Up-regulation of galanin and corticotropin-releasing hormone mRNAs in the key hypothalamic and amygdaloid nuclei in a mouse model of visceral pain

Nishii, Hisae; Nomura, Masayoshi; Aono, Hisami; Fujimoto, Naohiro; Matsumoto, Tetsuro

doi:10.1016/j.regpep.2006.12.022

Cited by 22 publications

(25 citation statements)

References 50 publications

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“…Galanin levels are reported to increase in sensory neurons in models of chemically induced ileitis (Pidsudko et al, 2003) and cystitis (Callsen-Cencic and Mense, 1997), although a similar study reported no significant change (Zvarova and Vizzard, 2006). In this model, galanin also increased in the hypothalamus and amygdala (Nishii et al, 2007). Galanin also increases after noxious colorectal distension (in the absence of inflammation) (Lu et al, 2005a) and in chronic diverticular disease (Simpson et al, 2009), indicative of a role in visceral as well as somatic pain modulation.…”

Section: Galanin Family Peptides and Receptorsmentioning

confidence: 62%

Physiology, Signaling, and Pharmacology of Galanin Peptides and Receptors: Three Decades of Emerging Diversity

et al. 2014

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Section: Galanin Family Peptides and Receptorsmentioning

confidence: 62%

Physiology, Signaling, and Pharmacology of Galanin Peptides and Receptors: Three Decades of Emerging Diversity

et al. 2014

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“…Pain-related plasticity within the AMG has been demonstrated in rats in multiple models including acute-onset models of arthritis and colitis, in a model of neuropathic pain, and in a cyclophosphamide-induced cystitis pain model in mice (Han and Neugebauer, 2004; Ikeda et al, 2007; Neugebauer et al, 2003; Nishii et al, 2007). Neuroendocrine peptide expression is upregulated in the CeA following cyclophosphamide-induced cystitis of the urinary bladder, and chemical stimulation of the CeA via stereotaxic application of corticosteroids results in facilitation of spinal dorsal horn neuronal responses to bladder distension (Nishii et al, 2007; Qin et al, 2003c).…”

Section: Discussionmentioning

confidence: 99%

Lesions of the central amygdala and ventromedial medulla reduce bladder hypersensitivity produced by acute but not chronic foot shock

et al. 2017

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Both acute and chronic stress has been shown to exacerbate symptoms of chronic visceral pain conditions such as interstitial cystitis. Studies using animal models support these findings in that both acute and chronic exposure to foot shock induced stress (FS) augment nociceptive reflex responses to urinary bladder distension (UBD). Only a few studies have examined the neural substrates mediating these phenomena and it is not clear whether acute and chronic stress engage the same or different substrates to produce bladder hypersensitivity. The present studies examined the role of two important central nervous system structures – the amygdala (AMG) and the ventromedial medulla (VMM) – in mediating/modulating hypersensitivity evoked by acute versus chronic FS using responses to graded UBD in adult, female Sprague-Dawley rats. Bladder hypersensitivity produced by acute FS was significantly reduced by either bilateral central AMG or VMM lesions using measures generated by graded UBD, but these lesions had no significant effects using the same measures on bladder hyperalgesia produced by chronic FS. Our findings provide evidence that neural substrates underlying bladder hypersensitivity produced by chronic stress differ from those produced by acute stress. These findings suggest that while the AMG and VMM participate in pain processing during periods of limited exposure to stress, prolonged stress may recruit a new set of neural substrates not initially activated by acute exposure to stress.

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“…However, extracellular signal-regulated kinase (ERK) phosphorylation is observed in the CeA after intraplantar formalin [30] or in acid-induced muscle pain [32]. Last, in visceral pain models but also in more persistent pain models, such as knee intraarticular injection of kaolin-carrageenan, or neuropathic models based on sciatic nerve ligation, major changes can be observed in the CeA (Table 1), such as an increase in spontaneous and evoked activity [33, 34, 37], an enhancement of synaptic transmission at the PB-CeA and the BLA-CeA synapses [35, 38], an increase in the phosphorylation of NR1 glutamatergic subunit [36], an increased expression of CRF, of group I metabotropic glutamatergic receptors (mGluRs) and of corticosterone receptor [26, 29, 35, 39, 40] and an increased cell proliferation [41]. …”

Section: Reviewmentioning

confidence: 99%

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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Up-regulation of galanin and corticotropin-releasing hormone mRNAs in the key hypothalamic and amygdaloid nuclei in a mouse model of visceral pain

Cited by 22 publications

References 50 publications

Physiology, Signaling, and Pharmacology of Galanin Peptides and Receptors: Three Decades of Emerging Diversity

Physiology, Signaling, and Pharmacology of Galanin Peptides and Receptors: Three Decades of Emerging Diversity

Lesions of the central amygdala and ventromedial medulla reduce bladder hypersensitivity produced by acute but not chronic foot shock

The amygdala between sensation and affect: a role in pain

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