N-Methyl-d-aspartate (NMDA) and non-NMDA glutamate receptor antagonists differentially suppress dorsal horn neuron responses to mechanical stimuli in rats with peripheral nerve injury

Leem, Joong Woo; Choi, Eun Jin; Park, Eun Sun; Paik, Kwang Se

doi:10.1016/0304-3940(96)12714-2

Cited by 49 publications

(33 citation statements)

References 14 publications

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“…The role of spinal AMPA receptors in neuropathic pain behaviors after nerve injury, as demonstrated in the present study, is consistent with previous studies (Mao et al, 1992a,b;Leem et al, 1996;Kondo et al, 2002;Garry et al, 2003). For instance, activation of spinal AMPA receptors has been shown to induce nociceptive behaviors including thermal hyperalgesia (Yamamoto and Sakashita, 1998;Menéndez et al, 2003) and vocalization (Kontinen and Meert, 2002).…”

Section: Discussionsupporting

confidence: 93%

“…Ionotropic glutamate receptors including alpha-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid (AMPA) receptors are localized both presynaptically and postsynaptically within superficial laminae of spinal cord dorsal horn. AMPA receptors have been shown to play a significant role in the mechanisms of neuropathic pain and spinal nociceptive processing (Mao et al, 1992a,b;Leem et al, 1996;Kondo et al, 2002;Garry et al, 2003). The AMPA receptor consists of several subunits and previous studies have indicated that spinal AMPA receptor expression was altered after either peripheral nerve injury or inflammation, which contributed to the development of pathological pain conditions in rats (Harris et al, 1996;Alvarez et al, 2000).…”

Section: Introductionmentioning

confidence: 99%

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Intrathecal midazolam regulates spinal AMPA receptor expression and function after nerve injury in rats

Lim

Sung

et al. 2006

Brain Research

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Spinal γ-aminobutyric acid (GABA) and alpha-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid (AMPA) receptors have been implicated in the mechanisms of neuropathic pain after nerve injury; however, how these two receptors interact at the spinal level remains unclear. Here we show that intrathecal midazolam through activation of spinal GABAA receptors attenuated the expression and function of spinal AMPA receptors in rats following peripheral nerve injury. Thermal hyperalgesia and mechanical allodynia induced by chronic constriction nerve injury (CCI) in rats were attenuated by the short-acting benzodiazepine midazolam (20=10>5 μg > vehicle) administered intrathecally once daily for seven postoperative days. CCI-induced upregulation of AMPA receptors within the spinal cord dorsal horn was also significantly reduced by the intrathecal midazolam (10, 20 μg) treatment. The inhibitory effects of midazolam (10, 20 μg) on neuropathic pain behaviors and AMPA receptor expression were prevented by co-administration of midazolam with the GABAA receptor antagonist bicuculline (3 μg), whereas intrathecal treatment with bicuculline (1 or 3 μg) alone in naive rats induced the upregulation of spinal AMPA receptor expression and nociceptive responses, indicating a tonic regulatory effect from endogenous GABAergic activity on the AMPA receptor expression and spinal nociceptive processing. These results indicate that modulation of spinal AMPA receptor expression and function by the GABAergic activity may serve as a mechanism contributory to the spinal nociceptive processing.

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Section: Discussionsupporting

confidence: 93%

Section: Introductionmentioning

confidence: 99%

Intrathecal midazolam regulates spinal AMPA receptor expression and function after nerve injury in rats

Lim

Sung

et al. 2006

Brain Research

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“…It has been reported that gabapentin decreases glutamate concentrations and inhibits the release of glutamate and glutamatergic synaptic transmission presynatically (15)(16)(17). Glutamate acts on the NMDA receptor and non-NMDA receptor and shows the excitatory effect (18,19). Further, AMPAevoked neuronal response is inhibited by gabapentin (20,21).…”

Section: Discussionmentioning

confidence: 99%

Spinal Gabapentin and Antinociception: Mechanisms of Action

2003

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Spinal gabapentin has been known to show the antinociceptive effect. Although several assumptions have been suggested, mechanisms of action of gabapentin have not been clearly established. The present study was undertaken to examine the action mechanisms of gabapentin at the spinal level. Male SD rats were prepared for intrathecal catheterization. The effect of gabapentin was assessed in the formalin test. After pretreatment with many classes of drugs, changes of effect of gabapentin were examined. General behaviors were also observed. Intrathecal gabapentin produced a suppression of the phase 2 flinching, but not phase 1 in the formalin test. The antinociceptive action of intrathecal gabapentin was reversed by intrathecal NMDA, AMPA, D-serine, CGS 15943, atropine, and naloxone. No antagonism was seen following administration of bicuculline, saclofen, prazosin, yohimbine, mecamylamine, L-leucine, dihydroergocristine, or thapsigargin. Taken together, intrathecal gabapentin attenuated only the facilitated state. At the spinal level, NMDA receptor, AMPA receptor, nonstrychnine site of NMDA receptor, adenosine receptor, muscarinic receptor, and opioid receptor may be involved in the antinociception of gabapentin, but GABA receptor, L-amino acid transporter, adrenergic receptor, nicotinic receptor, serotonin receptor, or calcium may not be involved.

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“…On the other hand, sertraline (Sert) produced hypoglycaemic effects in non-diabetic and diabetic rats most likely related to increased insulin output, decreased gluconeogenesis and increased insulin receptor sensitivity 16 . The role of K + channel has also been described for the hypoglycaemic effects of sertraline 19 .…”

Section: Discussionmentioning

confidence: 99%

“…When Ami and Sert were studied for pain sensitivity measurement, their results indicate that both the drugs produced almost complete reversal of thermal hyper-analgesia in diabetic ratsl Sert effects being more prominent 19 . Recent studies have indicated that the neurons in the spinal cord that release the neurotransmitter, 5-HT and NE from nerve endings inhibit pain transmission .…”

Section: Discussionmentioning

confidence: 99%

Amitriptyline and Sertraline in Diabetic Neuropathy: A Comparative View

Jawaid¹,

Shakya²,

Mm³

et al. 2009

Int J Health Res

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an online international journal allowing free unlimited access to abstract and full-text of published articles. The journal is devoted to the promotion of health sciences and related disciplines (including medicine, pharmacy, nursing, biotechnology, cell and molecular biology, and related engineering fields). It seeks particularly (but not exclusively) to encourage multidisciplinary research and collaboration among scientists, the industry and the healthcare professionals. It will also provide an international forum for the communication and evaluation of data, methods and findings in health sciences and related disciplines. The journal welcomes original research papers, reviews and case reports on current topics of special interest and relevance. All manuscripts will be subject to rapid peer review. Those of high quality (not previously published and not under consideration for publication) will be published without delay. The maximum length of manuscripts should normally be 10,000 words (20 single-spaced typewritten pages) for review, 6,000 words for research articles, 3,000 for technical notes, case reports, commentaries and short communications. Submission of Manuscript:The International Journal of Health Research uses a journal management software to allow authors track the changes to their submission. All manuscripts must be in MS Word and in English and should be submitted online at http://www.ijhr.org. Authors who do not want to submit online or cannot submit online should send their manuscript by e-mail attachment (in single file) to the editorial office below. Submission of a manuscript is an indication that the content has not been published or under consideration for publication elsewhere. Authors may submit the names of expert reviewers or those they do not want to review their papers. Enquiries

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N-Methyl-d-aspartate (NMDA) and non-NMDA glutamate receptor antagonists differentially suppress dorsal horn neuron responses to mechanical stimuli in rats with peripheral nerve injury

Cited by 49 publications

References 14 publications

Intrathecal midazolam regulates spinal AMPA receptor expression and function after nerve injury in rats

Intrathecal midazolam regulates spinal AMPA receptor expression and function after nerve injury in rats

Spinal Gabapentin and Antinociception: Mechanisms of Action

Amitriptyline and Sertraline in Diabetic Neuropathy: A Comparative View

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