PubMed · 8909280
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J C Kolb, J Krupnick. 1996. Shoulder reduction without anesthesia.. https://doi.org/10.1016/s0196-0644(96)70124-5
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The work in our laboratory has been designed to characterize the transducer mechanisms coupled to neurotransmitter receptors in the plasma membrane. Particular attention has been paid to the physiological/pharmacological effects mediated by the opioid system. Antisense oligodeoxynucleotides have proved useful in correlating opioid receptor clones with those defined pharmacologically. The involvement of the cloned opioid receptors mu, delta, and kappa in analgesia has been determined by means of in vivo injection of ODNs directed to the receptor mRNAs. Using this strategy the classes of G-transducer proteins regulated by each type/subtype of opioid receptor in the promotion of antinociception have also been characterized. After displaying different patterns of binding to their receptors, opioids trigger a variety of intracellular signals. The physiological implications and therapeutic potential of these findings merit consideration.
The effect of weak electromagnetic stimulation on the emergence of conditioned analgesia was examined in the adult rat. Subjects were conditioned to associate a continuous 20 kHz ultrasonic tone (CS) with 0.2 mA footshock (UCS-) over five successive days. For 30 min either before or after conditioning sessions, rats were exposed to sham or pulsed (primed burst potentiation) magnetic fields (500 nT). At the end of the conditioning phase, all animals were evaluated for anticipatory analgesia following CS presentation using a hotplate analgesiometer. Data analysis suggested a statistically significant attenuation of fear-conditioned analgesia in rats exposed to electromagnetic stimulation prior to conditioning, whereas post-conditioning exposure potentiated the reduction in pain sensitivity compared to baseline measures. The present results suggest that the emergence of fear-conditioned responses is sensitive to whole body exposure to a magnetic field pattern that has been shown to induce long-term potentiation in hippocampal slices.
Synthetic cannabinoids produce behavioral analgesia and suppress pain neurotransmission, raising the possibility that endogenous cannabinoids serve naturally to modulate pain. Here, the development of a sensitive method for measuring cannabinoids by atmospheric pressure-chemical ionization mass spectrometry permitted measurement of the release of the endogenous cannabinoid anandamide in the periaqueductal gray (PAG) by in vivo microdialysis in the rat. Electrical stimulation of the dorsal and lateral PAG produced CB1 cannabinoid receptor-mediated analgesia accompanied by a marked increase in the release of anandamide in the PAG, suggesting that endogenous anandamide mediates the behavioral analgesia. Furthermore, pain triggered by subcutaneous injections of the chemical irritant formalin substantially increased the release of anandamide in the PAG. These findings indicate that the endogenous cannabinoid anandamide plays an important role in a cannabinergic pain-suppression system existing within the dorsal and lateral PAG. The existence of a cannabinergic pain-modulatory system may have relevance for the treatment of pain, particularly in instances where opiates are ineffective.