Acute corticosterone treatment is sufficient to induce anxiety and amygdaloid dendritic hypertrophy

Proceedings of the National Academy of Sciences of the United States of America - Tập 105 Số 14 - Trang 5573-5578 - 2008
Rupshi Mitra1, Robert M. Sapolsky2,3
1Department of Biology, Stanford University, Gilbert Building, Stanford, CA 94305, USA.
2Department of Biology, Stanford University, Gilbert Building, Stanford, CA 94305
3The Rockefeller University, New York, NY

Tóm tắt

Stress is known to induce dendritic hypertrophy in the basolateral amygdala (BLA) and to enhance anxiety. Stress also leads to secretion of glucocorticoids (GC), and the BLA has a high concentration of glucocorticoid receptors. This raises the possibility that stress-induced elevation in GC secretion might directly affect amygdaloid neurons. To address the possible effects of GC on neurons of amygdala and on anxiety, we used rats treated either acutely with a single dose or chronically with 10 daily doses of high physiological levels of corticosterone (the rat-specific glucocorticoid). Behavior and morphological changes in neurons of BLA were measured 12 days after the initiation of treatment in both groups. A single acute dose of corticosterone was sufficient to induce dendritic hypertrophy in the BLA and heightened anxiety, as measured on an elevated plus maze. Moreover, this form of dendritic hypertrophy after acute treatment was of a magnitude similar to that caused by chronic treatment. Thus, plasticity of BLA neurons is sufficiently sensitive so as to be saturated by a single day of stress. The effects of corticosterone were specific to anxiety, as neither acute nor chronic treatment caused any change in conditioned fear or in general locomotor activity in these animals.

Từ khóa


Tài liệu tham khảo

10.1016/0006-8993(92)91597-8

10.1016/S0006-3223(00)00964-1

10.1038/nrn849

10.1037/0735-7044.110.6.1321

10.1177/1534582306289043

10.1016/S0306-4522(00)00050-6

10.1016/0006-8993(94)91778-7

10.1073/pnas.0504011102

10.1523/JNEUROSCI.22-15-06810.2002

10.1037/0735-7044.118.6.1450

10.31887/DCNS.2006.8.4/ssmith

10.1615/CritRevNeurobiol.v10.i3-4.50

10.1016/j.yfrne.2003.07.001

10.1046/j.1365-2826.2001.00688.x

10.1615/CritRevNeurobiol.v10.i2.10

10.1111/j.1749-6632.1994.tb39223.x

10.1002/hipo.450020410

10.1016/0306-4522(95)00259-L

10.1016/S0031-9384(98)00225-X

10.1523/JNEUROSCI.5740-03.2004

10.1523/JNEUROSCI.0680-07.2007

10.1046/j.1460-9568.2002.02172.x

10.1523/JNEUROSCI.18-19-07836.1998

10.1016/j.ceca.2005.01.008

10.1523/JNEUROSCI.22-18-08042.2002

10.1016/j.yebeh.2005.08.007

10.1074/jbc.M003388200

10.1007/s11010-006-9320-6

10.1016/S0021-9258(18)45700-6

10.1074/jbc.M305350200

10.3109/10253890009001124

10.1016/0166-2236(94)90094-9

10.1037/0735-7044.110.5.1074

10.1016/j.neuropharm.2006.07.007

10.1523/JNEUROSCI.4623-04.2005

10.1016/j.jphysparis.2006.03.006

10.1016/S0165-0173(02)00248-5

10.1016/j.neubiorev.2005.04.004

10.1016/j.bbr.2007.02.001

10.1016/j.neuroscience.2004.07.013

10.1111/j.1749-6632.2003.tb07095.x

KC Evans, et al., A functional MRI study of amygdala responses to angry schematic faces in social anxiety disorder. Depress Anxiety, 2007).

HM Lesscher, et al., Amygdala protein kinase C epsilon regulates corticotropin-releasing factor and anxiety-like behavior. Genes Brain Behav, 2007).

10.1016/S0014-2999(03)01282-2

10.1371/journal.pone.0000167

10.1017/S146114570600664X

10.1016/j.biopsych.2005.12.003

10.1073/pnas.0337480100

10.1523/JNEUROSCI.2574-04.2004

10.1523/JNEUROSCI.4664-03.2004

10.1037/0735-7044.118.2.274

10.1523/JNEUROSCI.0499-06.2006

10.1016/j.nlm.2006.03.003

10.1038/sj.npp.1300899

10.1016/0031-9384(88)90097-2

10.1016/0091-3057(85)90286-2

10.1523/JNEUROSCI.14-09-05373.1994

10.1016/S0014-2999(03)01279-2

Thông tin
Thông tin xuất bản

Proceedings of the National Academy of Sciences of the United States of America

Tập 105 Số 14

5573-5578

Thông tin tác giả