Acute stress imposed during adolescence yields heightened anxiety in Sprague Dawley rats that persists into adulthood: Sex differences and potential involvement of the Medial Amygdala

Lovelock, Dennis F.

doi:10.1016/j.brainres.2019.146392

Cited by 28 publications

(23 citation statements)

References 72 publications

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“…On the other hand, it has been reported that peripubertal stress leads to increased risk-taking behavior and novelty seeking in Wistar Han male and female rats with more pronounced effect in females (Toledo-Rodriguez and Sandi 2011). Our findings from adolescent female and male rats are also consistent with another recent publication (Lovelock and Deak 2019), which used acute footshock stress during adolescence (30 PND) and reported long-term increased anxiety-like behavior in males but decreased anxiety-like behavior in females in adulthood (70 PND) (Lovelock and Deak 2019).…”

Section: Discussionsupporting

confidence: 92%

Age- and sex- dependent changes in locus coeruleus physiology and anxiety-like behavior in response to acute stress

Borodovitsyna

Chandler²

2020

Preprint

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Adolescence is a critical period of development with increased sensitivity toward psychological stressors. Many psychiatric conditions emerge during adolescence and animal studies have shown that that acute stress has long-term effects on hypothalamic pituitary adrenal axis function and behavior. We recently demonstrated that acute stress produces long-term electrophysiological changes in locus coeruleus and long-lasting anxiety-like behavior in adolescent male rats. Based on prior reports of increased stress sensitivity during adolescence and increased sensitivity of female locus coeruleus toward corticotropin releasing factor, we hypothesized that the same acute stressor would cause different behavioral and physiological responses in adolescent female and adult male rats one week after stressor exposure. In this study, we assessed age and sex differences in how an acute psychological stressor affects corticosterone release, anxiety-like behavior, and locus coeruleus physiology at short- and long-term intervals. All groups of animals responded to stress with elevated corticosterone levels at the acute time point. One week after stressor exposure, adolescent females showed decreased firing of locus coeruleus neurons upon current injection and increased exploratory behavior compared to controls. The results were in direct contrast to changes observed in adolescent males, which showed increased anxiety-like behavior and increased spontaneous and induced firing locus coeruleus neurons a week after stressor exposure. Adult males were both behaviorally and electrophysiologically resilient to the long-term effects of acute stress. Therefore, there may be a normal developmental trajectory for locus coeruleus neurons which promotes stress resilience in adults, but stressor exposure during adolescence perturbs their function. Furthermore, while locus coeruleus neurons are more sensitive to stressor exposure during adolescence, the effect varies between adolescent males and females. These findings suggest that endocrine, behavioral, and physiological responses to stress vary among animals of different age and sex, and therefore these variables should be taken into account when selecting models and designing experiments to investigate the effects of stress. These differences in animals may also allude to age and sex differences in the prevalence of various psychiatric illnesses within the human population.

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Section: Discussionsupporting

confidence: 92%

Age- and sex- dependent changes in locus coeruleus physiology and anxiety-like behavior in response to acute stress

Borodovitsyna

Chandler²

2020

Preprint

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“…Although there are various investigated brain regions responsible for mood regulation [32,33], the majority of studies in the field of behavioral alterations are focused on the hippocampus [34,35]. It is worth noticing that increased oxidative damage in all specific brain regions responsible for mood regulation correlates with mood disorders [36,37].…”

Section: Discussionmentioning

confidence: 99%

N-Acetylcysteine Protects against the Anxiogenic Response to Cisplatin in Rats

et al. 2019

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Since cisplatin therapy is usually accompanied with numerous toxicities, including neurotoxicity, that involve tissue oxidative damage, the aim of this study was to evaluate the possible protective effect of N-acetylcysteine (NAC) on the anxiogenic response to cisplatin (CIS). Thirty-two male Wistar albino rats divided into four groups (control, cisplatin, NAC, and CIS + NAC). All treatments were delivered intraperitoneally. On day one, the control and cisplatin groups received saline while the NAC and CIS + NAC groups were administered with NAC (500 mg/kg). On the fifth day, the control group received saline while the CIS group was treated with cisplatin (7.5 mg/kg), the NAC group again received NAC (500 mg/kg), and the CIS + NAC group was simultaneously treated with cisplatin and NAC (7.5 and 500 mg/kg, respectively). Behavioral testing, performed on the tenth day in the open field (OF) and elevated plus maze (EPM) tests, revealed the anxiogenic effect of cisplatin that was significantly attenuated by NAC. The hippocampal sections evaluation showed increased oxidative stress (increased lipid peroxidation and decline in antioxidant enzymes activity) and proapoptotic action (predominantly by diminished antiapoptotic gene expression) following a single dose of cisplatin. NAC supplementation along with cisplatin administration reversed the prooxidative and proapoptotic effects of cisplatin. In conclusion, the results obtained in this study confirmed that antioxidant supplementation with NAC may attenuate the cisplatin-induced anxiety. The mechanism of anxiolytic effect achieved by NAC may include the decline in oxidative damage that down regulates increased apoptosis and reverses the anxiogenic action of cisplatin.

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“…Furthermore, rats infused in the PFC with an adeno-associated virus carrying a dominant negative form of SGK1 (S422A) caused helplessness-and anhedoniclike behaviors (Licznerski et al, 2015). A very recent study on adult rats, subjected to acute stress during adolescence, revealed no significant changes in SGK1 mRNA levels in anxiety-related brain regions such as central amygdala, medial amygdala, ventral hippocampus, and paraventricular nucleus (Lovelock and Deak, 2019). Despite the high comorbidity between MDD and PTSD, the modulation of SGK1 expression could be mediated by distinct signaling pathways.…”

Section: Sgk1 and L-hpa Axis Activitymentioning

confidence: 99%

The Emerging Role of SGK1 (Serum- and Glucocorticoid-Regulated Kinase 1) in Major Depressive Disorder: Hypothesis and Mechanisms

et al. 2020

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Major depressive disorder (MDD) is a heterogeneous psychiatric disease characterized by persistent low mood, diminished interests, and impaired cognitive and social functions. The multifactorial etiology of MDD is still largely unknown because of the complex genetic and environmental interactions involved. Therefore, no established mechanism can explain all the aspects of the disease. In this light, an extensive research about the pathophysiology of MDD has been carried out. Several pathogenic hypotheses, such as monoamines deficiency and neurobiological alterations in the stress-responsive system, including the hypothalamic-pituitary-adrenal (HPA) axis and the immune system, have been proposed for MDD. Over time, remarkable studies, mainly on preclinical rodent models, linked the serum-and glucocorticoid-regulated kinase 1 (SGK1) to the main features of MDD. SGK1 is a serine/threonine kinase belonging to the AGK Kinase family. SGK1 is ubiquitously expressed, which plays a pivotal role in the hormonal regulation of several ion channels, carriers, pumps, and transcription factors or regulators. SGK1 expression is modulated by cell stress and hormones, including gluco-and mineralocorticoids. Compelling evidence suggests that increased SGK1 expression or function is related to the pathogenic stress hypothesis of major depression. Therefore, the first part of the present review highlights the putative role of SGK1 as a critical mediator in the dysregulation of the HPA axis, observed under chronic stress conditions, and its controversial role in the neuroinflammation as well. The second part depicts the negative regulation exerted by SGK1 in the expression of both the brain-derived neurotrophic factor (BDNF) and the vascular endothelial growth factor (VEGF), resulting in an anti-neurogenic activity. Finally, the review focuses on the antidepressant-like effects of anti-oxidative nutraceuticals in several preclinical model of depression, resulting from the restoration of the physiological expression and/or activity of SGK1, which leads to an increase in neurogenesis. In summary, the purpose of this review is a systematic analysis of literature depicting SGK1 as molecular junction of the complex mechanisms underlying the MDD in an effort to suggest the kinase as a potential biomarker and strategic target in modern molecular antidepressant therapy.

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Acute stress imposed during adolescence yields heightened anxiety in Sprague Dawley rats that persists into adulthood: Sex differences and potential involvement of the Medial Amygdala

Cited by 28 publications

References 72 publications

Age- and sex- dependent changes in locus coeruleus physiology and anxiety-like behavior in response to acute stress

Age- and sex- dependent changes in locus coeruleus physiology and anxiety-like behavior in response to acute stress

N-Acetylcysteine Protects against the Anxiogenic Response to Cisplatin in Rats

The Emerging Role of SGK1 (Serum- and Glucocorticoid-Regulated Kinase 1) in Major Depressive Disorder: Hypothesis and Mechanisms

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