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Skin fibroblast beta-adrenergic receptor function in manic-depressive illness
W H Berrettini1, J Bardakjian, C B Cappellari
1Clinical Neurogenetics Branch, DIRP, NIMH, Bethesda, MD 20892.
Biological Psychiatry
|December 1, 1987
Summary
Beta-adrenergic receptor function was normal in bipolar patients, with no differences in cyclic adenosine monophosphate (cAMP) response to isoproterenol. Receptor desensitization also did not distinguish bipolar patients from controls.
Area of Science:
- Neuroscience
- Cell Biology
- Pharmacology
Background:
- Bipolar disorder is a mood disorder with complex neurobiological underpinnings.
- Beta-adrenergic receptors play a role in neurotransmission and cellular signaling.
- Dysregulation of cellular signaling pathways has been implicated in mood disorders.
Purpose of the Study:
- To investigate beta-adrenergic receptor function in bipolar disorder.
- To assess the cyclic adenosine monophosphate (cAMP) response to isoproterenol in fibroblasts from bipolar patients and controls.
- To examine receptor desensitization as a potential biomarker in bipolar disorder.
Main Methods:
- Cultured skin fibroblasts were obtained from individuals with bipolar disorder and healthy volunteers.
- The cyclic adenosine monophosphate (cAMP) response to isoproterenol was measured.
- Fibroblasts were incubated with isoproterenol to assess receptor desensitization.
Main Results:
- No significant differences were observed in the basal cAMP response to isoproterenol between bipolar patients and controls.
- Following a 24-hour incubation with isoproterenol, subsensitivity to rechallenge did not differ between the groups.
- These findings suggest normal beta-adrenergic receptor function and desensitization regulation in bipolar disorder fibroblasts.
Conclusions:
- Beta-adrenergic receptor signaling, as measured by cAMP production, is not globally altered in fibroblasts from bipolar disorder patients.
- Receptor desensitization mechanisms appear to be intact in this cellular model of bipolar disorder.
- These results do not support a primary role for beta-adrenergic receptor dysfunction in the pathophysiology of bipolar disorder as assessed in skin fibroblasts.