To get to the bottom of things, neuroscientist Terra Barnes and her team at Washington University in St . Louisin Missouri produced mice with mutation in the Gnptab gene and studied whether it affected the ultrasonic vocalizations that newly born mouse pups emit when separated from their mothers.
In addition, mouse pups emit USV when they are separated from their mother or are under uncomfortable situations[11], [12].
Because previous studies showed that axonal rearrangement is more robust in younger animals than in older animals in other sensory systems [24], [25], we performed ME on mouse pups at P10, when the eye-specific projection patterns of RGC axons are mostly formed in the dLGN [10], [12].
This was based upon the knowledge that when mouse pups are cross-fostered to adoptive lactating dams, they are usually well accepted and nurtured [39], and on the fact that an adoption procedure carried out in the first postnatal days has a low impact on offspring's HPA functioning [40].
Moreover, µ-opioid receptor knockout mouse pups emitted fewer ultrasonic vocalizations when removed from their mothers, indicating a deficit in attachment behaviors [40].
Ultimately, although the rodent literature has helped inform us about experimental design for thimerosal studies, the small size of mouse pups represents significant challenges particularly when administering IM thimerosal (Harry et al. 2004).
Previous research has shown that female mice have more and healthier pups when they are paired with a male that they choose as opposed to a random male.
First, we showed that mouse pups move toward the thermoneutral temperature when offered a choice between a thermoneutral and cold environment, thus showing thermotaxis.
The treatment restored new neuron growth in the two brain structures controlling smell and memory, and it restored the mouse dads' ability to recognize their pups when they were full-grown.
When miR-150−/− mouse pups were exposed to hyperoxia, a moderate protection of the lung structure was noted at P9; however, no protection was evident at P13, where miR-150−/− mice and wild-type mice exhibited a comparable blunting of alveolarization in response to hyperoxia exposure.
