The role of the read through variant of acetylcholinesterase in anxiogenic effects of predator stress in mice.

Autor: Adamec R; Department of Psychology, Memorial University, 232 Elizabeth Avenue, St. John's, NF, A1B 3X9 Canada. radamec@mun.ca, Head D, Soreq H, Blundell J
Jazyk: angličtina
Zdroj: Behavioural brain research [Behav Brain Res] 2008 May 16; Vol. 189 (1), pp. 180-90. Date of Electronic Publication: 2008 Jan 05.
DOI: 10.1016/j.bbr.2007.12.023
Abstrakt: This study examined the role of the read through variant of acetylcholinesterase (AChE-R) in lasting changes in murine affective behavior produced by a brief predator stress. AChE-R is elevated by stress in limbic cholinergic circuits implicated in anxiogenic effects of predator stress. The expression of AChE-R was blocked with a systemically administered central acting antisense oligonucleotide for AChE-R (EN101). EN101 was injected at multiple points prior to and after a predator stress in male C57 mice. Seven days after the last injection, behavior was tested. Predator stress caused a significant increase in startle amplitude, which EN101 blocked. This effect was specific to EN101, as the negative control inactive form of EN101, INVEN101 was without effect on stress effects on startle. Neither EN101 nor INVEN101 altered the anxiogenic effects of predator stress on behavior in the elevated plus maze, and both drugs partially reduced stress suppression of time active in the hole board. In the light dark box test, INVEN101 exhibited a weak block of stress effects on behavior for reasons which are unclear. Taken together, findings support the view that multiple neural systems are responsible for the different changes in behavior produced by predator stress. Present findings also suggest a role for AChE-R in specific anxiogenic (hyperarousal) effects following predator stress. Since AChE-R manipulations took place starting 23 h prior to predator stress and continued 48 h after predator stress, further research is necessary to determine the role of AChE-R in initiation and/or consolidation of hyperarousal effects of predator stress.
Databáze: MEDLINE
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