Hypothyroidism is known to exert significant structural and functional changes to the developing centralnervous system, and can lead to the establishment of serious mental retardation and neurological prob-lems. The aim of the present study was to shed more light on the effects of gestational and/or lactationalmaternal exposure to propylthiouracil-induced experimental hypothyroidism on crucial brain enzymeactivities of Wistar rat offspring, at two time-points of their lives: at birth (day-1) and at 21 days of age(end of lactation). Under all studied experimental conditions, offspring brain acetylcholinesterase (AChE)activity was found to be significantly decreased due to maternal hypothyroidism, in contrast to the twostudied adenosinetriphosphatase (Na+,K+-ATPase and Mg2+-ATPase) activities that were only found tobe significantly altered right after birth (increased and decreased, respectively, following an exposure togestational maternal hypothyroidism) and were restored to control levels by the end of lactation. As ourfindings regarding the pattern of effects that maternal hypothyroidism has on the above-mentioned cru-cial offspring brain enzyme activities are compared to those reported in the literature, several differencesare revealed that could be attributed to both the mode of the experimental simulation approach followedas well as to the time-frames examined. These findings could provide the basis for a debate on the need ofa more consistent experimental approach to hypothyroidism during neurodevelopment as well as for afurther evaluation of the herein presented and discussed neurochemical (and, ultimately, neurodevelop-mental) effects of experimentally-induced maternal hypothyroidism, in a brain region-specific manner.