Although immature rats and mice generally demonstrate poor behavioral inhibitory capacities, some recent evidence may indicate the presence of substantial inhibitory control. The present experiment investigated the possibility that gamma-aminobutyric acid (GABA) systems may mediate some behavioral inhibition during early development. Mice 9-100 days old were injected with the GABA-elevating agent amino-oxyacetic acid (AOAA) and tested for behavioral activity. High levels of locomotor activity characteristic of immature control mice were attenuated following AOAA injection, whereas AOAA had little effect on the activity of adult mice. Moreover, AOAA produced a period of rebound hyperactivity for young but not for adult mice. These findings suggest that although GABA systems may mediate early behavioral inhibition, coordination between excitatory and inhibitory capacities matures slowly. In a second experiment the dopamine-beta-hydroxylase inhibitor FLA-63 prevented rebound hyperactivity in young mice pretreated with AOAA, suggesting that the excitatory component may be mediated by noradrenergic systems.

No abstract

To assess the effects of early postnatal undernutrition upon the developing abilities of infant and juvenile mice to acquire and retain a passive-avoidance response, we reared mice following birth in either "normally nourished" or "undernourished" conditions by maintaining litter sizes of 6 or 16, respectively. At ages ranging from 7 to 21 days, mice from each nutritional condition were trained to withhold stepping off from a small vibrating platform in order to avoid shock. Following training to a common criterion, separate groups of mice were retained to the same criterion either 1 or 24 hr later. From the comparisons with yoked control groups at each age and retention interval, we conclude that although undernutrition results in some age-related differences in the ability to withhold responding, these are quite small during acquisition within each age group. In contrast, the retention data suggest that undernutrition delayed the development of both short- and long-term memory abilities on this task. In general, these results are similar to earlier data involving discriminated shock-escape wherein undernutrition had little apparent effect upon acquisition at the early ages but rather marked effects upon developing memory system.

In order to determine the age at which Swiss-Webster mice first became capable of learning and exhibiting 24-h retention of a directional, one-way active avoidance response, six separate groups of 20 mice received 25 active avoidance training trials at selected ages between 11 and 21 days of age. Equal numbers of yoked-shock control mice received identical amounts of shock and handling as their trained littermates on each trial. Following a 24-h retention interval, all groups received 25 active avoidance training trials. The acquisition results indicated that, while all age groups were capable of emitting some successful avoidances, within-session improvement was not apparent until 17 days of age. Comparisons of retest scores by trained mice with their formerly yoked-shocked littermates revealed that reliably more avoidances were made by mice with prior training beginning at 17 days of age. In general, the results suggest that the ability to acquire and remember for 24 h an active avoidance response emerges around 15-17 days of age for Swiss mice on this directional task.

To determine the effects of early undernutrition on learning and long-term memory, Swiss mice were cross-fostered randomly at birth to produce litter sizes of 6 and 16, thereby providing "normally nourished" and "undernourished" conditions. At 28 days of age, the pups were housed in groups of 3 and 4, with ad-lib access to food and water until testing began at 60 days of age. Each mouse received 50 active-avoidance training trials daily for 14 consecutive days. Retention testing began 14 days after the end of original training and consisted of 50 trials daily for 5 days. Overall, mice reared in large litters suffered deficits in learning but not in long-term memory.