Modality-specific hyperexcitability of dorsal horn neurons to mechanical stimuli in herpetic mice

Nishikawa, Yukitoshi; Sasaki, Atsushi; Andoh, Tsugunobu; Nishimura, Hiroshi; Shiraki, Kimíyasu; Kuraishi, Yasushi

doi:10.1097/wnr.0b013e32832e0cc1

Cited by 4 publications

(1 citation statement)

References 20 publications

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“…Our recent study has demonstrated that the excitatory response of spinal dorsal horn neurons to brush stimulation of the lesional skin was increased in herpetic mice, while the response of the tibial nerve, a branch of the sciatic nerve innervating the affected skin, to brush stimulation was decreased (11). These findings suggest that dynamic allodynia in the affected dermatome is due to the increased excitability of spinal dorsal horn neurons, but not primary afferents, to brush stimulation.…”

Section: Introductionmentioning

confidence: 73%

Blockade of Glycine Transporter (GlyT) 2, but Not GlyT1, Ameliorates Dynamic and Static Mechanical Allodynia in Mice With Herpetic or Postherpetic Pain

2010

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Abstract.Glycine is an inhibitory neurotransmitter in the spinal dorsal horn and its extracellular concentration is regulated by glial glycine transporter (GlyT) 1 and neuronal GlyT2. This study was conducted to elucidate the effects of intrathecal injections of GlyT1 and GlyT2 inhibitors on two distinct types of mechanical allodynia, dynamic and static allodynia, in mice with herpetic or postherpetic pain. The GlyT2 inhibitor ALX1393, but not the GlyT1 inhibitor sarcosine, suppressed dynamic and static allodynia at the herpetic and postherpetic stages. Intrathecal ALX1393 suppressed dynamic allodynia induced by intrathecal strychnine and N -methyl-D -aspartate (NMDA). Intrathecal sarcosine suppressed dynamic allodynia induced by intrathecal strychnine, but not NMDA. Expression level of GlyT1, but not GlyT2, mRNA in the lumbar dorsal horn was decreased at the herpetic and postherpetic stages. Glycine receptor α 1-subunit mRNA was decreased in the lumbar dorsal horn at the herpetic, but not postherpetic stage, without alteration in α 3-subunit mRNA. The results suggest that GlyT2 is a potential target for treatment of dynamic and static allodynia in patients with herpes zoster and postherpetic neuralgia. The lack of efficacy of GlyT1 inhibitor may be explained by activation of NMDA receptors and the down-regulation of GlyT1 in the lumbar dorsal horn.

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Section: Introductionmentioning

confidence: 73%

Blockade of Glycine Transporter (GlyT) 2, but Not GlyT1, Ameliorates Dynamic and Static Mechanical Allodynia in Mice With Herpetic or Postherpetic Pain

2010

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Animal Models and Pharmacology of Herpetic and Postherpetic Pain

Kuraishi

Sasaki

2014

Behavioral Neurobiology of Chronic Pain

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Varicella-zoster virus (VZV) causes varicella upon primary infection and subsequently becomes latent in the sensory ganglia. Reactivation of latent VZV in the sensory ganglion results in herpes zoster, which usually begins with pain and dysesthesia. Pain that persists long after healing of the rash is termed postherpetic neuralgia. VZV inoculation into rats induces mechanical allodynia and thermal hyperalgesia without causing herpes zoster. As with VZV, herpes simplex virus 1 (HSV1) is an alphaherpesvirus. HSV1 also becomes latent in the sensory ganglia after primary infection, and reactivation of latent HSV1 in the sensory ganglion results in herpes simplex. HSV1 inoculation into mice causes zoster-like skin lesions together with mechanical allodynia and mechanical hyperalgesia. A marked difference between the two rodent models is whether the herpes virus proliferates in the nervous system after inoculation. VZV-inoculated rats are useful for investigating mechanical allodynia induced by latent infection with herpes virus. HSV1-inoculated mice are useful for investigating mechanical allodynia induced by the proliferation of herpes virus in sensory neurons and for assessing the effects of acute herpetic pain on the incidence of postherpetic allodynia.

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A Memoir of My Research on Pain and Analgesia for 39 Years

Kuraishi

2014

YAKUGAKU ZASSHI

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This review describes my research for the past 39 years regarding the pharmacology of pain and analgesia. We have demonstrated that the descending noradrenergic system is involved in the analgesic eŠect of morphine injected into the nucleus reticularis gigantocellularis, and that noradrenaline exerts antinociception mediated by a-adrenoceptors. We have found that noxious mechanical and thermal stimuli to the skin increase the release of substance P and somatostatin, respectively, from the dorsal horn in situ, and that noradrenaline inhibits the release of substance P and glutamate from primary aŠerents. We developed an animal model of cancer pain using melanoma cells. We have shown that the suppression of cancer pain results in the inhibition of tumor growth and lung metastasis, and that melanoma cells release several algogenic substances including ATP, endothelin-1, and bradykinin. We investigated neuropathic allodynia induced by the chemotherapeutic drugs paciltaxel, oxaliplatin, vincristine, and bortezomib. Single administration of these drugs caused allodynia with similar time-courses. However, antiallodynic actions of adjuvant analgesics, including gabapentin and limaprost, were dependent on the chemotherapeutic drugs used. Limaprost experiments have revealed that a decrease in peripheral blood ‰ow is involved in allodynia exacerbation after the administration of paciltaxel and oxaliplatin. We have developed animal models of herpetic pain and postherpetic neuralgia using herpes simplex virus 1. We have demonstrated that nitric oxide, prostaglandin E 2 , and galectin-3 are involved in herpetic allodynia, that risk factors associated with postherpetic allodynia include severe herpetic pain, nociceptin, and major histocompatibility complex, and that deaŠerentation and nitric oxide are involved in postherpetic allodynia.Key words-neuropathic pain; descending noradrenergic system; nociceptive transmitter; cancer pain

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Modality-specific hyperexcitability of dorsal horn neurons to mechanical stimuli in herpetic mice

Cited by 4 publications

References 20 publications

Blockade of Glycine Transporter (GlyT) 2, but Not GlyT1, Ameliorates Dynamic and Static Mechanical Allodynia in Mice With Herpetic or Postherpetic Pain

Blockade of Glycine Transporter (GlyT) 2, but Not GlyT1, Ameliorates Dynamic and Static Mechanical Allodynia in Mice With Herpetic or Postherpetic Pain

Animal Models and Pharmacology of Herpetic and Postherpetic Pain

A Memoir of My Research on Pain and Analgesia for 39 Years

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