ChemInform Abstract: Synthesis and Determination of Acute and Chronic Pain Activities of 1‐[1‐(3‐Methylphenyl)(tetralyl)]piperidine (I) as a New Derivative of Phencyclidine via Tail Immersion and Formalin Tests.

Ahmadi, Abbas; Khalili, Mohsen; Mihandoust, Farnaz; Barghi, Leila

doi:10.1002/chin.201032149

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“…The time taken to withdraw the tail was noted as reaction time (22). Prior to the experiment the mice were screened for the sensitivity test by immersing the tail of the mice gently in hot water maintained at 55 o C (23). A cut off time of 10 sec was maintained at 55°C to prevent tissue damage.…”

Section: Tail-immersion Testmentioning

confidence: 99%

Evaluation of the Effects of Novel Nafimidone Derivatives on Thermal Hypoalgesia in Mice with Diabetic Neuropathy

et al. 2013

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The worldwide diabetes epidemic has shown no signs of abatement. Its prevalence has more than doubled since 1980 (1). Diabetic neuropathy (DN) is the most common diabetic complication, afflicting over 50% of all diabetics. The possible biochemical pathomechanisms include oxidative stress, activation of the polyol pathway, increased advanced glycation end products (AGEs) and their receptors, impaired ionic homeostasis of cells and activation of protein kinases (PKC and PKA), and mitogen-activated protein kinases (MAPK), and inducible nitric oxide synthase (2-6).Understanding the biochemical mechanisms underlying diabetic neuropathic pain and sensory disorders requires preclinical studies in animal models. The streptozotocin (STZ)-induced diabetic rodent is the most commonly used animal model of diabetes (7,8). On the other hand, existing animal models of diabetic painful and insensate neuropathy, however, have serious limitations. Diabetic rats and mice have limited life span and rarely show evidence of overt neuropathy, such as demyelination, axonal degeneration, fiber loss, or axonal regeneration in their peripheral nerves. This makes diabetic rodents unsuitable for studying the contribution of these phenomena of DN to pain or to loss of sensory function (9). Nonetheless, despite these limitations, assessment of behavioral responses to external stimuli in diabetic rats and mice (i.e., thermal and mechanical hyper and hypoalgesia, tactile allodynia, as well as formalin-induced spontaneous nociceptive behavior) has led to identification of a number of mechanisms of loss of sensation and/or pain in diabetes (10).Decades of research elucidating the pathophysiology of diabetic neuropathy have failed, thus far, to produce a treatment that prevents or reverses its development and progression. Recently, however, numerous competing or parallel pathological pathways have begun to intersect and complement each other, illuminating potential pharmacologic targets. The current foci of diabetic neuropathy research are excessive activation of sodium channels and corrupted molecular mechanisms of cellular pathways of related kinases (11).Voltage-gated sodium channels (Na v Chs) are a necessary component of normal sensation, emotions, thoughts and movements and are of particular interest as target for neuro- ABSTRACTObjective: Diabetic neuropathy (DN) is a common complication in Diabetes Mellitus. The streptozotocin-induced diabetic rodent is the most commonly used animal model of diabetes and increased sodium channel expression and activity were revealed in this model. At this study, we evaluated the effect of three different nafimidone derivatives which have possible anticonvulsant activity on disorders of thermal pain sensation in diabetic mice.Study Design: Randomized animal experiment.Material and Methods: Mice were divided randomly into five groups (5 mice per group): Control, Diabetes, Dibetes+C1, Diabetes+C2, Diabetes+C3. We used hot and cold plate, and tail-immersion tests for assessment of thermal nociceptive response...

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Section: Tail-immersion Testmentioning

confidence: 99%