AI Article Synopsis
- Research indicates that adrenergic alpha2A receptors (ADRA2A) play a key role in regulating water intake, particularly in patients with schizophrenia.
- A study involving patients with schizophrenia showed that using clonidine (an ADRA2A-agonist) worsened excessive drinking (polydipsia), while mianserin (an ADRA2A-antagonist) improved it, linking drinking behavior to the central adrenergic system.
- However, a study examining the C-1291G polymorphism in the ADRA2A gene among Japanese patients found no significant association with polydipsia, suggesting this genetic variation might not affect susceptibility to the condition in this population.
Article Abstract
Several lines of studies have shown the existence of an important inhibitory mechanism for the control of water intake involving adrenergic alpha2A receptors (ADRA2A). A human study using patients with schizophrenia demonstrated an exacerbation of polydipsia by the administration of clonidine, an ADRA2A-agonist, and a relief of polydipsia by mianserin, an ADRA2A-antagonist, suggesting the involvement of the central adrenergic system in the drinking behavior of patients with schizophrenia. Based on these findings we examined a possible association between the C-1291G polymorphism in the promoter region of the ADRA2A gene and polydipsia in schizophrenia using a Japanese case-control sample. Our sample includes 348 patients with schizophrenia (DSM-IV) (84 with polydipsia and 264 without polydipsia). No significant association between the ADRA2A C-1291G polymorphism and polydipsia was found. Our result suggests that the ADRA2A C-1291G polymorphism may not confer susceptibility to polydipsia in schizophrenia in our sample. Further studies with larger samples are warranted.
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| http://dx.doi.org/10.1016/j.pnpbp.2009.01.012 | DOI Listing |
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