Neuroscience
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It is well-known that the onset of puberty is associated with changes in mood as well as cognition. Stress can have an impact on these outcomes, which in many cases, can be more influential in females, suggesting that gender differences exist. The adolescent period is a vulnerable time for the onset of certain psychopathologies, including anxiety disorders, depression and eating disorders, which are also more prevalent in females. ⋯ Spatial learning and synaptic plasticity are also adversely impacted at puberty, likely a result of increased expression of α4βδ GABARs on the dendritic spines of CA1 hippocampal pyramidal cells, which are essential for consolidation of memory. This review will focus on the role of these receptors in mediating behavioral changes at puberty. Stress-mediated changes in mood and cognition in early adolescence may have relevance for the expression of psychopathologies in adulthood.
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Accumulating evidence suggests that adolescence represents a sensitive period during which social stressors influence adult behavior and stress reactivity. However, relatively little is known about the impact of social stress in adolescence on behaviors or stress reactivity in females. In this study, we exposed adolescent or adult female rats to the repeated social stress of defeat for seven consecutive days. ⋯ Using exposure to a novel restraint to assess stress reactivity, we found that stress during adolescence and adulthood led to lower basal adrenocorticotropic hormone concentrations and that both stressed and control adolescent groups exhibited a delay in recovery in adulthood compared to stressed and control adult groups. Fos protein analysis further suggested that cortical/thalamic structures serve as potential substrates that mediate these long-term impacts of stress during adolescence. Thus, repeated social stress during adolescence produces different patterns of effects as compared with repeated social stress during adulthood.
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Review
From the stressed adolescent to the anxious and depressed adult: investigations in rodent models.
Anxiety and depression are the most prevalent of the psychiatric disorders. The average age of onset of these disorders is in adolescence, and stressful experiences are recognized as an important pathway to such dysfunction. ⋯ The focus of the review is investigations in which adolescent rodents were exposed to chronic stressors, describing our research using social instability stress and that of other researchers using various social and non-social stressors. The evidence to date suggests stress in adolescence alters the trajectory of brain development, and particularly that of the hippocampus, increasing anxiety and depressive behaviour in adulthood.
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In adult rodents, endocannabinoids (eCBs) regulate fast glucocorticoid (GC) feedback in the hypothalamus-pituitary adrenal (HPA) axis, acting as retrograde messengers that bind to cannabinoid receptors (CB1R) and inhibit glutamate release from presynaptic CRH neurons in the paraventricular nucleus of the hypothalamus (PVN). During the first two weeks of life, rat pups exhibit significant CRH and ACTH responses to stress although the adrenal GC output remains reduced. At the same time, pups also display increased sensitivity to GC feedback, but it is unclear whether eCBs play a role in mediating fast GC feedback in neonatal life. ⋯ Methylprednisolone suppressed ACTH stress responses although AM251 still delayed restoration of ACTH levels to the baseline. This suggests that the eCB effect on ACTH secretion in neonates is most evident when there is a dynamic fluctuation of corticosterone levels. Interestingly, AM251 increased basal and stimulated corticosterone secretion in all treatments including MET, suggestive of a direct action of CB1R blockade on adrenal steroidogenesis.
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In the last decade, early-onset of affective illness has been recognized as a major public health problem. However, clinical studies indicate that although children experience the symptoms of anxiety and depression in much the same way as adults, they display and react to those symptoms differently (Bostic et al., 2005). Recently, we have demonstrated that similar differences in symptoms are found also between adult and juvenile rats (Jacobson-Pick and Richter-Levin, 2010). ⋯ Exposure to forced swim stress resulted in significant alterations of dentate gyrus activity and plasticity in male rats with differences between adult and pre-pubertal animals. Stress had far less impact on females' dentate electrophysiology. The results are in agreement with the differences in behavioral response to stress between pre-pubertal and adult rats, and with reported differences for the sensitivity of male and female rats in performing hippocampus-dependent tasks under stress, such as the active avoidance task.