Involvement of adenosine in the anti-allodynic effect of amitriptyline in streptozotocin-induced diabetic rats

Ulugöl, Ahmet; Karadağ, Çetin Hakan; Tamer, Melek; Fırat, Zeki; Aslantas, Aysegul; Dökmeci, İsmet

doi:10.1016/s0304-3940(02)00491-3

Cited by 68 publications

(29 citation statements)

References 17 publications

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“…A variety of mechanisms have been suggested to explain amitriptyline antinociceptive actions, including block of uptake of NA and 5-HT, engagement of opioid mechanisms, inhibition of ion channel activity, block of N-methyl-D-aspartic acid receptors, increased γ-aminobutyric acid receptor activity, and modulation of immune function (Mico et al 2006;Dick et al 2007). Adenosine mechanisms are also implicated in antinociception produced by systemic (Ulugol et al 2002) and peripherally administered amitriptyline (Sawynok et al 1999;Ulugol et al 2002) in models of chronic pain. Adenosine A1 receptors (A1Rs) mediate suppression of Escape latency (s) Fig.…”

Section: Discussionmentioning

confidence: 99%

Depression-like behavior and mechanical allodynia are reduced by bis selenide treatment in mice with chronic constriction injury: a comparison with fluoxetine, amitriptyline, and bupropion

2010

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These data demonstrate an important dissociation between the antiallodynic and antidepressant effects in mice when tested in a model of neuropathic pain. Depressive behavior in CCI mice was reversed by bis selenide and amitriptyline but not by the conventional antidepressants fluoxetine and buproprion. Bis selenide was more potent than the other drugs tested for antidepressant-like and antiallodynic effects in mice.

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Section: Discussionmentioning

confidence: 99%

Depression-like behavior and mechanical allodynia are reduced by bis selenide treatment in mice with chronic constriction injury: a comparison with fluoxetine, amitriptyline, and bupropion

2010

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“…One week after surgery, a single intraperitoneal dose of streptozotocin (STZ; Future Bioscience Pvt. Ltd., Delhi, India; 40 mg/ml in 0.1 mol/l phosphate/0.4 mol/l citrate buffer, pH 6.5) at a dose of 45 mg/kg body weight (selection of dose after standardization) was injected in uninephrectomized animals [6]. The diagnosis of diabetes was established 48 h after the STZ injection by the determination of the tail vein blood glucose and animals having a 4- to 6-hour fasting blood glucose concentration of less than 200 mg/dl were excluded from the study.…”

Section: Design and Methodsmentioning

confidence: 99%

Investigating the Effect of CoCl<sub>2</sub> Administration on Diabetic Nephropathy and Associated Aortic Dysfunction

Deshmukh

Patel²,

Prajapati³

et al. 2012

Kidney Blood Press Res

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Aim: Endothelial dysfunction appears to be a consistent finding in diabetic nephropathy. The study aimed to investigate the effect of cobalt chloride in the amelioration of endothelial dysfunction in uninephrectomized diabetic rats. Methods: We examined the effect of CoCl₂ (10 mg/kg, i.p., OD = once a day) treatment on contractile responses to angiotensin II (10^–10 to 10^–6M) in an aortic preparation of control rats and uninephrectomized diabetic control rats. Blood glucose, plasma urea, creatinine, uric acid, aortic endothelial nitric oxide synthase (eNOS), nitrate/nitrite (NOx), superoxide dismutase, catalase and reduced glutathione levels were checked in the different groups. Results: A significant attenuation of the augmented responses to angiotensin II was observed in CoCl₂-treated animals along with a fall in plasma urea, creatinine and uric acid levels. A significant reduction in blood glucose and an increase in aortic eNOS and NOx levels along with antioxidants levels were observed. Conclusion: Chronic hypoxia augments angiotensin II responses in the thoracic aorta of uninephrectomized diabetic control rats. CoCl₂ attenuates these enhanced vascular responses with a significant decrease in blood glucose signifying stabilization of the hypoxia-inducible factor in the alleviation of endothelial dysfunction in diabetic nephropathy.

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“…Such doses of caffeine inhibit antinociception by acetaminophen (Siegers 1973;Godfrey et al 2006), amitriptyline (Esser and Sawynok 2000;Ulugol et al 2002;Yaba et al 2006, Sawynok et al 2008, carbamazepine and oxcarbazepine (Tomić et al 2004) and cizolirtine (Aubel et al 2007). This antagonism may reflect block of adenosine A 1 receptors recruited by increased endogenous levels of adenosine.…”

Section: Summary Of Analgesia-modifying Properties Of Caffeinementioning

confidence: 98%

“…Aminophylline (10 mg kg À1 ), also inactive alone, inhibited antinociception by the antidepressants clomipramine, maprotiline, imipramine and zimelidine (writhing test, mice) (Sierralta et al 1995). Caffeine, generally between 5 and 10 mg kg À1 , inhibits antinociception by amitriptyline in several further models of pain -in the spinal nerve ligation model (thermal hyperalgesia, rats) (Esser and Sawynok 2000), in the streptozotocin-induced diabetic model (mechanical allodynia, rats) (Ulugol et al 2002) and in the formalin model (2% formalin, mice) (Sawynok et al 2008). Caffeine (5 mg kg À1 ) also inhibits the action of a newer antidepressant, venlafaxine (hot plate test, mice) (Yaba et al 2006).…”

Section: Antidepressantsmentioning

confidence: 99%

“…Local administration of caffeine inhibits antinociception produced by peripherally administered amitriptyline in the formalin test in rats (as does 8-phenyltheophylline) (Sawynok et al 1999), in the spinal nerve ligation model in rats (thermal hyperalgesia) (Esser and Sawynok 2000) and in the streptozotocin-induced diabetes model in rats (mechanical allodynia) (Ulugol et al 2002). Caffeine was no longer able to inhibit the peripheral action of amitriptyline in adenosine A 1 receptor knockout mice (Sawynok et al 2008).…”

Section: Antidepressantsmentioning

confidence: 99%

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Methylxanthines and Pain

Sawynok

2010

Methylxanthines

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Caffeine, an antagonist of adenosine A(1), A(2A) and A(2B) receptors, is known as an adjuvant analgesic in combination with non-steroidal anti-inflammatory drugs (NSAIDs) and acetaminophen in humans. In preclinical studies, caffeine produces intrinsic antinociceptive effects in several rodent models, and augments the actions of NSAIDs and acetaminophen. Antagonism of adenosine A(2A) and A(2B) receptors, as well as inhibition of cyclooxygenase activity at some sites, may explain intrinsic antinociceptive and adjuvant actions. When combined with morphine, caffeine can augment, inhibit or have no effect depending on the dose, route of administration, nociceptive test and species; inhibition reflects spinal inhibition of adenosine A(1) receptors, while augmentation may reflect the intrinsic effects noted above. Low doses of caffeine given systemically inhibit antinociception by several analgesics (acetaminophen, amitriptyline, oxcarbazepine, cizolirtine), probably reflecting block of a component of action involving adenosine A(1) receptors. Clinical studies have demonstrated adjuvant analgesia, as well as some intrinsic analgesia, in the treatment of headache conditions, but not in the treatment of postoperative pain. Caffeine clearly exhibits complex effects on pain transmission; knowledge of such effects is important for understanding adjuvant analgesia as well as considering situations in which dietary caffeine intake may have an impact on analgesic regimens.

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Involvement of adenosine in the anti-allodynic effect of amitriptyline in streptozotocin-induced diabetic rats

Cited by 68 publications

References 17 publications

Depression-like behavior and mechanical allodynia are reduced by bis selenide treatment in mice with chronic constriction injury: a comparison with fluoxetine, amitriptyline, and bupropion

Depression-like behavior and mechanical allodynia are reduced by bis selenide treatment in mice with chronic constriction injury: a comparison with fluoxetine, amitriptyline, and bupropion

Investigating the Effect of CoCl<sub>2</sub> Administration on Diabetic Nephropathy and Associated Aortic Dysfunction

Methylxanthines and Pain

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