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Opiate-dependent modulation of adenylate cyclase
Summary
Opiate receptors initially inhibit, then increase, adenylate cyclase activity in neuroblastoma cells. This suggests opiates shift the enzyme balance toward a higher-activity form, requiring protein synthesis.
Area of Science:
- Neuroscience
- Biochemistry
- Cell Biology
Background:
- Opiate receptors are known to inhibit adenylate cyclase.
- Neuroblastoma X glioma NG108-15 hybrid cells are a model for studying receptor-mediated signaling.
Purpose of the Study:
- To investigate the long-term effects of opiate receptor activation on adenylate cyclase activity.
- To elucidate the mechanisms underlying the observed changes in enzyme activity.
Main Methods:
- Treatment of NG108-15 cells with opiate agonists.
- Measurement of basal- and stimulated-adenylate cyclase activity.
- Use of NaF, guanosine 5'-(beta, gamma-imido)triphosphate, and cycloheximide to probe enzyme regulation.
Main Results:
- Opiate treatment led to increased basal, prostaglandin E1-, and 2-chloroadenosine-stimulated adenylate cyclase activity.
- NaF and guanosine 5'-(beta, gamma-imido)triphosphate largely abolished these differences, indicating involvement of G-proteins.
- Cycloheximide partially inhibited the opiate-dependent increase, suggesting a role for protein synthesis.
Conclusions:
- Opiate receptor activation induces a conversion of adenylate cyclase to a form with altered, higher activity.
- This conversion is partly dependent on protein synthesis.
- Opiates may regulate the enzyme by shifting the equilibrium between low- and high-activity forms of adenylate cyclase.