Aα-Opiate Receptor in 7315c Tumor Tissue Mediates Inhibition of Immunoreactive Prolactin Release and Adenylate Cyclase Activity

Publisher Website
Google Scholar
Abstract
Cells of the 7315c tumor released immunoreactive PRL [prolactin] (IR-PRL). Cholera toxin enhanced this release. Morphine and other opiate agonists inhibited IR-PRL release from both untreated and cholera toxin-treated tumor cells. The opiate-induced inhibition of IR-PRL release was concentration dependent and naloxone sensitive. Cholera toxin also enhanced the adenylate cyclase activity of 7315c tumor tissue. Opiates inhibited enzyme activity in both untreated and cholera toxin-treated 7315c tissue in a concentration-dependent and naloxone-sensitive manner. FK 33824 [(D-ala2-mephery-met(O5)-O1)enkephalin] was more potent than [D-Ala2,D-Leu5]enkephalin in inhibiting IR-PRL release and adenylate cyclase activity. In cholera toxin-treated 7315c tumor tissue, GTP was required for opiate-induced inhibition of adenylate cyclase activity. Nonhydrolyzable analogs of GTP inhibited toxin-stimulated cyclase activity in the absence of an opiate. The 7315c tumor possesses a .mu.-opiate receptor; stimulation of this receptor inhibits both IR-PRL release and adenylate cyclase activity. An inhibitory guanyl nucleotide component may link the .mu.-opiate receptor to adenylate cyclase.