Differential impact of juvenile stress and corticosterone in juvenility and in adulthood, in male and female rats

Jacobson‐Pick, Shlomit; Richter‐Levin, Gal

doi:10.1016/j.bbr.2010.05.036

Cited by 91 publications

(78 citation statements)

References 48 publications

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“…This contrasts with previous reports of increased anxiety (Giovanoli et al, 2013;Jacobson-Pick et al, 2008;Maslova et al, 2002aMaslova et al, , 2002bTsoory et al, 2007;Yee et al, 2011), although negative or inconsistent results have also been reported (Avital and Richter-Levin, 2005;Bourke and Neigh, 2011;Jacobson-Pick and Richter-Levin, 2010;McCormick et al, 2007;Peleg-Raibstein and Feldon, 2011;Pohl et al, 2007;Toledo-Rodríguez and Sandi, 2007). This is likely related to a differential susceptibility to stress among the different strains of rats and mice used (e.g., Maslova et al, 2002aMaslova et al, , 2002b.…”

Section: Accepted M Manuscriptcontrasting

confidence: 85%

Behavioral and neuroendocrine consequences of juvenile stress combined with adult immobilization in male rats

Fuentes

Carrasco

Armario

et al. 2014

Hormones and Behavior

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Exposure to stress during childhood and adolescence increases vulnerability to developing several psychopathologies in adulthood and alters the activity of the hypothalamic-pituitaryadrenal (HPA) axis, the prototypical stress system. Rodent models of juvenile stress appear to support this hypothesis because juvenile stress can result in reduced activity/exploration and enhanced anxiety, although results are not always consistent. Moreover, an in-depth characterization of changes in the HPA axis is lacking. In the present study, the long-lasting effects of juvenile stress on adult behavior and HPA function were evaluated in male rats. The juvenile stress consisted of a combination of stressors (cat odor, forced swim and footshock) during postnatal days 23-28. Juvenile stress reduced the maximum amplitude of the adrenocorticotropic hormone (ACTH) levels (reduced peak at lights off), without affecting the circadian corticosterone rhythm, but other aspects of the HPA function (negative glucocorticoid feedback, responsiveness to further stressors and brain gene expression of corticotrophin-releasing hormone and corticosteroid receptors) remained unaltered. The behavioral effects of juvenile stress itself at adulthood were modest (decreased activity in the circular corridor) with no evidence of enhanced anxiety. Imposition of an acute severe stressor (immobilization on boards, IMO) did not increase anxiety in control animals, as evaluated one week later in the elevated-plus maze (EPM), but it potentiated the acoustic startle response (ASR). However, acute IMO did enhance anxiety in the EPM, in juvenile stressed rats, thereby suggesting that juvenile stress sensitizes rats to the effects of additional stressors.

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Section: Accepted M Manuscriptcontrasting

confidence: 85%

Behavioral and neuroendocrine consequences of juvenile stress combined with adult immobilization in male rats

Fuentes

Carrasco

Armario

et al. 2014

Hormones and Behavior

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“…During the early postnatal period, maternal separation, a commonly used experimental early-life stress, leads to increased anxiety-, depression-, and schizophrenialike behavior in adulthood Ellenbroek et al, 1998;Huot et al, 2001;Martisova et al, 2012;Romeo et al, 2003). In addition, juvenile rodents exposed to stressful events after weaning show increased depressionand anxiety-like behavior in adulthood (Jacobson-Pick and Richter-Levin, 2010;Pohl et al, 2007;Wilkin et al, 2012).…”

Section: Effects Of Early-life Experiences On Adult Neurogenesis and mentioning

confidence: 99%

Adult Neurogenesis and Mental Illness

Schoenfeld

Cameron

2014

Neuropsychopharmacol

162

108

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Several lines of evidence suggest that adult neurogenesis, the production of new neurons in adulthood, may play a role in psychiatric disorders, including depression, anxiety, and schizophrenia. Medications and other treatments for mental disorders often promote the proliferation of new neurons; the time course for maturation and integration of new neurons in circuitry parallels the delayed efficacy of psychiatric therapies; adverse and beneficial experiences similarly affect development of mental illness and neurogenesis; and ablation of new neurons in adulthood alters the behavioral impact of drugs in animal models. At present, the links between adult neurogenesis and depression seem stronger than those suggesting a relationship between new neurons and anxiety or schizophrenia. Yet, even in the case of depression there is currently no direct evidence for a causative role. This article reviews the data relating adult neurogenesis to mental illness and discusses where research needs to head in the future.

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“…Modulating GABA contributes to the mechanism of action of anxiolytics, mood stabilizers and antidepressants [43,46]. The composition of GABA A R α subunits changes during different stages of development such that the relative expression of α2 and α3 subunits is high early in life compared with the level of expression of α1, and this pattern reverses into adulthood [47]. Subjecting adult juvenile-stressed rats to emotional challenges in adulthood (i.e.…”

Section: Post-weaning To Pre-pubertal (Juvenile) Stress Modelmentioning

confidence: 99%

Post-Weaning to Pre-Pubertal (‘Juvenile’) Stress: A Model of Induced Predisposition to Stress-Related Disorders

et al. 2012

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Human studies suggest that childhood trauma predisposes individuals to develop stress-related disorders such as depression and post-traumatic stress disorder (PTSD). Recent years have witnessed growing interest in effectively modeling in animals the long-term effects of childhood emotional trauma on stress responses in adulthood. Most studies concerned with the impact of early-life stress on subsequent stress responses in adulthood in rodents have focused on the post-natal pre-weaning period. However, psychiatric studies often refer to human childhood rather than infancy when investigating the patients’ traumatic history of stress-related psychopathologies. In accordance with that, we have examined the consequences of stress exposure at a later early-life period, the post-weaning, pre-puberty (juvenile) period, which holds greater resemblance to human childhood. This review summarizes a series of studies examining the impact of exposure of rats to stressors during ‘juvenility’ (‘juvenile stress’) on the ability of these animals to cope with stress later in life. Exposure to relatively brief but significant stress experience during juvenility was found to impair the ability of animals to cope with stressful challenges in adulthood. These behavioral manifestations were associated with lasting alterations in limbic system brain regions of neuromodulatory pathways, such as alterations in the expression of cell adhesion molecules, GABAergic system functioning and alterations in levels of circulating corticosterone. Importantly, these studies have also demonstrated considerable individual and sex differences, which call for the development of adequate analysis approaches. The juvenile stress model combined with characterization of individual profiles is presented as a useful model to study in rodents different facets of stress-related disorders and neural mechanisms of vulnerability and resilience to stress.

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Differential impact of juvenile stress and corticosterone in juvenility and in adulthood, in male and female rats

Cited by 91 publications

References 48 publications

Behavioral and neuroendocrine consequences of juvenile stress combined with adult immobilization in male rats

Behavioral and neuroendocrine consequences of juvenile stress combined with adult immobilization in male rats

Adult Neurogenesis and Mental Illness

Post-Weaning to Pre-Pubertal (‘Juvenile’) Stress: A Model of Induced Predisposition to Stress-Related Disorders

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