Stimulation by corticotropin-releasing factor of the release of immunoreactive dynorphin A from mouse spinal cords in vitro

Song, Zhijing; Takemori, A. E.

doi:10.1016/0014-2999(92)90458-g

Cited by 29 publications

(20 citation statements)

References 30 publications

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“…There are a few reports suggesting that KOR activation can elicit CRF release, establishing the potential for interaction between these systems in vivo (Nikolarakis et al, 1986;Song and Takemori, 1992). Additionally, it has been reported recently that reinstatement to drug seeking in squirrel monkeys may be mediated by KOR activation that is dependent on CRF 1 -R activation (Valdez et al, 2007).…”

Section: Discussionmentioning

confidence: 99%

The Dysphoric Component of Stress Is Encoded by Activation of the Dynorphin κ-Opioid System

Land¹,

Bruchas²,

Lemos³

et al. 2008

J. Neurosci.

545

582

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Stress is a complex human experience having both positive and negative motivational properties. When chronic and uncontrollable, the adverse effects of stress on human health are considerable and yet poorly understood. Here, we report that the dysphoric properties of chronic stress are encoded by the endogenous opioid peptide dynorphin acting on specific stress-related neuronal circuits. Using different forms of stress presumed to evoke dysphoria in mice, we found that repeated forced swim and inescapable footshock both produced aversive behaviors that were blocked by a -opioid receptor (KOR) antagonist and absent in mice lacking dynorphin. Injection of corticotropin-releasing factor (CRF) or urocortin III, key mediators of the stress response, produced place aversion that was also blocked by dynorphin gene deletion or KOR antagonism. CRF-induced place aversion was blocked by the CRF 2 receptor antagonist antisauvigine-30, but not by the CRF 1 receptor antagonist antalarmin. In contrast, place aversion induced by the KOR agonist U50,488 was not blocked by antisauvigine-30. These results suggest that the aversive effects of stress were mediated by CRF 2 receptor stimulation of dynorphin release and subsequent KOR activation. Using a phospho-selective antibody directed against the activated KOR to image sites of dynorphin action in the brain, we found that stress and CRF each caused dynorphin-dependent KOR activation in the basolateral amygdala, nucleus accumbens, dorsal raphe, and hippocampus. The convergence of stress-induced aversive inputs on the dynorphin system was unexpected, implicates dynorphin as a key mediator of dysphoria, and emphasizes -receptor antagonists as promising therapeutics.

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Section: Discussionmentioning

confidence: 99%

The Dysphoric Component of Stress Is Encoded by Activation of the Dynorphin κ-Opioid System

Land¹,

Bruchas²,

Lemos³

et al. 2008

J. Neurosci.

545

582

View full text Add to dashboard Cite

show abstract

“…CRF and dynorphin are co-expressed in the hypothalamus [64,65] and central amygdala [66,67] . CRF causes dynorphin release [68,69] and dynorphin-dependent κ opioid receptor activation in several anxiety-related brain regions [30] . Land et al (2008) reported that CRF-induced anxiety-like behaviors were blocked by a κ opioid receptor antagonist [30] .…”

Section: Rodent Models Of Anxietymentioning

confidence: 99%

The role of the dynorphin/κ opioid receptor system in anxiety

Hang

Wang

et al. 2015

Acta Pharmacol Sin

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Anxiety disorders are the most common and prevalent forms of psychiatric disease, although the biological basis of anxiety is not well understood. The dynorphin/κ opioid receptor system is widely distributed in the central nervous system and has been shown to play a critical role in modulating mood and emotional behaviors. In the present review, we summarize current literature relating to the role played by the dynorphin/κ opioid receptor system in anxiety and κ opioid receptor antagonists as potential therapeutic agents for the treatment of anxiety disorders.

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“…Likewise, depletion of DA from the striatum increases both response latencies and omissions (Cole and Robbins, 1989;Baunez and Robbins, 1999), a pattern of effects similar to that which we observed after CRF administration. CRF stimulates dynorphin release (Nikolarakis et al, 1986;Song and Takemori, 1992), which can in turn inhibit DA release via KOR activation at terminals of midbrain DA neurons (Donzanti et al, 1992;Svingos et al, 1999), creating a hypo-dopaminergic state. Additionally, there is evidence that the DRN sends direct projections to the striatum that regulates DA release: activation of 5HT receptors in the striatum increases extracellular concentrations of DA (Benloucif and Galloway, 1991;Benloucif et al, 1993), whereas CRF reduces 5HT release in the striatum (Price et al, 1998), raising the possibility that CRF-induced decreases in 5HT may reduce DA activity in this region.…”

Section: Kor Antagonism Blocks Crf Effects On Attentionmentioning

confidence: 99%

Corticotropin-Releasing Factor (CRF)-Induced Disruption of Attention in Rats Is Blocked by the κ-Opioid Receptor Antagonist JDTic

Veer

Yano

Carroll

et al. 2012

Neuropsychopharmacol

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Stress often disrupts behavior and can lead to psychiatric illness. Considerable evidence suggests that corticotropin-releasing factor (CRF) plays an important role in regulating the effects of stress. CRF administration produces stress-like effects in humans and laboratory animals, and CRF levels are elevated in individuals with stress-related illness. Recent work indicates that k-opioid receptor (KOR) antagonists can block CRF effects, raising the possibility that at least some of the effects of stress are mediated via KORs. Here we examined the effects of CRF on performance in the 5-choice serial reaction time task (5CSRTT), a test used to quantify attention in rodents, as well as functional interactions between CRF and KORs. Male Sprague-Dawley rats were trained in the 5CSRTT and then each was implanted with an intracerebroventricular (ICV) cannula. After recovery and restabilization of performance, they received a single intraperitoneal (IP) injection of vehicle or JDTic (10 mg/kg), a KOR antagonist with long-lasting (414 days) effects. In subsequent sessions, rats received ICV infusions of CRF (0.25-1.0 mg) or vehicle and were tested 60 min later. CRF dose-dependently disrupted performance as reflected by decreases in correct responding, increases in omission errors, increases in latencies to respond correctly, and increases in time to complete the session. JDTic attenuated each of these CRF-induced deficits while having no effects on its own. The persistent ability of JDTic to disrupt KOR function was confirmed using the tail immersion assay. These findings indicate that KOR antagonists can prevent acute stress-related effects that degrade performance in tasks requiring attention.

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Stimulation by corticotropin-releasing factor of the release of immunoreactive dynorphin A from mouse spinal cords in vitro

Cited by 29 publications

References 30 publications

The Dysphoric Component of Stress Is Encoded by Activation of the Dynorphin κ-Opioid System

The Dysphoric Component of Stress Is Encoded by Activation of the Dynorphin κ-Opioid System

The role of the dynorphin/κ opioid receptor system in anxiety

Corticotropin-Releasing Factor (CRF)-Induced Disruption of Attention in Rats Is Blocked by the κ-Opioid Receptor Antagonist JDTic

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