are highly comorbid in humans and have partially overlapping symptomatic profiles. The aim of these studies was to examine the effects of traumatic stress (and stress reactivity) on alcohol-related behaviors and neuronal activation patterns. Male Wistar rats were trained to respond for alcohol, were exposed to predator odor (bobcat urine) paired with context and were tested for short- and long-term avoidance of the predator odor-paired context, alcohol self-administration and compulsivity of alcohol responding. Rats were re-exposed to the odor-paired context for western blot analysis of ERK phosphorylation in subregions of the medial prefrontal cortex (mPFC) and the amygdala. Rats that avoided the predator-paired chamber (Avoiders) exhibited persistent avoidance up to 6 weeks post conditioning. Avoiders exhibited increases in operant alcohol responding over weeks, as well as more compulsive-like responding for alcohol adulterated with quinine. Following re-exposure to the predator odor-paired context, Avoiders and Non-Avoiders exhibited unique patterns of neuronal activation in subregions of the mPFC and the amygdala, which were correlated with changes in avoidance and alcohol drinking. Furthermore, activity of upstream regions was differentially predictive of downstream regional activity in the Avoiders versus Non-Avoiders. An animal model for assessing the effect of traumatic stress on alcohol drinking reveals individual differences in neuronal activation patterns associated with re-exposure to traumatic stress-related stimuli, and may provide insight into the neural mechanisms underlying excessive alcohol consumption in humans with PTSD.

Show MeSH
Related in: MedlinePlus