Anticholinesterase treatment of chicken retinal cells increases acetylcholinesterase protein independently of protein kinase C

It has been reported that anticholinesterase exposure, e.g. by environmenta l toxins or nerve gases, can increase acetylcholinesterase (AChE) protein, possibly as an autoregulatory stress response. We earlier have transfected retinal cells of the chick embryo with a pSVK3-AChE(rab)-cDNA vector to het erologously express rabbit AChE, which concomitantly also increased AChE pr otein from chick. To analyse further the cell-internal pathways of these di fferent paradigms (anticholinesterase treatment vs. AChE transfection) whic h both lead to an AChE increase, we here show that AChE overexpression by t ransfection leads to an increase in protein kinase C (PKC). Most remarkably , when cells independently of, or in addition to their transfection are tre ated with 10 muM of the AChE inhibitor BW284c51,AChE protein levels are muc h more dramatically increased up to 20-fold. This treatment, however, does not affect PKC. These data show that (i) retinal cells respond to anticholi nesterase insult by a massive increase of AChE protein; (ii) the response t o BW284c51 is not PKC-mediated; and (iii) both strategies of AChE increase follow different cell-internal pathways, their effects being additive. The ecological and biomedical implications of these findings are briefly discus sed. (C) 2001 Elsevier Science Ireland Ltd. All rights reserved.