Enhanced nociceptive responding in two rat models of depression is associated with alterations in monoamine levels in discrete brain regions

Burke, Nikita N.; Hayes, Elizabeth S.; Calpin, Pádraig; Kerr, Daniel M.; Moriarty, Orla; Finn, David P.; Roche, Michelle

doi:10.1016/j.neuroscience.2010.10.030

Cited by 61 publications

(70 citation statements)

References 74 publications

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“…In accordance with previous published data from our group (Burke et al, 2010, Burke et al, 2013a, OB animals displayed enhanced nociceptive responding to both mechanical and cold stimuli and enhanced cold allodynia following SNL. Neither acute nor chronic minocycline administration altered basal mechanical thresholds of either sham or OB rats.…”

Section: Acute Minocycline Pretreatment Prevents the Development Of Nsupporting

confidence: 93%

“…Recent data from our laboratory and others have demonstrated that OB rats exhibit mechanical allodynia, enhanced formalin-evoked nociceptive behaviour (Burke et al, 2013a, Burke et al, 2010, Wang et al, 2010, increased nociceptive behaviours to electrical stimulation of the dura mater (Liang et al, 2011), and altered nociceptive behaviour following SNL (Burke et al, 2013a). This latter effect has been shown to be associated with altered central expression of the cytokines IL-6 and IL-10 ( Burke et al, 2013a).…”

Section: Introductionmentioning

confidence: 90%

“…Bilateral olfactory bulbectomy (OB) was performed on rats anaesthetised with isoflurane (Abbot Laboratories, UK [3% induction, 1.5% maintenance in 0.5 l/min O 2 ]) as described previously (Roche et al, 2007, Burke et al, 2010, Burke et al, 2013a. In brief, two burr holes of 2mm diameter were drilled into the skull, 5mm rostral to bregma and 2mm lateral to the midline and the olfactory bulbs removed by gentle aspiration.…”

Section: Bilateral Olfactory Bulbectomy (Ob) Surgery -Model Of Depresmentioning

confidence: 99%

“…Two weeks following sham/OB surgery, animals were placed singly into a brightly-lit (lux 200) novel open field arena (diameter 75cm) with a white floor (plastic-covered wood flooring) and reflective walls for a 5 minute period. Locomotor activity (distance moved, cm) was assessed using a computerised video tracking system (EthoVision®, Version 8 Noldus, Netherlands) as previously described (Burke et al, 2013a, Burke et al, 2010, Roche et al, 2007.…”

Section: Open Field Testmentioning

confidence: 99%

“…Recent data from animal studies support this clinical relationship and indicate that inflammatory and neuropathic pain-related responding is enhanced in various animal models of depression including olfactory bulbectomy (OB) (Burke et al, 2013a, Burke et al, 2010, early life stress (Uhelski andFuchs, 2010, Burke et al, 2013b) and the Wistar-Kyoto rat (Burke et al, 2010, Zeng et al, 2008, Rea et al, 2014. However, the neurobiological substrates mediating altered nociceptive responding in depression remain ambiguous.…”

Section: Introductionmentioning

confidence: 99%

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Minocycline modulates neuropathic pain behaviour and cortical M1–M2 microglial gene expression in a rat model of depression

Burke¹,

Kerr²,

Moriarty³

et al. 2014

Brain, Behavior, and Immunity

140

106

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Section: Acute Minocycline Pretreatment Prevents the Development Of Nsupporting

confidence: 93%

Section: Introductionmentioning

confidence: 90%

Section: Bilateral Olfactory Bulbectomy (Ob) Surgery -Model Of Depresmentioning

confidence: 99%

Section: Open Field Testmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

See 3 more Smart Citations

Minocycline modulates neuropathic pain behaviour and cortical M1–M2 microglial gene expression in a rat model of depression

Burke¹,

Kerr²,

Moriarty³

et al. 2014

Brain, Behavior, and Immunity

140

106

View full text Add to dashboard Cite

The analgesic efficacy of morphine varies with rat strain and experimental pain model: implications for target validation efforts in pain drug discovery

Hestehave

Abelson

Pedersen

et al. 2018

European Journal of Pain

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Background Translating efficacy of analgesic drugs from animal models to humans remains challenging. Reasons are multifaceted, but lack of sufficiently rigorous preclinical study design criteria and phenotypically relevant models may be partly responsible. To begin to address this fundamental issue, we assessed the analgesic efficacy of morphine in three inbred rat strains (selected based on stress reactivity and affective/pain phenotypes), and outbred Sprague Dawley ( SD ) rats supplied from two vendors. Methods Sensitivity to morphine (0.3–6.0 mg/kg, s.c.) was evaluated in the hot plate test of acute thermal nociception, the Complete Freund's Adjuvant ( CFA ) model of inflammatory‐induced mechanical hyperalgesia, and in a locomotor motility assay in male rats from the following strains; Lewis ( LEW ), Fischer (F344), Wistar Kyoto ( WKY ), and SD 's from Envigo and Charles River. Results F344 and SD rats were similarly sensitive to morphine in hot plate and CFA ‐induced inflammatory hyperalgesia (Minimum Effective Dose ( MED ) = 3.0 mg/kg). WKY rats developed a less robust mechanical hypersensitivity after CFA injection, and were less sensitive to morphine in both pain tests ( MED = 6.0 mg/kg). LEW rats were completely insensitive to morphine in the hot plate test, in contrast to the reversal of CFA ‐induced hyperalgesia ( MED = 3.0 mg/kg). All strains exhibited a dose‐dependent reduction in locomotor activity at 3.0–6.0 mg/kg. Conclusion Sensory phenotyping in response to acute thermal and inflammatory‐induced pain, and sensitivity to morphine in various inbred and outbred rat strains indicates that different pathophysiological mechanisms are engaged after injury. This could have profound implications for translating preclinical drug discovery efforts into pain patients. Significance The choice of rat strain used in preclinical pain research can profoundly affect the outcome of experiments in relation to (a) nociceptive threshold responses, and (b) efficacy to analgesic treatment, in assays of acute and tonic inflammatory nociceptive pain.

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Neurobiology of Stress-Induced Hyperalgesia

Olango

Finn

2014

Behavioral Neurobiology of Chronic Pain

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The intensity and severity of perceived pain does not correlate consistently with the degree of peripheral or central nervous system tissue damage or with the intensity of primary afferent or spinal nociceptive neurone activity. In this respect, the modulation of pain by emotion and context is now widely recognized. In particular, stress, fear and anxiety exert potent, but complex, modulatory influences on pain. Stress can either suppress pain (stress-induced analgesia) or exacerbate it (stress-induced hyperalgesia; SIH) depending on the nature, duration and intensity of the stressor. Herein, we review the methods and models used to study the phenomenon of SIH in rodents and humans and then present a detailed discussion of our current understanding of neural substrates and neurobiological mechanisms. The review provides perspectives and challenges for the current and future treatment of pain and the co-morbidity of pain with stress-related psychiatric disorders including anxiety and depression.

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Enhanced nociceptive responding in two rat models of depression is associated with alterations in monoamine levels in discrete brain regions

Cited by 61 publications

References 74 publications

Minocycline modulates neuropathic pain behaviour and cortical M1–M2 microglial gene expression in a rat model of depression

Minocycline modulates neuropathic pain behaviour and cortical M1–M2 microglial gene expression in a rat model of depression

The analgesic efficacy of morphine varies with rat strain and experimental pain model: implications for target validation efforts in pain drug discovery

Neurobiology of Stress-Induced Hyperalgesia

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