Function of delta opioid receptors in cultured cells

Opiate‐Inhibited Adenylate Cyclase in Rat Brain Membranes Depleted of Gs‐Stimulated Adenylate Cyclase

“…The second messenger system most commonly associated with opiate receptors is opiate-inhibited adenylate cyclase, first described in brain membranes by Collier and Roy (1974) and later explored in detail in NG 108-15 neuroblastoma X glioma hybrid cells (Sharma et al, 1975;Traber et al, 1975;Blume et al, 1979). Many of the properties of opiate-inhibited adenylate cyclase have been determined in the neuroblastoma cell systems, where the signal for inhibition of adenylate cyclase is relatively large (Gilbert and Richelson, 1983). However, many important questions cannot be determined in these simplified cell systems.…”

Opioid-Induced Reductions in Amygdala Lateral Paracapsular GABA Neuron Circuit Activity

“…Acutely, opioids decrease adenylyl cyclase activity through the activation of G i coupled signal transduction mechanisms [32][33][34][35]. However, prolonged exposure increases adenylyl cyclase (likely as an adaption to suppressed activity), resulting in increased cAMP sensitivity during acute morphine withdrawal [23,32].…”

Enkephalins and Endorphins

“…On one hand, ME may be subject of enkephalinase present in the membrane of PM; and a decrease of BAOS production is induced either by inhibition of H excretion from cells or by releasing biologically active break down products of ME. On the other hand, it was reported by Gilbert and Richelson (1983) that delta opiate receptors which are coupled inhibiting to adenylate cyclase in cultured murine neuroblastoma clones and their glioma hybrids, after incubation with the high concentrations of ME may form clusters with a positive coupling to the adenylate cyclase system. This change in the receptor coupling serves as a form of down regulation at the post-receptor level without any reduction in the number of affinity of delta receptors.…”

“…Experiments were carried out applying two further peptides which bind to specific receptor on the surface of leukocytes (Thomas and Hoffman, 1984;Bhathena et al, 1981) and which are well known immunomodulators (Weinstock and Kassab, 1984;Payan et al, 1984;Foris et al, 1985). Like At II, somatostatin (SS) and Met-enkaphalin (ME) exert their effect on target tissues through specific receptors which are coupled to the adenylate cyclase system in an inhibiting way, since all of the applied NPs affect their targets elevating the intracellular level of cGMP (Gilbert and Richelson, 1983;Wodcock and Johnston, 1982;Spada et al, 1984).…”