1.Opioid analgesia in the mouse: evidence for multiple receptors using beta-FNA.
Sánchez-Blázquez P;Garzón J NIDA Res Monogr. 1986;75:465-8.
The icv injection of morphine or DADLE ED50 a few min before the alkylating agent beta-FNA resulted in complete protection of their respective analgesic effects when evaluated 24h later, although a little cross-protection could be observed. The analgesia evoked by DADLE was partially protected using higher doses of morphine before beta-FNA. However, higher doses of DADLE did not protect the analgesia induced by morphine. On the other hand, the antagonistic action of KCl on opioid analgesia was found to be dependent on the opioid utilized to protect the opioid receptor against the effect of beta-FNA. These results are discussed in terms of multiple receptors mediating opioid analgesia at supraspinal level in the mouse.
2.Down-regulation of delta but not mu opioid receptors in the hippocampal slice associated with loss of physiological response.
Dingledine R;Valentino RJ;Bostock E;King ME;Chang KJ Life Sci. 1983;33 Suppl 1:333-6.
In rat hippocampal slices, opioids potentiate the synaptic activation of pyramidal neurons as revealed by the shift to the left in the input-output curve constructed by plotting the population spike as a function of the field EPSP. The peak effect was obtained within 12-25 min with D-Ala2,D-Leu5-enkephalin (DADLE), morphiceptin and morphine. However, the effect of both peptides declined during constant superfusion. About 60% peak effect was lost after 1 hr superfusion with morphiceptin or after 4 hr with DADLE. In contrast, the effect of morphine gradually increased over a 4 hr incubation. Following superfusion of the slices for 4 hr in DADLE or morphine, or 1.5 hr in morphiceptin, the membrane particulate fractions were prepared from the homogenate of slices. Opiate receptor binding activities were measured with 125I-DADLE (delta-receptors) and 125I-FK 33824 (mu-receptors). A significant reduction in delta- but not mu-receptor binding was detected in slices treated with DADLE. This seems to correlate to the development of desensitization to DADLE. Neither mu-receptor nor delta-receptor binding activity was altered by the superfusion of morphine or morphiceptin despite the development of desensitization to morphiceptin.
3.A possible role for an enkephalinergic system in the internal defense mechanism of Biomphalaria alexandrina exposed to Schistosoma mansoni.
Osman AM;Gomma M;Saad AH J Egypt Soc Parasitol. 2003 Dec;33(3):841-61.
The present study documents that in Bioniphalaria alexandrina coordinated responses to Schistosoma mansoni infection are modulated by receptor-mediated opioid signals. Rather comprehensive tests in susceptible and resistant snails have demonstrated: I- the presence of an endogenaus opioids in the snail hemolymph (in particular, Leu-enkephalin-like material). II- in vitro treatment of snail hemocytes with synthetic Leu-enkephalin analogue (DADLE) resulted in the modulation of cellular adherence, and phagocytic activity. III- the addition of Naloxone, either alone or in combination whith DADLE, generally reduced hemocyte activity indicating opioid-receptor-mediated mechanism. V- the presence of DADLE or Naloxone modulated the level of IL-2-, TNF-gamma- and FNF-alpha-like molecules in S. mansoni resistant and susceptible snails. Specifically, DADLE and DADLE in combination with Naloxone generally were found to be capable of modulating resistant snail hemocytes at concentrations of 10(-6) and 10(-8) M. Similar actions after incubation with the same concentrations were not detected in the susceptible snails. These observations demonstrate the existence of a complete opioid system in B. alexandrina, associated with susceptibility and resistance to S.
