Roles of β- and α2-Adrenoceptors Within the Central Nucleus of the Amygdala in the Visceral Pain–Induced Aversion in Rats

Deyama, Satoshi; Takishita, Azusa; Tanimoto, Sachi; Ide, Soichiro; Nakagawa, Takayuki; Satoh, Masamichi; Minami, Masabumi

doi:10.1254/jphs.10139sc

Cited by 14 publications

(16 citation statements)

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“…Injection of cholinergic agonists Naïve- Decreased thermal sensitivity, reduced jaw opening reflex- Decreased vocalizations[63, 65, 66] 7. Injection of noradrenergic α 2 ligands Naïve- Agonist induced mechanical and thermal hypoalgesia[64, 80]- Antagonist reduced stress-induced thermal hypoalgesia Acetic acid- Agonist decreased pain-induced CPA[81] 8. Injection of noradrenergic β antagonists Acetic acid- Decreased pain-induced CPA[81] 9.…”

Section: Reviewmentioning

confidence: 99%

“…Injection of noradrenergic α 2 ligands Naïve- Agonist induced mechanical and thermal hypoalgesia[64, 80]- Antagonist reduced stress-induced thermal hypoalgesia Acetic acid- Agonist decreased pain-induced CPA[81] 8. Injection of noradrenergic β antagonists Acetic acid- Decreased pain-induced CPA[81] 9. Injection of CGRP receptor ligands Naïve- CGRP decreased mechanical and thermal reflexes[59] Naïve- CGRP increased mechanical reflexes- CGRP increased vocalizations[82] Arthritis- CGRP1 antagonist inhibited the enhanced reflex to mechanical stimulus- CGRP1 antagonist decreased vocalizations[83] 10.…”

Section: Reviewmentioning

confidence: 99%

“…A widely used test to assess the affective/emotional component of pain, is the pain-induced conditioned place aversion. This behavior is suppressed in the intraplantar formalin and intraperitoneal acetic acid models by bilateral lesions of the CeA [72, 73] or by injection of β-adrenoceptor antagonist [81]. Similarly, intra-CeA administration of a GABA-A receptor agonist, a NMDA antagonist or a group I mGluR antagonist reduces the place avoidance behavior in neuropathic rats [74, 75].…”

Section: Reviewmentioning

confidence: 99%

“…It is also not yet known how the opioid system interacts with other neurotransmission systems within the CeA, but several studies suggest that the CeA opioid system act downstream to agents that promote antinociception such as galanin or BDNF [60, 68]. Finally, adrenoceptors modulate pain processes in the CeA [64, 80, 81], especially through α 2 adrenoceptors located on PB-CeA pre-synaptic elements which strongly regulate glutamate release [100].

Figure 3 Molecular actors in nociceptive processing in the CeA during arthritic pain.…”

Section: Reviewmentioning

confidence: 99%

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The amygdala between sensation and affect: a role in pain

2013

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The amygdala is a structure of the temporal lobe thought to be involved in assigning emotional significance to environmental information and triggering adapted physiological, behavioral and affective responses. A large body of literature in animals and human implicates the amygdala in fear. Pain having a strong affective and emotional dimension, the amygdala, especially its central nucleus (CeA), has also emerged in the last twenty years as key element of the pain matrix. The CeA receives multiple nociceptive information from the brainstem, as well as highly processed polymodal information from the thalamus and the cerebral cortex. It also possesses the connections that allow influencing most of the descending pain control systems as well as higher centers involved in emotional, affective and cognitive functions. Preclinical studies indicate that the integration of nociceptive inputs in the CeA only marginally contributes to sensory-discriminative components of pain, but rather contributes to associated behavior and affective responses. The CeA doesn’t have a major influence on responses to acute nociception in basal condition, but it induces hypoalgesia during aversive situation, such as stress or fear. On the contrary, during persistent pain states (inflammatory, visceral, neuropathic), a long-lasting functional plasticity of CeA activity contributes to an enhancement of the pain experience, including hyperalgesia, aversive behavioral reactions and affective anxiety-like states.

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Section: Reviewmentioning

confidence: 99%

Section: Reviewmentioning

confidence: 99%

Section: Reviewmentioning

confidence: 99%

Figure 3 Molecular actors in nociceptive processing in the CeA during arthritic pain.…”

Section: Reviewmentioning

confidence: 99%

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The amygdala between sensation and affect: a role in pain

2013

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“…In addition, recent studies in rats showed that a aversion to a noxious stimuli can also be assessed with a conditioned place aversion (CPA) test after intraperitoneal (i.p.) injection of acetic acid (AA) (Deyama et al, 2010) or intraplantar injection of complete Freund’s adjuvant (Johansen et al, 2001; Zhang et al, 2013). These studies revealed that several limbic brain areas, such as the anterior cingulate cortex (Deyama et al, 2007; Johansen and Fields, 2004; Johansen et al, 2001), central amygdala (Deyama et al, 2010), and bed nucleus of the stria terminalis (Deyama et al, 2008, 2007), mediate this CPA.…”

Section: Introductionmentioning

confidence: 99%

Expression and pharmacological modulation of visceral pain-induced conditioned place aversion in mice

et al. 2016

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Pain encompasses both a sensory as well as an affective dimension and these are differentially processed in the brain and periphery. It is therefore important to develop animal models to reflect the non-reflexive assays in pain. In this study, we compared effects of the mu opioid receptor agonist morphine, the nonsteroidal anti-inflammatory drug ketoprofen and the kappa receptor opioid agonist U50,488H and antagonist JDTic on acetic acid-induced stretching and acetic acid-induced aversion in the condition place aversion (CPA) test in male ICR mice. Intraperitoneal administration of acetic acid (0.32–1%) was equipotent in stimulating stretching and CPA. Ketoprofen, morphine and U50,488H all inhibited the acid-induced stretching. Ketoprofen and morphine also blocked the acid-induced CPA but U50,488H failed to do so. The reversal ability of ketoprofen and morphine on acid-induced CPA is unique to pain-stimulated place aversion since these drugs failed to reduce non-noxious LiCl-induced CPA. Overall, this study characterized and validated a preclinical mouse model of pain-related aversive behavior that can be used to assess genetic and biological mechanisms of pain as well as improving the predictive validity of preclinical studies on candidate analgesics.

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