Premium
Alpha‐1A adrenergic receptor modulates anxiety and depression in mice
Author(s) -
Luger Elizabeth Joan,
Fettig Megan,
Darsie Belle,
Wald Jenna,
Berntson Sarah,
Boese Sarah,
Haselton James,
Handel Evelyn,
Talbot Jeffery,
Rorabaugh Boyd,
Doze Van
Publication year - 2009
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.23.1_supplement.962.3
Subject(s) - elevated plus maze , tail suspension test , anxiolytic , behavioural despair test , anxiety , knockout mouse , open field , agonist , endocrinology , receptor , medicine , genetically modified mouse , adrenergic receptor , antidepressant , chemistry , psychology , transgene , psychiatry , biochemistry , gene
Norepinephrine (NE), an endogenous neurotransmitter, is involved in cognition as well as anxiety and depression. NE mediates its actions through the activation of adrenergic receptors (ARs). This study explored the effects of increased α 1A AR activation on anxiety and depression in mice. Different sets of mice with varying degrees of α 1A AR expression and activation were used in behavioral tests for anxiety and depression. The mice sets included transgenic mice with increased α 1A AR expression, transgenic mice with a knockout of the α 1A AR, mice treated with the α 1A AR agonist cirazoline, and groups of normal control mice. The tail suspension and forced swim tests were used as models of depression and the light/dark, marble burying and elevated plus‐maze tests were used as measurements of anxiety. In addition, the open field test was used to determine the mobility of these animals. It was found that mice with increased α 1A AR activation, in comparison to normal mice, demonstrated anxiolytic and antidepressant‐like behavior in several of these models. The mobility of these animals was similar. These results suggest that activation of the α 1A AR reduces anxiety and depression in mice without affecting their mobility. This study was supported by NSF CAREER 0347259, NSF REU Site 0639227, NIH P20 RR016741, UND REFUNDU Program, American Physiological Society, and the Bower, Bennet & Bennet Endowed Research Award from ONU.