Little has been investigated about the effects of stress on synaptic communication at prepubertal age, a stage considered as juvenile. This period of development is related to socialization through play. Our group has studied the changes of neuronal morphology in limbic structures caused by stress at prenatal and at early postnatal ages (before weaning) in the rat. In the present study, we assessed the effect of restraint stress at juvenile ages. Male Sprague-Dawley rats from postnatal day (PD) 21 to PD35 were restrained (from movement) for 2 hrs. Locomotor activity in a novel environment was evaluated at three different ages, prepubertal PD38, pubertal PD50, and postpubertal PD68. Using the Golgi-Cox procedure, the dendritic morphology was evaluated in the pyramidal neurons of the prefrontal cortex (PFC), hippocampus, and basolateral amygdala (BLA). Juvenile stress caused a reduced locomotor activity at PD38 and PD68 together with reduction in dendritic spines after puberty in the PFC and at all the studied ages in the BLA. In addition, dendritic length was also reduced in the PFC at PD38 and PD68 and CA1 of the ventral hippocampus at PD50 and PD68. Our results suggest that stress in the juvenile stage can cause changes at the level of behavior and synaptic communication with an effect that remains until adulthood.

Diabetes mellitus (DM) is characterized by high levels of blood glucose. In recent years, its prevalence has increased, which was 422 million in the world in 2014. In elderly patients, DM is associated with deficits in memory and learning processes. The cognitive deficits lead to dementia. With the development of animal models in DM, it has been possible to better understand quantitative morphological changes in numerous neuronal structures belonging to the limbic system, such as the prefrontal cortex (PFC), the hippocampus and basolateral amygdala (BLA). These structures are in close relationship with processes of memory and learning. Several reports have demonstrated that chronic hyperglycemia reduces spinogenesis and dendritic arborization in the aforementioned regions along with a decline in memory and learning processes, especially in streptozotocin (STZ)‐induced diabetic rats. In the present review, we discuss animal models, the effects of chronic hyperglycemia on dendritic morphology of limbic regions and memory and learning processes, the effect on neural transmission in these regions, the pathologic mechanisms involved, and the relevance of dendritic morphology in diabetes. All of this information can help us to have a better understanding of dementia in diabetes mellitus and propose strategies for its prevention and treatment.