Quantitative analysis of nociceptive and motor reflexes in genetically modified mice

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alpha-Adrenoceptor agonists, dexmedetomidine and xylazine inhibited spinal motor and nociceptive reflex potentials. In the alpha2A receptor-functional deficient D79N mice, the inhibitory effect on nociceptive but not motor reflex potentials by these agonists was attenuated. alpha2A-Receptors are suggested to be involved in the alpha2-agonist-evoked analgesia but not the inhibition of motor reflex. Adenosine and hydrogen sulfide (H2S) influence spinal neuronal activity. In the spinal astrocytes, the adenosine metabolic inhibitors released adenosine, while Ca2+-removal released ATP, which was degraded to adenosine. In the neurons, H2S is produced by the synthase CST/MPST.