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.
Highlights
Of inflammation and gene expression during the recovery period[12,13,14]
Postischemic mechanical allodynia produced by spinal mechanisms in mice
We found that mechanical thresholds for hindpaw-withdrawal reflex were reduced after ischemic treatment
Summary
Of inflammation and gene expression during the recovery period[12,13,14]. postischemic mechanical allodynia is induced very quickly after transient hindpaw ischemia. If neural changes reflecting postischemic tingling sensation are found, these changes may be useful for investigating the neural mechanisms that trigger neuropathic pain. Activity-dependent flavoprotein fluorescence signals reflect aerobic energy metabolism in mitochondria[15], and are useful for investigating fine neural activities and plasticity[16,17,18]. A modality shift from tactile sensation to nociception can be visualized as reappearance of S1 responses to tactile stimulation in mice with ipsilateral dorsal column lesioning[7]. It is because the tactile sensation is mediated via the ipsilateral dorsal column to the contralateral S123, while nociception is mediated via the contralateral spinothalamic tract[24]. We confirmed that such a modality shift from tactile sensation to nociception was produced within 30 min after ischemic treatment
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