Bradykinin into amygdala induces thermal hyperalgesia in rats

Dalmolin, Gerusa Duarte; Silva, C.R.; Bellé, N.A.V.; Rubin, Maribel Antonello; Mello, Carlos Fernando; Calixto, João B.; Ferreira, Juliano

doi:10.1016/j.npep.2006.12.007

Cited by 16 publications

(6 citation statements)

References 53 publications

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“…Imaging studies show an activation of the amygdala in response to different painful stimuli (53,54). Intervention studies in rodents confirmed the central role of the amygdala in pain perception (55)(56)(57)(58).…”

Section: Amygdalamentioning

confidence: 82%

Depression and pain

Michael¹

2009

Front Biosci

138

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Depression and pain disorders are often diagnosed in the same patients. Here we summarize the shared pathophysiology between both disorders and the importance of addressing all symptoms in patients with comorbid pain and depression. We describe anatomical structures that are activated and/or altered in response to both depression and pain--examples include the insular cortex, the prefrontal cortex, the anterior cingulate cortex, the amygdala, and the hippocampus. Both disorders activate common neurocircuitries (e.g. the hypothalamic-pituitary-adrenal axis, limbic and paralimbic structures, ascending and descending pain tracks), common neurochemicals (e.g. monoamines, cytokines, and neurotrophic factors), and are associated with common psychological alterations. One explanation for the interaction and potentiation of the disease burden experienced by patients affected by both pain and depression is provided by the concept of allostasis. In this model, patients accumulate allostatic load through internal and external stressors, which makes them more susceptible to disease. To break this cycle, it is important to treat all symptoms of a patient. Therapeutic approaches that address symptoms of both depression and pain include psychotherapy, exercise, and pharmacotherapy.

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Section: Amygdalamentioning

confidence: 82%

Depression and pain

Michael¹

2009

Front Biosci

138

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“…To evaluate the hypersensitivity to heat stimulation, we used the paw immersion test . Briefly, animals were held, and the right hind paw was immersed in a water bath at 48 °C.…”

Section: Methodsmentioning

confidence: 99%

“…To evaluate the hypersensitivity to heat stimulation, we used the paw immersion test. 22 Briefly, animals were held, and the right hind paw was immersed in a water bath at 48°C. The time elapsed between onset of the stimulus and manifestation of the paw withdrawal response was measured automatically and was taken as an index of the thermal nociceptive threshold.…”

Section: Chronic Inflammation Evaluationmentioning

confidence: 99%

Free and nanoencapsulated vitamin D₃: effects on E‐NTPDase and E‐ADA activities in an animal model with induced arthritis

Silveira

Thorstenberg

et al. 2016

Cell Biochemistry & Function

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Evaluation of the effects on the E-NTPDase and E-ADA activities in an animal model of induced arthritis. Two formulations of vitamin D3 were used: form oral solution and nanoencapsulated. Vitamin D3 seems to contribute to the inflammatory process induced by CFA. Vitamin D3 possibly alters the E-NTPDase and E-ADA activities. Vitamin D3 may be an alternative supplementary treatment for chronic arthritis.

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“…Tail-flick test. The warm-water tail-flick test was performed using a water bath with temperature at 48 ± 0.2 ° [23]. Before injection, baseline latency was determined.…”

Section: Methodsmentioning

confidence: 99%

Antinociceptive Effect of a Novel Tosylpyrazole Compound in Mice

Oliveira¹,

Gewehr²,

Dalmolin³

et al. 2009

Basic Clin Pharma Tox

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Pain is the most common complaint in the medical field and the identification of compounds that can effectively treat painful states without induction of side-effects remains a major challenge in biomedical research. The aim of the present study was to investigate the antinociceptive effect of a novel compound, 3-(4-fluorophenyl)-5-trifluoromethyl-1 H -1-tosylpyrazole (compound A) in several models of pain in mice and compare with those produced by the known trifluoromethyl-containing pyrazole compound celecoxib. Compound A or celecoxib were administrated by oral (78-780 μ mol/kg), intrathecal (9-22.5 nmol/site) or intracerebroventricular (9-22.5 nmol/site) routes. Oral administration of either compound A or celecoxib abolished the mechanical allodynia, but not the oedema caused by intraplantar injection of carrageenan. Similarly, compound A reduced the overt nociception, but not the oedema, produced by bradykinin or capsaicin. However, compound A (500 μ mol/kg, orally) did not alter nociception nor oedema caused by intraplantar injection of prostaglandin E 2 or glutamate, whereas celecoxib reduced only the nociception induced by the former. Moreover, oral and intrathecal administration of compound A or celecoxib also reduced the nociception induced by acetic acid. However, only celecoxib reduced the acetic acid-induced nociception when it was injected by the intracerebroventricular route. Finally, neither compound A nor celecoxib was able to produce antinociceptive effect in the tail-flick test or to alter the motor performance and the body temperature. Besides, compound A or celecoxib did not induce gastric lesion. Thus, compound A seems to be an interesting prototype for the development of novel analgesic drugs.

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Bradykinin into amygdala induces thermal hyperalgesia in rats

Cited by 16 publications

References 53 publications

Depression and pain

Depression and pain

Free and nanoencapsulated vitamin D₃: effects on E‐NTPDase and E‐ADA activities in an animal model with induced arthritis

Antinociceptive Effect of a Novel Tosylpyrazole Compound in Mice

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Bradykinin into amygdala induces thermal hyperalgesia in rats

Cited by 16 publications

References 53 publications

Depression and pain

Depression and pain

Free and nanoencapsulated vitamin D3: effects on E‐NTPDase and E‐ADA activities in an animal model with induced arthritis

Antinociceptive Effect of a Novel Tosylpyrazole Compound in Mice

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Product

Resources

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Free and nanoencapsulated vitamin D₃: effects on E‐NTPDase and E‐ADA activities in an animal model with induced arthritis