To investigate the effects of aging on coordination of plantar flexor muscles during bipedal and unipedal stances, we examined a relationship between the center of pressure sway and electromyographic activity of these muscles, and also the common neural input, using a coherence analysis. Healthy young and elderly adults were asked to perform bipedal and unipedal standing. The electromyograms were recorded unilaterally from the medial and lateral gastrocnemius (MG and LG) and soleus (SL) muscles, and the common input was analyzed for MG-LG, MG-SL, and LG-SL pairs in two frequency bands: a delta band, that is associated with force variability, and a beta band, that could reflect the corticospinal drive. Main results indicated that the MG and SL muscles worked for lateral sway, while the LG muscle worked for medial sway during the unipedal stance. The delta-band coherence for the MG-SL pair and the beta-band coherences for all the pairs were larger during the unipedal than bipedal stance for both groups. The delta-band coherence for the MG-SL pair was larger for the elderly than young adults during the unipedal stance. In addition, the beta-band coherence for the MG-SL pair was larger than the other pairs during the unipedal stance for the elderly. These findings suggest that the oscillatory activity between the MG and SL muscles is strongly involved in the control of unipedal stance, and aging would increase the cortical drive to these muscles to deal with the postural sway that could be affected by forces generated cooperatively by them.

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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.