We studied the effect of cholecystokinin (CCK-8) and yohimbine - (alpha)-2-adrenoreceptor antagonist administered locally into lateral reticular formation (LRF) on the bioelectrical response to the pain stimulation. The experiments were carried out on 8 concious rabbits with bilatrally implanted electrodes into: motor-sensory cortex, ventro-postero-lateral thalamic nuclei, hippocampus and LRF. Nociceptive stimulation was performed by means of electrical pulses applied to the front paw. Bioelectrical activity (BA) of the chosen brain structures was analysed by means of spectral analysis (FFT) and directed transfer function (DTF). The results of our study may suggest that supraspinal administration of CCK-8 together with yohimbine have inhibitory effect on nociceptive transmission.
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Drugs able to inhibit calmodulin activation can prevent some consequences of the rise in intracellular calcium. It has recently been shown that intrathecal injection of calmodulin inhibitors induce analgesia in rats. We study here the effect induced by the calmodulin inhibitor, calmidazolium, on the activity of dorsal horn neurons driven by noxious and non-noxious stimuli. Extracellular recordings of convergent (n = 12), low-threshold mechanoreceptive (n = 5) and proprioceptive (n = 5) units were made in the presence of calmidazolium. Calmidazolium (600 mg) reduced the noxious (50oC) heat-evoked responses obtained in convergent neurons. On the contrary, the non-noxious tactile responses obtained in low-threshold mechanoreceptive neurons as well as the joint movement-evoked responses obtained in proprioceptive units remained unmodified. We conclude that calmidazolium can block nociceptive processing in the spinal cord and that this fact can help to explain the analgesic effects that intrathecal W-7 and calmidazolium induce in behavioral tests.
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