Thermal Allodynia (thermal + allodynia)

Distribution by Scientific Domains


Selected Abstracts


Neuropathic pain is enhanced in ,-opioid receptor knockout mice

EUROPEAN JOURNAL OF NEUROSCIENCE, Issue 3 2006
Xavier Nadal
Abstract We have evaluated the possible involvement of ,-opioid receptor (DOR) in the development and expression of neuropathic pain. For this purpose, partial ligation of the sciatic nerve was performed in DOR knockout mice and wild-type littermates. The development of mechanical and thermal allodynia, as well as thermal hyperalgesia was evaluated by using the von Frey filament model, the cold-plate test and the plantar test, respectively. In wild-type and DOR knockout mice, sciatic nerve injury led to a neuropathic pain syndrome revealed in these nociceptive behavioural tests. However, the development of mechanical and thermal allodynia, and thermal hyperalgesia was significantly enhanced in DOR knockout mice. These results reveal the involvement of DOR in the control of neuropathic pain and suggest a new potential therapeutic use of DOR agonists. [source]


Markedly attenuated acute and chronic pain responses in mice lacking adenylyl cyclase-5

GENES, BRAIN AND BEHAVIOR, Issue 2 2007
K.-S. Kim
Chronic inflammatory and neuropathic pain is often difficult to manage using conventional remedies. The underlying mechanisms and therapeutic strategies required for the management of chronic pain need to be urgently established. The cyclic AMP (cAMP) second messenger system has been implicated in the mechanism of nociception, and the inhibition of the cAMP pathway by blocking the activities of adenylyl cyclase (AC) and protein kinase A has been found to prevent chronic pain in animal models. However, little is known regarding which of the 10 known isoforms of AC are involved in nociceptive pathways. Therefore, we investigated the potential pronociceptive function of AC5 in nociception using recently developed AC5 knockout mice (AC5,/,). We found that AC5,/, mice show markedly attenuated pain-like responses in acute thermal and mechanical pain tests as compared with the wildtype control. Also, AC5,/, mice display hypoalgesic responses to inflammatory pain induced by subcutaneous formalin injection into hindpaws, and to non-inflammatory and inflammatory visceral pain induced by injecting magnesium sulfate or acetic acid into the abdomen. Moreover, AC5,/, mice show strongly suppressed mechanical and thermal allodynia in two nerve injury-induced neuropathic pain models. These results suggest that AC5 is essential for acute and chronic pain, and that AC5 knockout mice provide a useful model for the evaluation of the pathophysiological mechanisms of pain. [source]


A MOUSE MODEL FOR PERIPHERAL NEUROPATHY PRODUCED BY A PARTIAL INJURY OF THE NERVE SUPPLYING THE TAIL

JOURNAL OF THE PERIPHERAL NERVOUS SYSTEM, Issue 4 2002
SK Back
We attempted to develop a mouse model for peripheral neuropathy by a partial injury of the nerve supplying the tail. Under enflurane anesthesia, the unilateral superior caudal trunk was resected between the S3 and S4 spinal nerves. Tests for thermal allodynia were conducted by immersing the tail into 4 or 38C water. The mechanical allodynia was assessed by stimulating the tail with a von Frey hair (1.96 mN, 0.2 g). After the nerve injury, the experimental animals had shorter tail withdrawal latencies to cold and warm water immersion than the presurgical latency, and exhibited an increase in tail response to von Frey stimulation. We interpret these abnormal sensitivities as the signs of mechanical, cold and warm allodynia following the superior caudal trunk injury in the mouse. [source]


Targeted Pharmacotherapy of Evoked Phenomena in Neuropathic Pain: A Review of the Current Evidence

PAIN MEDICINE, Issue 1 2007
BSc(Med), Ron Granot MB BS
ABSTRACT Objective., Evoked phenomena in clinical neuropathic pain are viewed as a window into the underlying pathophysiology. They are also potential therapeutic targets. This study sought evidence for the effect on such evoked phenomena of currently used agents. Design., We reviewed MEDLINE (1966,2006) and EMBASE (1980,2006) to locate all randomized, double-blind, placebo-controlled trials examining therapeutic responses of evoked neuropathic pain phenomena, including dynamic mechanical allodynia, pin prick hyperalgesia, and thermal allodynia. We also noted the methods of elicitation of these evoked pain phenomena. Results., We found 40 articles meeting our inclusion criteria. A wide variety of methods was used to evoke neuropathic pain phenomena. For dynamic mechanical allodynia, there is some evidence for the efficacy of ketamine, alfentanil, and morphine, but only when administered intravenously. For other agents and other evoked pain phenomena, there is insufficient evidence to draw firm conclusions. Conclusions., There is minimal evidence to guide clinicians in treating evoked pain phenomena in clinical neuropathic pain states. There is little clinical evidence to either support or refute theoretical arguments for efficacy of specific agents in evoked neuropathic pain phenomena. More and larger trials are needed to examine these phenomena. Consensus is required with respect to methods used to elicit these evoked phenomena. [source]