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We have reported that neonatal handling leads to increased sweet food preference in adult life. Our aim was to verify if these differences in feeding behavior appear before puberty, and whether other types of intervention in periadolescence (such as exposure to toys) could interfere with sweet food consumption later in life. Nests of Wistar rats were (1) non-handled or (2) handled (10 min/day) on days 1–10 after birth. Males from these groups were subdivided in two subgroups: one was habituated to sweet food (Froot Loops—Kellogs®) in a new environment for 4 days and tested for sweet food preference at age 27 days, before submitting to a new habituation and test for sweet food ingestion again in adult life. The other subgroup was habituated and tested only in adulthood. In another set of experiments, neonatally non-handled rats were exposed or not to a new environment with toys in periadolescence, and tested for sweet food ingestion as adults. Neonatal handling increases sweet food consumption only if the habituation and tests are performed after puberty. Interestingly, infant exposure to sweet food had a similar effect as neonatal handling, since controls that were exposed to sweet food at age 22 to 27 days increased their ingestion as adults. Exposure to toys in periadolescence had the same effect. We suggest that an intervention during the first postnatal days or exposure to an enriched environment later in the pre-pubertal period leads to behavioral alterations that persist through adulthood, such as increased sweet food ingestion.

It has been reported that animals submitted to repeated restraint stress present various adaptation responses which are dependent on the sex. These adaptations include changes in nociception and adenine nucleotide hydrolysis. In this study, we report the effect of chronic administration of a gonadal steroid (17beta-estradiol) on ATP, ADP and AMP hydrolysis in spinal cord synaptosomes of adult ovariectomized (OVX) Wistar rats submitted to repeated restraint stress over 40 days. We also measured nociceptive threshold in these animals using the tail-flick test. The results show that tail-flick latencies were decreased in both stressed groups, OVX and OVX rats receiving estradiol replacement therapy, indicating reduced nociceptive threshold after exposure to repeated stress. Repeated restraint stress caused no effect on ATPase or ADPase activities. On the other hand, AMP hydrolysis in spinal cord synaptosomes from repeatedly stressed rats was decreased in OVX rats compared to non-stressed OVX ones, indicating reduced extracellular adenosine production; this effect was reversed by hormonal replacement. These observations suggest that nociceptive sensitivity to noxious stimuli is affected by repeated stress and that modulation of neurotransmission by adenine nucleotides in spinal cord may be altered by the interaction of sexual hormones and psychological factors, such as exposure to stress.