Evaluation of ketamine, nimodipine, gabapentin and imipramine in
partial sciatic nerve transection model of neuropathic pain in rat:
An experimental study

Hota, Debasish; Bansal, Vinod; Pattanaik, Smita

doi:10.1358/mf.2007.29.7.1074689

Cited by 12 publications

(15 citation statements)

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“…Both clinical and animal studies have shown that ketamine can be applied for treating many kinds of chronic pain, such as neuropathic pain, cancer pain, and complex regional pain syndrome [4,5,37] . The present results show that a low dose of ketamine (30 g/kg) administration did not affect the pain threshold of the neuropathic rats, while 100 g/kg ketamine showed obvious effects on mechanical allodynia.…”

Section: Discussionmentioning

confidence: 99%

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Ketamine Depresses Toll-Like Receptor 3 Signaling in Spinal Microglia in a Rat Model of Neuropathic Pain

et al. 2011

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Reports suggest that microglia play a key role in spinal nerve ligation (SNL)-induced neuropathic pain, and toll-like receptor 3 (TLR3) has a substantial role in the activation of spinal microglia and the development of tactile allodynia after nerve injury. In addition, ketamine application could suppress microglial activation in vitro, and ketamine could inhibit proinflammatory gene expression possibly by suppressing TLR-mediated signal transduction. Therefore, the present study was designed to disclose whether intrathecal ketamine could suppress SNL-induced spinal microglial activation and exert some antiallodynic effects on neuropathic pain by suppressing TLR3 activation. Behavioral results showed that intrathecal ketamine attenuated SNL-induced mechanical allodynia, as well as spinal microglial activation, in a dose-dependent manner. Furthermore, Western blot analysis displayed that ketamine application downregulated SNL-induced phosphorylated-p38 (p-p38) expression, which was specifically expressed in spinal microglia but not in astrocytes or neurons. Besides, ketamine could reverse TLR3 agonist (polyinosine-polycytidylic acid)-induced mechanical allodynia and spinal microglia activation. It was concluded that intrathecal ketamine depresses TLR3-induced spinal microglial p-p38 mitogen-activated protein kinase pathway activation after SNL, probably contributing to the antiallodynic effect of ketamine on SNL-induced neuropathic pain.

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Section: Discussionmentioning

confidence: 99%

“…tors, nicotinic receptors, voltage-gated ion channels, and the gamma-aminobutyric acid (GABA) receptor are all involved in the analgesia of ketamine [2,3,[5][6][7][8][9] . Very interestingly, some other studies have suggested that glia are also involved in opioid receptor, NMDA receptor, serotonergic receptor, and GABA receptor function [10][11][12][13] .…”

mentioning

confidence: 99%

Ketamine Depresses Toll-Like Receptor 3 Signaling in Spinal Microglia in a Rat Model of Neuropathic Pain

et al. 2011

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“…Although imipramine given daily at 3 mg/kg needed 21 days to modulate hyperalgesia in the partial sciatic nerve transaction model of neuropathy [15] , we have observed that a single subcutaneous injection of imipramine could be enough to relieve allodynia in rats for a relatively prolonged time (70 min when administering 0.5 mg).…”

Section: Discussionmentioning

confidence: 78%

“…Amitriptyline suppressed mechanical allodynia following peripheral administration, but not following intraperitoneal injection, in a rat model of neuropathic pain [14] . Hota et al [15] reported that imipramine modulated hyperalgesia and allodynia in a partial sciatic nerve transaction model of neuropathic pain. No clear data on the effect of doxepin administered alone in animal models of allodynia are available.…”

Section: Introductionmentioning

confidence: 99%

Analgesic and Antiallodynic Effects of Antidepressants after Infiltration into the Rat

García

Valle²,

Escribano³

et al. 2010

Pharmacology

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Tricyclic antidepressants (TCA) have potent local anesthetic properties and may produce a long-lasting pain blockade that could be of interest in relieving chronic pain states such as neuropathic pain, but there are only few data comparing their dose-response curves of analgesic activity under the same experimental conditions. This study examines the time course of pain-relieving properties of 7 TCA in heat-induced paw withdrawal after subcutaneous administration. Mixed inhibitors of norepinephrine and serotonin uptake (amitriptyline, nortriptyline, imipramine, desipramine, doxepin) and selective inhibitors of serotonin uptake (fluoxetine and fluvoxamine) were assayed. The TCA with the longest analgesic activity were selected to test its antiallodynic effect in the neuropathic pain model of chronic sciatic nerve constriction injury. Bupivacaine was used as a reference drug in both experiments. A dose versus time of maximal analgesic effect curve was constructed for each drug. The longest analgesic effect was obtained for doxepin and imipramine. Although low doses of amitriptyline showed the same activity than doxepin, higher doses failed to reach the same effect. Selective inhibitors of serotonin showed no action at all doses tested. In the chronic sciatic nerve constriction injury model, doxepin and, to a smaller degree, amitriptyline and imipramine protected from allodynia; bupivacaine was ineffective. The antiallodynic effect always lasted less long than the analgesic effect. These observations provide support for the potential use of TCA as durable analgesics. Doxepin overall showed the most outstanding results in pain relief.

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“…98,99 Tricyclic antidepressants (imiprimine and reuptake inhibitors [paroxetine and milnacipran]) reduce both thermal and mechanical hyperalgesia. 86,100 Amitriptyline is also effective as a post-treatment against thermal hyperalgesia. 101 …”

Section: Partial Sciatic Ligationmentioning

confidence: 99%

Behavioral Models of Pain States Evoked by Physical Injury to the Peripheral Nerve

Sorkin

Yaksh

2009

Neurotherapeutics

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Summary:Physical injury or compression of the root, dorsal root ganglion, or peripheral sensory axon leads to welldefined changes in biology and function. Behaviorally, humans report ongoing painful dysesthesias and aberrations in function, such that an otherwise innocuous stimulus will yield a pain report. These behavioral reports are believed to reflect the underlying changes in nerve function after injury, wherein increased spontaneous activity arises from the neuroma and dorsal root ganglion and spinal changes increase the response of spinal projection neurons. These pain states are distinct from those associated with tissue injury and pose particular problems in management. To provide for developing an understanding of the underlying mechanisms of these pain states and to promote development of therapeutic agents, preclinical models involving section, compression, and constriction of the peripheral nerve or compression of the dorsal root ganglion have been developed. These models give rise to behaviors, which parallel those observed in the human after nerve injury. The present review considers these models and their application.

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Evaluation of ketamine, nimodipine, gabapentin and imipramine in partial sciatic nerve transection model of neuropathic pain in rat: An experimental study

Cited by 12 publications

References 0 publications

Ketamine Depresses Toll-Like Receptor 3 Signaling in Spinal Microglia in a Rat Model of Neuropathic Pain

Ketamine Depresses Toll-Like Receptor 3 Signaling in Spinal Microglia in a Rat Model of Neuropathic Pain

Analgesic and Antiallodynic Effects of Antidepressants after Infiltration into the Rat

Behavioral Models of Pain States Evoked by Physical Injury to the Peripheral Nerve

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