Corticotropin releasing factor antagonist, α-helical CRF9–41, reverses nicotine-induced conditioned, but not unconditioned, anxiety

Tucci, Sonia; Cheeta, Survjit; Seth, Pallab; File, Sandra E.

doi:10.1007/s00213-003-1403-4

Cited by 36 publications

(22 citation statements)

References 49 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Lower doses of nicotine, covering the dose used in this study, are capable of inducing a conditioned place preference, while higher doses of nicotine are capable of eliciting a conditioned place aversion; although, a higher degree of variability has been observed in these experiments compared with conditioned place preference with more classical psychostimulants (Calcagnetti and Schechter 1994;Fudala and Iwamoto 1986;Fudala et al 1985;Jorenby et al 1990;Le Foll and Goldberg 2005;Shoaib et al 1994). Unconditioned as well as conditioned anxiety to nicotine at .1 mg/kg nicotine dose have been reported in the social interaction test and elevated plus maze (Irvine et al 2001a(Irvine et al , 2001bTucci et al 2003). We have previously reported conditioned locomotor hyperactivity in response to a context associated with nicotine or morphine but also yohimbine, an anxiogenic α2 antagonist (Schiltz et al 2005;Schroeder et al 2000Schroeder et al , 2001Schroeder et al , 2003Schroeder and Kelley 2002).…”

Section: Conditioned Locomotor Arousalmentioning

confidence: 70%

Acute Stress and Nicotine Cues Interact to Unveil Locomotor Arousal and Activity-Dependent Gene Expression in the Prefrontal Cortex

Schiltz

Kelley

Landry

2007

Biological Psychiatry

View full text Add to dashboard Cite

show abstract

Section: Conditioned Locomotor Arousalmentioning

confidence: 70%

Acute Stress and Nicotine Cues Interact to Unveil Locomotor Arousal and Activity-Dependent Gene Expression in the Prefrontal Cortex

Schiltz

Kelley

Landry

2007

Biological Psychiatry

View full text Add to dashboard Cite

show abstract

“…For example, the phenomenon of test-specific conditioned anxiety to an anxiogenic dose of nicotine has been demonstrated in both the social interaction and the elevated plus-maze tests (File et al, 2002a;Tucci et al, 2002). The corticotrophin releasing factor antagonist, a-helical CRF 9-41 reversed this conditioned anxiety, but not nicotine-induced unconditioned anxiety, providing evidence that conditioned anxiety is mediated by a different mechanism from unconditioned anxiety (Tucci et al, 2003a). More recently, we have also shown conditioned anxiety after a mid-high dose of the cannabinoid agonist CP 55,940 in the social interaction test (Genn et al, 2004a).…”

Section: Conditioned Anxiety and Conditioned Fearmentioning

confidence: 95%

Nicotine and cannabinoids: Parallels, contrasts and interactions

Viveros

Marco

File

2006

Neuroscience & Biobehavioral Reviews

View full text Add to dashboard Cite

“…For example, acute injection of high doses of nicotine into the hippocampus has anxiogenic effects that may be mediated by activation of α7 nicotinic acetylcholine receptors (nAChRs) (36), whereas lower doses of nicotine tend to produce anxiolytic effects (37). Interestingly, the anxiogenic effects of nicotine in the hippocampus were induced only under experimental conditions involving an unfamiliar arena or high light (38), which indicates that nAChR stimulation can produce distinct behavioral outcomes depending on the level of stress generated by the test itself.…”

Section: Discussionmentioning

confidence: 99%

Cholinergic signaling in the hippocampus regulates social stress resilience and anxiety- and depression-like behavior

Mineur

Obayemi

Wigestrand

et al. 2013

Proc. Natl. Acad. Sci. U.S.A.

320

229

View full text Add to dashboard Cite

Symptoms of depression can be induced in humans through blockade of acetylcholinesterase (AChE) whereas antidepressant-like effects can be produced in animal models and some clinical trials by limiting activity of acetylcholine (ACh) receptors. Thus, ACh signaling could contribute to the etiology of mood regulation. To test this hypothesis, we administered the AChE inhibitor physostigmine to mice and demonstrated an increase in anxiety-and depression-like behaviors that was reversed by administration of nicotinic or muscarinic antagonists. The behavioral effects of physostigmine were also reversed by administration of the selective serotonin reuptake inhibitor fluoxetine. Administration of fluoxetine also increased AChE activity throughout the brain, with the greatest change in the hippocampus. To determine whether cholinergic signaling in the hippocampus could contribute to the systemic effects of cholinergic drugs, we infused physostigmine or virally delivered shRNAs targeting AChE into the hippocampus. Both pharmacological and molecular genetic decreases in hippocampal AChE activity increased anxietyand depression-like behaviors and decreased resilience to repeated stress in a social defeat paradigm. The behavioral changes due to shRNA-mediated knockdown of AChE were rescued by coinfusion of an shRNA-resistant AChE transgene into the hippocampus and reversed by systemic administration of fluoxetine. These data demonstrate that ACh signaling in the hippocampus promotes behaviors related to anxiety and depression. The sensitivity of these effects to fluoxetine suggests that shRNA-mediated knockdown of hippocampal AChE represents a model for anxiety-and depression-like phenotypes. Furthermore, abnormalities in the cholinergic system may be critical for the etiology of mood disorders and could represent an endophenotype of depression.psychosocial stress | affective disorders D epression affects one in six individuals worldwide, resulting in a substantial personal and economic burden. Although the precise etiology of depression is not known, a constellation of findings suggests that predisposing factors, including individual genetic makeup, interacting with stressful life events, can precipitate depressive disorders. Currently available antidepressants are effective at treating both depression and anxiety, but the therapeutic response remains variable. Only 30% of patients achieve remission during the first line of treatment with a selective serotonin reuptake inhibitor (SSRI) such as fluoxetine, and many patients show only limited improvements. Thus, it is critical to identify the neurobiological factors that predispose individuals to stress susceptibility and depression to understand the etiology and develop therapeutics for the disorder.A recent human imaging study has suggested that acetylcholine (ACh) levels are elevated in patients who are actively depressed, as measured by occupancy of nicotinic receptors throughout the brain, and remain high in patients who have a history of depression (1). In addition, de...

show abstract

Corticotropin releasing factor antagonist, α-helical CRF9–41, reverses nicotine-induced conditioned, but not unconditioned, anxiety

Abstract: CRF is an important mediator of the conditioned anxiety to nicotine, but may not play a role in mediating the acute anxiogenic effects.

Cited by 36 publications

References 49 publications

Acute Stress and Nicotine Cues Interact to Unveil Locomotor Arousal and Activity-Dependent Gene Expression in the Prefrontal Cortex

Acute Stress and Nicotine Cues Interact to Unveil Locomotor Arousal and Activity-Dependent Gene Expression in the Prefrontal Cortex

Nicotine and cannabinoids: Parallels, contrasts and interactions

Cholinergic signaling in the hippocampus regulates social stress resilience and anxiety- and depression-like behavior

Contact Info

Product

Resources

About