Noxious thermal input from the rat tail: Modulation by descending inhibitory influences

Necker, Reinhold; Hellon, R. F.

doi:10.1016/0304-3959(77)90135-x

Cited by 142 publications

(49 citation statements)

References 17 publications

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“…This reflex is relayed in the distal part of the spinal cord and persists after spinal cord transection (Irwin et al 1951), indicating that the motor response does not rely on cognitive processing and requires minimum coordination. The tail flick reflex is under a tonic descending inhibitory mechanism (Necker and Hellon 1978); this inhibitory mechanism appears to be mediated through the endogenous opioid systems . On the other hand, the jumping response in the hot plate test is a coordinated reflex involving higher degree of cognitive processing (Jacob 1966;Jacob and Ramabadran 1983;Ramabadran and Bansinath 1986).…”

Section: Discussionmentioning

confidence: 99%

The hyperalgesic effect of naloxone is attenuated in streptozotocin-diabetic mice

et al. 1989

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In mice with streptozotocin-induced hyperglycemia, nociception was tested after naloxone administration in hot plate and tail immersion tests. The choice of these two tests was to include a supra-spinal nociceptive reflex indicative of higher cognitive process (hot-plate test) as well as a reflex which predominantly represents lower spinal motor mechanisms (tail immersion test). Naloxone-induced hyperalgesia was attenuated in both tests in mice with streptozotocin-induced diabetes. In mice with hyperglycemia induced by intraperitoneal dextrose administration, naloxone hyperalgesia was significantly enhanced in the hot plate test. The basal nociceptive threshold in streptozotocin-treated animals was decreased in the immersion but not in the hot plate test. These results indicate that hyperglycemia per se does not adequately explain the changes in naloxone hyperalgesia in experimental models of diabetes. They also suggest that acute hyperglycemia may modify the interaction of endogenous opioid peptides with their receptors only at supra-spinal sites. However, chronic hyperglycemia appears to affect endogenous opioid peptides both at spinal and supra-spinal levels and their interaction with the opiate receptors.

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Section: Discussionmentioning

confidence: 99%

The hyperalgesic effect of naloxone is attenuated in streptozotocin-diabetic mice

et al. 1989

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“…11,13,14) Thermal heat hyperalgesia was assessed by the tail immersion test as described by Necker and Hellon. 15) Tail heat-hyperalgesia was noted with the immersion of terminal part of the tail (1 cm) in water, maintained at a temperature of 52Ϯ1.0°C. The tail withdrawal latency was recorded, as a response of heat thermal sensation, and a cut-off time of 20 s was maintained.…”

Section: Experimental Animalsmentioning

confidence: 99%

“…15) Tail coldhyperalgesia was noted with the immersion of terminal part of the tail (1 cm) in water maintained at a temperature of 0-4°C. The tail withdrawal latency was recorded as a response of cold thermal sensation and a cut-off time of 20 s was maintained.…”

Section: Experimental Animalsmentioning

confidence: 99%

Ameliorative Potential of Pralidoxime in Tibial and Sural Nerve Transection-Induced Neuropathic Pain in Rats

Kaur

Jaggi

Singh

2010

Biological & Pharmaceutical Bulletin

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The present study was designed to investigate the ameliorative potential of pralidoxime in tibial and sural nerve transection-induced neuropathy in rats. Tibial and sural nerve transection was performed by sectioning tibial and sural nerve portions (2 mm) of the sciatic nerve, and leaving the common peroneal nerve intact. The pinprick, acetone, hot and cold tail immersion tests were performed to assess the degree of motor functions, mechanical hyperalgesia, cold allodynia, heat and cold hyperalgesia respectively. Biochemically, the tissue thio-barbituric acid reactive species (TBARS), super-oxide anion contents (the markers of oxidative stress) and total calcium levels were measured. Tibial sural nerve transection resulted in the development of mechanical hyperalgesia, cold allodynia, heat and cold hyperalgesia along with the rise in oxidative stress and calcium levels. However, administration of pralidoxime (10, 20 mg/kg intraperitoneally (i.p.)) for 14 d attenuated tibial and sural nerve transection-induced cold allodynia, mechanical, hot and cold hyperalgesia. Furthermore, pralidoxime also attenuated tibial and sural nerve transection induced increase in oxidative stress and calcium levels. It may be concluded that pralidoxime has ameliorative potential in attenuating the painful neuropathic state associated with tibial and sural nerve transection, which may possibly be attributed to decrease in oxidative stress and calcium levels.

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“…Thermal hyperalgesia and allodynia were assessed by the tail immersion test [15] . The tail of the rat was immersed in cold water maintained at noxious (4 ° C) or non-noxious (10 ° C) temperature, until the tail was withdrawn.…”

Section: Methodsmentioning

confidence: 99%

Vincristine-Induced Neuropathy in the Rat Is Not Modified by Drug-Drug Interactions with the P-Glycoprotein Inhibitor Verapamil

Balayssac¹,

Cayre²,

Ling³

et al. 2008

Chemotherapy

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Background: Cancer patients can be exposed to drug interactions during treatment with toxic anticancer drugs. The peripheral nervous system is a target for neurotoxic anticancer drugs. P-glycoprotein is essential for the functional integrity of blood-tissue barriers, and P-glycoprotein inhibition due to possible drug interactions could lead to adverse neurotoxic reactions. Methods: In a rat model of vincristine-induced neuropathy, we assessed the consequences of potential drug interactions of vincristine with some P-glycoprotein-inhibiting drugs, chosen because of their potency to increase the incorporation of ^99mTc-sestamibi in nervous tissue. Results: Quinidine (30 mg/kg) increased ^99mTc-sestamibi incorporation in dorsal root ganglia (DRG) but was toxic for rats. Verapamil (30 mg/kg) increased the tracer incorporation in the spinal cord, DRG and sciatic nerve. Combination treatment with the verapamil-vincristine regimen had a tendency to lower weight gain and altered nociceptive thresholds of neuropathic animals. Conclusion: Behavioral pain tests did not reveal an increase in vincristine neurotoxicity following combination treatment with verapamil and vincristine. This regimen only led to a slight increase in general toxicity.

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Noxious thermal input from the rat tail: Modulation by descending inhibitory influences

Cited by 142 publications

References 17 publications

The hyperalgesic effect of naloxone is attenuated in streptozotocin-diabetic mice

The hyperalgesic effect of naloxone is attenuated in streptozotocin-diabetic mice

Ameliorative Potential of Pralidoxime in Tibial and Sural Nerve Transection-Induced Neuropathic Pain in Rats

Vincristine-Induced Neuropathy in the Rat Is Not Modified by Drug-Drug Interactions with the P-Glycoprotein Inhibitor Verapamil

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