Abstrakt
Brain acetylcholinesterase (AChE) variant AChE(R) expression increases with acute stress, and this persists for an extended period, although the timing, strain and laterality differences, have not been explored previously. Acute stress transiently increases acetylcholine release, which in turn may increase activity of cholinesterases.
Also the AChE gene contains a glucocorticoid response element (GRE), and stress-inducible AChE transcription and activity changes are linked to increased glucocorticoid levels. Corticotropin-releasing hormone knockout (CRH-KO) mice have basal glucocorticoid levels similar to wild type (WT) mice, but much lower levels during stress.
Hence we hypothesized that CRH is important for the cholinesterase stress responses, including butyrylcholinesterase (BChE). We used immobilization stress, acute (30 or 120min) and repeated (120min dailyx7) in 48 male mice (24WT and 24 CRH-KO) and determined AChE(R), AChE and BChE mRNA expression and AChE and BChE activities in left and right brain areas (as cholinergic signaling shows laterality).
Immobilization decreased BChE mRNA expression (right amygdala, to 0.5, 0.3 and 0.4, xcontrol respectively) and AChE(R) mRNA expression (to 0.5, 0.4 and 0.4, xcontrol respectively). AChE mRNA expression increased (1.3, 1.4 and 1.8-fold, respectively) in the left striatum (Str).
The AChE activity increased in left Str (after 30min, 1.2-fold), decreased in right parietal cortex with repeated stress (to 0.5xcontrol). BChE activity decreased after 30min in the right CA3 region (to 0.4xcontrol) but increased (3.8-fold) after 120min in the left CA3 region.
The pattern of changes in CRH-KO differed from that in WT mice.