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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

Sensory modality shift induced by ischemic treatment.(a) Lesion in the left dorsal column at T11 level. (b) Example of the right S1 responses modified by the left column lesioning and ischemic treatment applied to the left thigh. (c) Example of the right S1 responses modified by the left column lessoning and sham treatment applied to the left thigh. (d) Response amplitudes immediately after dorsal column lesioning, and at 30 min and 60 min after ischemic or sham treatment.
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f4: Sensory modality shift induced by ischemic treatment.(a) Lesion in the left dorsal column at T11 level. (b) Example of the right S1 responses modified by the left column lesioning and ischemic treatment applied to the left thigh. (c) Example of the right S1 responses modified by the left column lessoning and sham treatment applied to the left thigh. (d) Response amplitudes immediately after dorsal column lesioning, and at 30 min and 60 min after ischemic or sham treatment.

Mentions: Potentiation in S1 after ischemic treatment may be produced by a modality shift from tactile sensation to nociception, as observed after partial denervation7. When we disrupted the ipsilateral dorsal column at the T11 level (Fig. 4a), S1 responses elicited by hindpaw stimulation were abolished (Fig. 4b). However, S1 responses reappeared at 30 and 60 min after ischemic treatment applied to the hindpaw (Fig. 4b). As no such response was observed in sham-treated mice (Fig. 4c), the reappearing S1 responses cannot be attributed to spontaneous recovery from the injury caused by dorsal column lesioning. The difference in S1 responses in the operated mice was statistically significant at 30 and 60 min after hindpaw ischemia or sham treatment (P < 0.01 for both, Fig. 4d). The reappearing S1 responses suggest that the modality shift from tactile sensation to nociception was induced within 30 min after ischemic treatment.


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)

Sensory modality shift induced by ischemic treatment.(a) Lesion in the left dorsal column at T11 level. (b) Example of the right S1 responses modified by the left column lesioning and ischemic treatment applied to the left thigh. (c) Example of the right S1 responses modified by the left column lessoning and sham treatment applied to the left thigh. (d) Response amplitudes immediately after dorsal column lesioning, and at 30 min and 60 min after ischemic or sham treatment.
© Copyright Policy - open-access
Related In: Results  -  Collection

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

f4: Sensory modality shift induced by ischemic treatment.(a) Lesion in the left dorsal column at T11 level. (b) Example of the right S1 responses modified by the left column lesioning and ischemic treatment applied to the left thigh. (c) Example of the right S1 responses modified by the left column lessoning and sham treatment applied to the left thigh. (d) Response amplitudes immediately after dorsal column lesioning, and at 30 min and 60 min after ischemic or sham treatment.
Mentions: Potentiation in S1 after ischemic treatment may be produced by a modality shift from tactile sensation to nociception, as observed after partial denervation7. When we disrupted the ipsilateral dorsal column at the T11 level (Fig. 4a), S1 responses elicited by hindpaw stimulation were abolished (Fig. 4b). However, S1 responses reappeared at 30 and 60 min after ischemic treatment applied to the hindpaw (Fig. 4b). As no such response was observed in sham-treated mice (Fig. 4c), the reappearing S1 responses cannot be attributed to spontaneous recovery from the injury caused by dorsal column lesioning. The difference in S1 responses in the operated mice was statistically significant at 30 and 60 min after hindpaw ischemia or sham treatment (P < 0.01 for both, Fig. 4d). The reappearing S1 responses suggest that the modality shift from tactile sensation to nociception was induced within 30 min after ischemic treatment.

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