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Background and Purpose: Hydrogen sulfide, a gasotransmitter, facilitates somatic pain signals via activation of Ca(v)3.2 T-type calcium channels in rats. Given evidence for the activation of transient receptor potential ankyrin-1 (TRPA1) channels by H(2)S, we asked whether TRPA1 channels, in addition to Ca(v)3.2 channels, contribute to the H(2)S-induced mechanical hyperalgesia and allodynia in mice.Experimental Approach: Mechanical hyperalgesia and allodynia were evaluated by the von Frey test in mice. Ca(v)3.2 or TRPA1 channels in the sensory neurons were silenced by repeated intrathecal administration of antisense oligodeoxynucleotides in mice.Key Results: Intraplantar administration of NaHS evoked hyperalgesia and allodynia in mice, an effect attenuated or abolished by NNC 55-0396 or mibefradil, T-type calcium channel blockers, and by ascorbic acid or zinc chloride, known to selectively inhibit Ca(v)3.2 channels, out of the three isoforms of T-type calcium channels. Silencing of Ca(v)3.2 channels in the sensory neurons also prevented the NaHS-induced hyperalgesia and allodynia in mice. The NaHS-induced hyperalgesia and allodynia in mice were significantly suppressed by AP18, a TRPA1 channel blocker, and by silencing of TRPA1 channels in the sensory neurons.Conclusions and Implications: Mechanical hyperalgesia and allodynia induced by NaHS/H(2)S required activation of both Ca(v)3.2 and TRPA1 channels in mice. [ABSTRACT FROM AUTHOR]

[Purpose] The soleus H-reflex is depressed at stimulation rates greater than 0.1 Hz. This reflex depression is referred to as postactivation depression. Postactivation depression reflects the reduced efficacy of the Ia-motoneurons synapses when they are evaluated after a previous activation. The aim of this study was to determine whether the recovery of motor functions in the lower extremities affects the PAD of the soleus H-reflex in patients with subacute stroke undergoing rehabilitation. [Subjects and Methods] Eight patients with subacute stroke patients were recruited. Postactivation depression, Fugl-Meyer score (lower-limb portion), walking velocity, the Modified Ashworth Scale, and center of pressure sway during standing were measured within three days of admission to rehabilitation and 50 days later. [Results] After rehabilitation, Fugl-Meyer scores, center of pressure path length, and walking velocity were significantly improved, and postactivation depression had significantly increased. There was a significant positive correlation between the rates of change of postactivation depression and center of pressure path length. [Conclusion] The results demonstrated that postactivation depression is partially normalized after rehabilitation in patients with subacute stroke, and suggested that the recovery in lower extremity function after stroke particularly standing stability is affected by spinal synaptic plasticity.