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Spinal mechanisms underlying potentiation of hindpaw responses observed after transient hindpaw ischemia in mice.

Watanabe T, Sasaki M, Komagata S, Tsukano H, Hishida R, Kohno T, Baba H, Shibuki K - Sci Rep (2015)

Bottom Line: The reduction in the threshold was blocked by spinal application of LY354740, a specific agonist of group II metabotropic glutamate receptors.Potentiation already appeared during ischemic treatment for 30 min.The present findings suggest that the postischemic potentiation shares spinal mechanisms, at least in part, with neuropathic pain.

View Article: PubMed Central - PubMed

Affiliation: 1] Department of Neurophysiology, Brain Research Institute, Niigata University,1-757 Asahi-machi, Chuo-ku, Niigata 951-8585, Japan [2] Department of Anesthesiology, School of Medicine, Niigata University, 1-757 Asahi-machi, Chuo-ku, Niigata 951-8510, Japan.

ABSTRACT
Transient ischemia produces postischemic tingling sensation. Ischemia also produces nerve conduction block that may modulate spinal neural circuits. In the present study, reduced mechanical thresholds for hindpaw-withdrawal reflex were found in mice after transient hindpaw ischemia, which was produced by a high pressure applied around the hindpaw for 30 min. The reduction in the threshold was blocked by spinal application of LY354740, a specific agonist of group II metabotropic glutamate receptors. Neural activities in the spinal cord and the primary somatosensory cortex (S1) were investigated using activity-dependent changes in endogenous fluorescence derived from mitochondrial flavoproteins. Ischemic treatment induced potentiation of the ipsilateral spinal and contralateral S1 responses to hindpaw stimulation. Both types of potentiation were blocked by spinal application of LY354740. The contralateral S1 responses, abolished by lesioning the ipsilateral dorsal column, reappeared after ischemic treatment, indicating that postischemic tingling sensation reflects a sensory modality shift from tactile sensation to nociception in the spinal cord. Changes in neural responses were investigated during ischemic treatment in the contralateral spinal cord and the ipsilateral S1. Potentiation already appeared during ischemic treatment for 30 min. The present findings suggest that the postischemic potentiation shares spinal mechanisms, at least in part, with neuropathic pain.

No MeSH data available.


Related in: MedlinePlus

Reduced mechanical thresholds for hindpaw-withdrawal reflex.(a) Application of high pressure (250 mm Hg) to the left thigh. (b) Mechanical thresholds for left hindpaw-withdrawal reflex before and after ischemic or sham treatment applied to the left thigh. Mean ± SEM are shown. (c) Mechanical thresholds for hindpaw-withdrawal reflex after hindpaw ischemia in mice with spinal application of LY354740 (10 nM, 5 μl) or saline alone. (d) Comparison of the thresholds for the left hindpaw-withdrawal reflex at 2 h after ischemic or sham treatment, with or without spinal application of LY354740. In the ischemia group, data were mixed in mice with or without spinal application of saline. In the sham-treated group, data were mixed in mice with sham treatment to the left thigh or to the right thigh.
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f1: Reduced mechanical thresholds for hindpaw-withdrawal reflex.(a) Application of high pressure (250 mm Hg) to the left thigh. (b) Mechanical thresholds for left hindpaw-withdrawal reflex before and after ischemic or sham treatment applied to the left thigh. Mean ± SEM are shown. (c) Mechanical thresholds for hindpaw-withdrawal reflex after hindpaw ischemia in mice with spinal application of LY354740 (10 nM, 5 μl) or saline alone. (d) Comparison of the thresholds for the left hindpaw-withdrawal reflex at 2 h after ischemic or sham treatment, with or without spinal application of LY354740. In the ischemia group, data were mixed in mice with or without spinal application of saline. In the sham-treated group, data were mixed in mice with sham treatment to the left thigh or to the right thigh.

Mentions: Because unpleasant postischemic tingling sensation is exacerbated by external mechanical forces, we measured the thresholds for hindpaw-withdrawal reflex using von Frey filaments25. The thresholds before hindpaw ischemia were 0.57 ± 0.10 g (mean ± SEM, n = 6). Mice were transiently anesthetized with 1% isoflurane, and a pressure of 250 mmHg was applied for 30 min to a rubber cuff set around the thigh (Fig. 1a). At 30 min after the ischemic treatment was finished, the mechanical thresholds were significantly reduced compared with the corresponding data in sham-treated mice with no pressure application (P < 0.01, Fig. 1b). The thresholds reached the minimal values of 0.07 ± 0.02 g (n = 6) at 2 h after the ischemic treatment (Fig. 1b), and were clearly and significantly smaller than the corresponding values in sham-treated mice (P < 0.005). Isoflurane anesthesia alone produced no reduction in the threshold in sham-treated mice (Fig. 1b).


Spinal mechanisms underlying potentiation of hindpaw responses observed after transient hindpaw ischemia in mice.

Watanabe T, Sasaki M, Komagata S, Tsukano H, Hishida R, Kohno T, Baba H, Shibuki K - Sci Rep (2015)

Reduced mechanical thresholds for hindpaw-withdrawal reflex.(a) Application of high pressure (250 mm Hg) to the left thigh. (b) Mechanical thresholds for left hindpaw-withdrawal reflex before and after ischemic or sham treatment applied to the left thigh. Mean ± SEM are shown. (c) Mechanical thresholds for hindpaw-withdrawal reflex after hindpaw ischemia in mice with spinal application of LY354740 (10 nM, 5 μl) or saline alone. (d) Comparison of the thresholds for the left hindpaw-withdrawal reflex at 2 h after ischemic or sham treatment, with or without spinal application of LY354740. In the ischemia group, data were mixed in mice with or without spinal application of saline. In the sham-treated group, data were mixed in mice with sham treatment to the left thigh or to the right thigh.
© Copyright Policy - open-access
Related In: Results  -  Collection

License
Show All Figures
getmorefigures.php?uid=PMC4499883&req=5

f1: Reduced mechanical thresholds for hindpaw-withdrawal reflex.(a) Application of high pressure (250 mm Hg) to the left thigh. (b) Mechanical thresholds for left hindpaw-withdrawal reflex before and after ischemic or sham treatment applied to the left thigh. Mean ± SEM are shown. (c) Mechanical thresholds for hindpaw-withdrawal reflex after hindpaw ischemia in mice with spinal application of LY354740 (10 nM, 5 μl) or saline alone. (d) Comparison of the thresholds for the left hindpaw-withdrawal reflex at 2 h after ischemic or sham treatment, with or without spinal application of LY354740. In the ischemia group, data were mixed in mice with or without spinal application of saline. In the sham-treated group, data were mixed in mice with sham treatment to the left thigh or to the right thigh.
Mentions: Because unpleasant postischemic tingling sensation is exacerbated by external mechanical forces, we measured the thresholds for hindpaw-withdrawal reflex using von Frey filaments25. The thresholds before hindpaw ischemia were 0.57 ± 0.10 g (mean ± SEM, n = 6). Mice were transiently anesthetized with 1% isoflurane, and a pressure of 250 mmHg was applied for 30 min to a rubber cuff set around the thigh (Fig. 1a). At 30 min after the ischemic treatment was finished, the mechanical thresholds were significantly reduced compared with the corresponding data in sham-treated mice with no pressure application (P < 0.01, Fig. 1b). The thresholds reached the minimal values of 0.07 ± 0.02 g (n = 6) at 2 h after the ischemic treatment (Fig. 1b), and were clearly and significantly smaller than the corresponding values in sham-treated mice (P < 0.005). Isoflurane anesthesia alone produced no reduction in the threshold in sham-treated mice (Fig. 1b).

Bottom Line: The reduction in the threshold was blocked by spinal application of LY354740, a specific agonist of group II metabotropic glutamate receptors.Potentiation already appeared during ischemic treatment for 30 min.The present findings suggest that the postischemic potentiation shares spinal mechanisms, at least in part, with neuropathic pain.

View Article: PubMed Central - PubMed

Affiliation: 1] Department of Neurophysiology, Brain Research Institute, Niigata University,1-757 Asahi-machi, Chuo-ku, Niigata 951-8585, Japan [2] Department of Anesthesiology, School of Medicine, Niigata University, 1-757 Asahi-machi, Chuo-ku, Niigata 951-8510, Japan.

ABSTRACT
Transient ischemia produces postischemic tingling sensation. Ischemia also produces nerve conduction block that may modulate spinal neural circuits. In the present study, reduced mechanical thresholds for hindpaw-withdrawal reflex were found in mice after transient hindpaw ischemia, which was produced by a high pressure applied around the hindpaw for 30 min. The reduction in the threshold was blocked by spinal application of LY354740, a specific agonist of group II metabotropic glutamate receptors. Neural activities in the spinal cord and the primary somatosensory cortex (S1) were investigated using activity-dependent changes in endogenous fluorescence derived from mitochondrial flavoproteins. Ischemic treatment induced potentiation of the ipsilateral spinal and contralateral S1 responses to hindpaw stimulation. Both types of potentiation were blocked by spinal application of LY354740. The contralateral S1 responses, abolished by lesioning the ipsilateral dorsal column, reappeared after ischemic treatment, indicating that postischemic tingling sensation reflects a sensory modality shift from tactile sensation to nociception in the spinal cord. Changes in neural responses were investigated during ischemic treatment in the contralateral spinal cord and the ipsilateral S1. Potentiation already appeared during ischemic treatment for 30 min. The present findings suggest that the postischemic potentiation shares spinal mechanisms, at least in part, with neuropathic pain.

No MeSH data available.


Related in: MedlinePlus