J.J. Bonica lecture[mdash ]2001: Role of spinal GABA in acute and persistent nociception

Hammond, Donna L.

doi:10.1053/rapm.2001.27835

Cited by 12 publications

(7 citation statements)

References 56 publications

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“…A sizable literature implicates the loss of GABA inhibition in the development of nerve injuryassociated pain (e.g., reviews by Hammond, 2001;Eaton, 2002; also recent reports by Malan et al, 2002;Baba et al, 2003;Miletic et al, 2003). This is not surprising given the postulated critical role of GABA inhibitory action to the normal function of numerous neuronal circuits (Paulsen and Moser, 1998).…”

Section: Discussionmentioning

confidence: 99%

“…The loss of GABA inhibition may at least partly contribute to the development of pain following peripheral nerve injury (reviews by Hammond, 2001;Eaton, 2002; also recent reports by Malan et al, 2002;Baba et al, 2003;Miletic et al, 2003). GABA-mediated inhibition appears critically dependent on the activity of the potassium-chloride co-transporter 2 (KCC2), one of four currently known members of the family of potassium-chloride co-transporters (Payne et al, 2003).…”

Section: Introductionmentioning

confidence: 99%

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Loose ligation of the sciatic nerve is associated with TrkB receptor-dependent decreases in KCC2 protein levels in the ipsilateral spinal dorsal horn

Miletić¹,

Miletić²

2008

Pain

110

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Significant decreases in the protein levels of potassium-chloride co-transporter 2 (KCC2) were detected in the ipsilateral spinal dorsal horn 4h following loose ligation of the sciatic nerve. These decreases were associated with a change in hindlimb weight distribution suggestive of pain behavior. In contrast, no changes in GABA-A receptor subunit alpha-1 levels were detected. The decreases in KCC2 coincided with a significant ipsilateral increase in BDNF protein levels. Both the decreases in KCC2 levels and the early pain behavior were prevented by intrathecal pre-treatment with the BDNF-sequestering TrkB/Fc chimera protein or the tyrosine kinase blocker K252a. The ligationassociated decreases in KCC2 levels were transient. In the ipsilateral spinal dorsal horn of ligated animals exhibiting weight-bearing pain behavior 7 days after the ligation the KCC2 levels were identical to those in control or sham-operated animals. These data suggested that TrkB-dependent reduction in KCC2 protein levels in the spinal dorsal horn was an early consequence of peripheral nerve injury. This decrease in KCC2 may have elicited an early increase in overall dorsal horn neuronal excitability perhaps through a loss of GABA inhibition which is critically dependent on KCC2 activity. The increased neuronal excitability may in turn have caused enhanced and exaggerated communication between primary afferents and dorsal horn neurons to contribute to the early behavioral signs of pain.

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Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Loose ligation of the sciatic nerve is associated with TrkB receptor-dependent decreases in KCC2 protein levels in the ipsilateral spinal dorsal horn

Miletić¹,

Miletić²

2008

Pain

110

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“…The function of GABA in the modulation of nociception is crucial and complex. Several reports have demonstrated the participation of the GABAergic system in the modulation of pain at the supraspinal and spinal level [1][2][3]21]. The involvement of GABA in spinal antinociceptive effects is well established [22].…”

mentioning

confidence: 99%

“…Antinociceptive effects can be induced by GABA agonists. The GA-BA receptors may mediate the antinociception induced by the GABA agonists [3,5,21,23]. Some studies have demonstrated that GABA receptors located at the spinal cord level are involved in the regulation of nociception.…”

mentioning

confidence: 99%

Oxysophoridine through Intrathecal Injection Induces Antinociception and Increases the Expression of the GABAAα1 Receptor in the Spinal Cord of Mice

Yang

Gao²,

Jia

et al. 2012

Planta Med

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Our researches in recent years have shown that oxysophoridine (OSR), an alkaloid extracted from Siphocampylus verticillatus, presents antinociception through systemic and intracerebroventricular (icv) administration, and that OSR can also increase the GABA-immunopositive cells number in the central nervous system in rats. The purpose of the present study was to investigate the antinociception produced by OSR administered spinally, the interaction between OSR and GABAA receptor (GABAAR) agonists or antagonists on acute thermal nociceptive models (tail-flick test), and the possible alterations on the mRNA and protein expression of GABAAα1 receptors in the spinal cord. ICR mice were tested for their tail withdrawal response to thermal stimulation (tail-flick test). Quantitative real-time PCR and Western blot were used to inspect the influence of OSR administered by intrathecal injection (i. t.) on mRNA and protein expression of the GABAAα1 receptor in mice spinal cord by the formalin test. The experiments showed that OSR (0.13-0.25 mg/site, i. t.) significantly increased the tail withdrawal threshold with a peak effect of 68.35 % MPE at 20 min (p < 0.01). When OSR (0.06 mg/site, i. t.) was administered with gamma aminobutyric acid (GABA) (30.0 µg/site, icv) or muscimol (MUS) (0.10 µg/site, icv), the value of tail-flick latency was remarkably larger than with OSR alone (at 10 min, 45.67 % or 31.45 %, p < 0.01). Picrotoxin (PTX) and bicuculine (BIC) can significantly antagonize the antinociception of OSR. OSR (0.25 mg/site, i. t.) can increase the expression of mRNA and protein of the GABAAα1 receptor in the spinal cord (L5-L6). The results reveal that i. t. administered OSR presents effective antinociception whose action is mainly located in the spinal cord. The antinociception of OSR results from the activation of the GABAA receptor and from the regulation of the GABAAα1 receptor-mediated neurotransmission.

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“…Several reports have demonstrated the participation of GABAergic system in modulation of pain at the supraspinal (Millan, 2002) and spinal level (Malcangio and Bowery, 1996;Hammond, 2001). In addition, studies have demonstrated a peripheral GABAergic antinociceptive action (Carlton and Zhou, 1998;Motta et al, 2004).…”

Section: Introductionmentioning

confidence: 98%

Involvement of chloride channel coupled GABAC receptors in the peripheral antinociceptive effect induced by GABAC receptor agonist cis-4-aminocrotonic acid

Reis

Duarte

2007

Life Sciences

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J.J. Bonica lecture[mdash ]2001: Role of spinal GABA in acute and persistent nociception

Cited by 12 publications

References 56 publications

Loose ligation of the sciatic nerve is associated with TrkB receptor-dependent decreases in KCC2 protein levels in the ipsilateral spinal dorsal horn

Loose ligation of the sciatic nerve is associated with TrkB receptor-dependent decreases in KCC2 protein levels in the ipsilateral spinal dorsal horn

Oxysophoridine through Intrathecal Injection Induces Antinociception and Increases the Expression of the GABAAα1 Receptor in the Spinal Cord of Mice

Involvement of chloride channel coupled GABAC receptors in the peripheral antinociceptive effect induced by GABAC receptor agonist cis-4-aminocrotonic acid

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