Blockade of CRF1 receptors in the central nucleus of the amygdala attenuates the dysphoria associated with nicotine withdrawal in rats

Bruijnzeel, Adrie W.; Ford, Jenna; Rogers, Jessica A.; Scheick, Stacey; Ji, Yue; Bishnoi, Mahendra; Alexander, Jon C.

doi:10.1016/j.pbb.2011.12.001

Cited by 56 publications

(40 citation statements)

References 49 publications

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“…reduces the nicotine withdrawal-dependent elevations in brain reward threshold (Bruijnzeel et al, 2012). In cannabinoid-dependent rats, precipitated withdrawal is associated with a marked elevation in extracellular CRF concentration in the CeA (Rodriguez de Fonseca et al, 1997).…”

Section: Discussionmentioning

confidence: 96%

CRF–CRF1 Receptor System in the Central and Basolateral Nuclei of the Amygdala Differentially Mediates Excessive Eating of Palatable Food

Iemolo

Blasio

Cyr

et al. 2013

Neuropsychopharmacol

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Highly palatable foods and dieting are major contributing factors for the development of compulsive eating in obesity and eating disorders. We previously demonstrated that intermittent access to palatable food results in corticotropin-releasing factor-1 (CRF 1 ) receptor antagonist-reversible behaviors, which include excessive palatable food intake, hypophagia of regular chow, and anxiety-like behavior. However, the brain areas mediating these effects are still unknown. Male Wistar rats were either fed chow continuously for 7 days/week (Chow/Chow group), or fed chow intermittently 5 days/week, followed by a sucrose, palatable diet 2 days/week (Chow/Palatable group). Following chronic diet alternation, the effects of microinfusing the CRF 1 receptor antagonist R121919 (0, 0.5, 1.5 mg/side) in the central nucleus of the amygdala (CeA), the basolateral nucleus of the amygdala (BlA), or the bed nucleus of the stria terminalis (BNST) were evaluated on excessive intake of the palatable diet, chow hypophagia, and anxiety-like behavior. Furthermore, CRF immunostaining was evaluated in the brain of diet cycled rats. Intra-CeA R121919 blocked both excessive palatable food intake and anxiety-like behavior in Chow/Palatable rats, without affecting chow hypophagia. Conversely, intra-BlA R121919 reduced the chow hypophagia in Chow/Palatable rats, without affecting excessive palatable food intake or anxiety-like behavior. Intra-BNST treatment had no effect. The treatments did not modify the behavior of Chow/Chow rats. Immunohistochemistry revealed an increased number of CRF-positive cells in CeA-but not in BlA or BNST-of Chow/Palatable rats, during both withdrawal and renewed access to the palatable diet, compared with controls. These results provide functional evidence that the CRF-CRF 1 receptor system in CeA and BlA has a differential role in mediating maladaptive behaviors resulting from palatable diet cycling.

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Section: Discussionmentioning

confidence: 96%

CRF–CRF1 Receptor System in the Central and Basolateral Nuclei of the Amygdala Differentially Mediates Excessive Eating of Palatable Food

Iemolo

Blasio

Cyr

et al. 2013

Neuropsychopharmacol

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“…This increase in CRF mRNA is also seen within the nucleus accumbens during nicotine withdrawal [73]. Furthermore, CRFR1 antagonists blunt nicotine withdrawal-induced anxiety-like behavior and dysphoria [74, 190]. This suggests that while chronic nicotine may lead to a decrease in HPA activity, brain CRF systems remain sensitized.…”

Section: Preclinical Studies Of Drug Administration and Stress Responmentioning

confidence: 99%

Substance use modulates stress reactivity: Behavioral and physiological outcomes

Fosnocht

Briand

2016

Physiology & Behavior

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Drug addiction is a major public health concern in the United States costing taxpayers billions in health care costs, lost productivity and law enforcement. However, the availability of effective treatment options remains limited. The development of novel therapeutics will not be possible without a better understanding of the addicted brain. Studies in both clinical and preclinical models indicate that chronic drug use leads to alterations in the body and brain’s response to stress. Dysregulation of the hypothalamic-pituitary-adrenal (HPA) axis may shed light on the ability of stress to increase vulnerability to relapse. Further, within both the HPA axis and limbic brain regions, corticotropin-releasing factor (CRF) is critically involved in the brain’s response to stress. Alterations in both central and peripheral CRF activity seen following chronic drug use provide a mechanism by which substance use can alter stress reactivity, thus mediating addictive phenotypes. While many reviews have focused on how stress alters drug-mediated changes in physiology and behavior, the goal of this review is to focus on how substance use alters responses to stress.

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“…These could be addressed by the respective (but not yet approved) k and CRF antagonists (Bruijnzeel et al, 2010; Bruijnzeel et al, 2012; Chartoff et al, 2012), which may also stabilize aberrant learning mechanisms since elevations in stress hormones and neurotransmitters (e.g., cortisol) repeatedly paired with stressful situations and consequent suicidality may become a conditioned stimulus and independently elicit suicidal psychological state of mind c.f., cortisol-primed drug craving (Elman et al, 2003). …”

Section: Therapeutic Considerationsmentioning

confidence: 99%

Pain and suicidality: Insights from reward and addiction neuroscience

Elman

Borsook

Volkow

2013

Progress in Neurobiology

180

147

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Suicidality is exceedingly prevalent in pain patients. Although the pathophysiology of this link remains unclear, it may be potentially related to the partial congruence of physical and emotional pain systems. The latter system’s role in suicide is also conspicuous during setbacks and losses sustained in the context of social attachments. Here we propose a model based on the neural pathways mediating reward and anti-reward (i.e., allostatic adjustment to recurrent activation of the reward circuitry); both are relevant etiologic factors in pain, suicide and social attachments. A comprehensive literature search on neurobiology of pain and suicidality was performed. The collected articles were critically reviewed and relevant data were extracted and summarized within four key areas: (1) physical and emotional pain, (2) emotional pain and social attachments, (3) pain-and suicide-related alterations of the reward and anti-reward circuits as compared to addiction, which is the premier probe for dysfunction of these circuits and (4) mechanistically informed treatments of co-occurring pain and suicidality. Pain-, stress- and analgesic drugs-induced opponent and proponent states of the mesolimbic dopaminergic pathways may render reward and anti-reward systems vulnerable to sensitization, cross-sensitization and aberrant learning of contents and contexts associated with suicidal acts and behaviors. These findings suggest that pain patients exhibit alterations in the brain circuits mediating reward (depressed function) and anti-reward (sensitized function) that may affect their proclivity for suicide and support pain and suicidality classification among other “reward deficiency syndromes” and a new proposal for “enhanced anti-reward syndromes”. We suggest that interventions aimed at restoring the balance between the reward and anti-reward networks in patients with chronic pain may help decreasing their suicide risk.

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Blockade of CRF1 receptors in the central nucleus of the amygdala attenuates the dysphoria associated with nicotine withdrawal in rats

Cited by 56 publications

References 49 publications

CRF–CRF1 Receptor System in the Central and Basolateral Nuclei of the Amygdala Differentially Mediates Excessive Eating of Palatable Food

CRF–CRF1 Receptor System in the Central and Basolateral Nuclei of the Amygdala Differentially Mediates Excessive Eating of Palatable Food

Substance use modulates stress reactivity: Behavioral and physiological outcomes

Pain and suicidality: Insights from reward and addiction neuroscience

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