Effects of Long-Term Adrenalectomy on Apoptosis and Neuroprotection in the Rat Hippocampus

Andrés, Sergio; Cárdenas, Sergio; Parra, C.; Bravo, Javier A.; Greiner, Monika; Rojas, Paulina S.; Morales, Paola; Lara, Hernán E.; Fiedler, Jenny L.

doi:10.1385/endo:29:2:299

Cited by 14 publications

(12 citation statements)

References 48 publications

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“…The trophic influence of adrenal steroids on granular neurone survival appears to be related to the regulation of intrinsic apoptotic signalling pathways . Evidence indicates that adrenalectomy increases mRNA expression of the proapoptotic gene bax and promotes the activation of cysteine protease caspase‐9 . This enzyme promotes the proteolytic cleavage of executor caspases that subsequently destroy several proteins, culminating in apoptosis.…”

Section: Gcs Stress and Neuroplasticitymentioning

confidence: 99%

Novel Aspects of Glucocorticoid Actions

Uchôa

Aguilera

Herman

et al. 2014

J Neuroendocrinology

125

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Normal hypothalamic-pituitary-adrenal (HPA) axis activity leading to rhythmic and episodic release of adrenal glucocorticoids is essential for body homeostasis and survival during stress. Acting through specific intracellular receptors in the brain and periphery, glucocorticoids regulate behavior, metabolic, cardiovascular, immune, and neuroendocrine activities. In contrast to chronic elevated levels, circadian and acute stress-induced increases in glucocorticoids are necessary for hippocampal neuronal survival and memory acquisition and consolidation, through inhibiting apoptosis, facilitating glutamate transmission and inducing immediate early genes and spine formation. In addition to its metabolic actions leading to increasing energy availability, glucocorticoids have profound effects on feeding behavior, mainly through modulation of orexigenic and anorixegenic neuropeptides. Evidence is also emerging that in addition to the recognized immune suppressive actions of glucocorticoids by counteracting adrenergic proinflammatory actions, circadian elevations have priming effects in the immune system, potentiating acute defensive responses. In addition, negative feedback by glucocorticoids involves multiple mechanisms leading to limiting HPA axis activation and preventing deleterious effects of excessive glucocorticoid production. Adequate glucocorticoid secretion to meet body demands is tightly regulated by a complex neural circuitry controlling hypothalamic corticotrophin releasing hormone (CRH) and vasopressin secretion, the main regulators of pituitary adrenocorticotrophic hormone (ACTH). Rapid feedback mechanisms, likely involving non-genomic actions of glucocorticoids, mediate immediate inhibition of hypothalamic CRH and ACTH secretion, while intermediate and delayed mechanisms mediated by genomic actions involve modulation of limbic circuitry and peripheral metabolic messengers. Consistent with their key adaptive roles, HPA axis components are evolutionarily conserved, being present in the earliest vertebrates. Understanding these basic mechanisms may lead to novel approaches for the development of diagnostic and therapeutic tools for disorders related to stress and alterations of glucocorticoid secretion.

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Section: Gcs Stress and Neuroplasticitymentioning

confidence: 99%

Novel Aspects of Glucocorticoid Actions

Uchôa

Aguilera

Herman

et al. 2014

J Neuroendocrinology

125

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“…Whole hippocampal homogenates were prepared as described earlier (Greiner et al, 2001;Andres et al, 2006). Seventy-five micrograms of protein from each homogenate were resolved by electrophoresis on 12% SDS-polyacrylamide gels, and electrotransferred onto 0.22-mm nitrocellulose membranes.…”

Section: Immunoblot Analysismentioning

confidence: 99%

Desipramine prevents stress-induced changes in depressive-like behavior and hippocampal markers of neuroprotection

Bravo

Dı́az-Véliz²,

Mora³

et al. 2009

Behavioural Pharmacology

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Extracellular signal-regulated kinases (ERKs) are widely implicated in multiple physiological processes. Although ERK1/2 has been proposed as a common mediator of antidepressant action in naive rodents, it remains to be determined whether the ERK1/2 pathway plays a role in depressive disorder. Here, we investigated whether chronic restraint stress (14 days) and antidepressant treatment [desipramine (DMI), 10 mg/kg intraperitoneally] induce changes in animal behavior and hippocampal levels of phospho-ERK1/2 and its substrate phospho-cAMP response element-binding protein (CREB). The results indicated that stress-induced depressive-like behaviors were correlated with an increase in P-ERK1/2 and P-CREB in the hippocampus evaluated by immunoblot analysis. As an indication of CREB activity, we evaluated changes in mRNA levels of its target genes. Brain-derived neurotrophic factor (BDNF) mRNA was reduced by stress, an effect prevented by DMI only in the CA3 area of hippocampus. Bcl-2 mRNA was reduced in all hippocampal regions by stress, an effect independent of DMI treatment. However, immunoblot from hippocampal extracts revealed that stress increased BCL-2 levels, an effect prevented by chronic DMI. These results suggest that ERKs and BDNF may be altered in depressive disorder, modifications that are sensitive to DMI action. In contrast, the stress-induced increase in BCL-2 may correspond to a neuroprotective response.

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“…Therefore, high neural level of GCs blunt negative feedback, which leads to a further increase in GCs and more damage to hippocampus as predicted by the GCs cascade hypothesis (reviewed in Sapolsky et al, 1986;De Kloet et al, 1998;Nichols et al, 2001). In support of this hypothesis, many studies, including recent ours, have approved that GCs play a negative role in brain function in general, and more precisely, in learning and memory process (Cameron and McKay, 1999;Montaron et al, 1999;Hibberd et al, 2000;Miller and O'Callaghan, 2005;Andrés et al, 2006;He et al, 2008).…”

Section: Introductionmentioning

confidence: 88%

Effect of corticosterone on developing hippocampus: Short‐term and long‐term outcomes

et al. 2008

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Many documents implicate that corticosterone plays a negative role in brain function, especially in learning and memory. However, less evidence confirms its direct actions on hippocampal development. In the work reported here, pro treatment, minimum corticosterone administration in infant mice, and con treatment, corticosterone deprivation by adrenalectomy, were used to examine the effects imposed by corticosterone on the structure and function of developing hippocampus. Our study shows that adrenalectomy induces decrease of plasma corticosterone levels and results in the impairment of learning performance and the degenerative changes not in CA regions of hippocampus but in dentate gyrus. Noteworthily, this damage effect is severer in 5-week-old mice than that in 10-week-old mice. In addition, the short-term effect of minimum corticosterone administration may accelerate the development of dentate gyrus of 10-day-old mice. Moreover, minimum corticosterone administration during infancy contributed to the learning performance and the structural integrity of hippocampal CA regions in different developing stages, while this phenomenon was not observed in dentate gyrus. In conclusion, corticosterone is necessary for the development of dentate gyrus, especially in relatively young individuals, and administration with minimum corticosterone in infancy has a long-term positive influence on the hippocampal structure and function in different developing stages.

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Effects of Long-Term Adrenalectomy on Apoptosis and Neuroprotection in the Rat Hippocampus

Cited by 14 publications

References 48 publications

Novel Aspects of Glucocorticoid Actions

Novel Aspects of Glucocorticoid Actions

Desipramine prevents stress-induced changes in depressive-like behavior and hippocampal markers of neuroprotection

Effect of corticosterone on developing hippocampus: Short‐term and long‐term outcomes

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