Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0040822 (tremor)
 18,428 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Beta-adrenergic receptor kinetics were measured in leukocytes from 17 drug-free, nondepressed patients with social phobia (generalized type) and 17 gender-matched and age-matched healthy controls. Binding was characterized using the highly specific beta-adrenergic ligand [125I]pindolol (125IPIN). Contrary to some studies in panic disorder and many studies in depression, no significant difference was found in Bmax or Kd values between social phobic patients and controls. Neither severity of social phobic symptoms nor the severity of certain symptoms of beta-adrenergic activation (i.e., tachycardia, tremor, blushing) influenced Bmax or Kd. To the extent that these peripheral indices can be considered reflective of central processes, these findings suggest that a simple defect in beta-adrenoceptor number of affinity is unlikely to explain the pathophysiology of generalized social phobia.
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PMID:Lymphocyte beta-adrenoceptors in social phobia. 839 92

Somatic symptoms include a range of physical experiences, such as pain, muscle tension, body shaking, difficulty in breathing, heart palpitation, blushing, fatigue, and sweating. Somatic symptoms are common in major depressive disorder (MDD), anxiety disorders, and some other psychiatric disorders. However, the etiology of somatic symptoms remains unclear. Somatic symptoms could be a response to emotional distress in patients with those psychiatric conditions. Increasing evidence supports the role of aberrant serotoninergic and noradrenergic neurotransmission in somatic symptoms. The physiological alterations underlying diminished serotonin (5-HT) and norepinephrine (NE) signaling may contribute to impaired signal transduction, reduced 5-HT, or NE release from terminals of presynaptic neurons, and result in alternations in function and/or number of receptors and changes in intracellular signal processing. Multiple resources of data support each of these mechanisms. Animal models have shown physiological responses, similar to somatic symptoms seen in psychiatric patients, after manipulations of 5-HT and NE neurotransmission. Human genetic studies have identified many single-nucleotide polymorphisms risk loci associated with somatic symptoms. Several neuroimaging findings support that somatic symptoms are possibly associated with a state of reduced receptor binding. This narrative literature review aimed to discuss the involvement of serotonergic and noradrenergic systems in the pathophysiology of somatic symptoms. Future research combining neuroimaging techniques and genetic analysis to further elucidate the biological mechanisms of somatic symptoms and to develop novel treatment strategies is needed.
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PMID:Dysfunction in Serotonergic and Noradrenergic Systems and Somatic Symptoms in Psychiatric Disorders. 3117 61