Environmental enrichment ameliorates chronic immobilisation stress-induced spatial learning deficits and restores the expression of BDNF, VEGF, GFAP and glucocorticoid receptors

Shilpa, BM; Bhagya, V.; Harish, G.; Bharath, MM Srinivas; Rao, B.S. Shankaranarayana

doi:10.1016/j.pnpbp.2017.02.025

Cited by 94 publications

(84 citation statements)

References 109 publications

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“…This was correlated with upregulation of GFAP, which, in turn, led to increased basolateral amygdala volumes, which also contributed to anxiety-like phenotype in stressed animals. These animals also exhibited defective hippocampal-dependent learning and memory in a partially baited radial arm maze task, with reduced GFAP and GRs in the hippocampus and PFC [21].…”

Section: Amygdalamentioning

confidence: 95%

“…Animals subjected to CUS show decreased GFAP expression with depressive-like behavior [19]. The reduction of the glial population [11] forms a very vital factor that may contribute to the reduction of volumes [20] due to elevation in GCs by lowering the GFAP levels [20,21]. Western blotting and immunohistological studies have shown that the decrease in the expression of GFAP and GFAP-expressing glial cells possibly due to excitotoxicity in the different areas of the hippocampus [22].…”

Section: Hippocampusmentioning

confidence: 99%

“…Chronic stress induces secretion of GCs, which are known to cause a significant redistribution of apical dendrites and alters spine density [26]. In addition, chronic stress causes significant reduction of GC receptors (GRs), which take part in metabolism and the regulation of stress and neurotrophic factors like brainderived neurotrophic factor (BDNF) and its receptor required for plasticity [21]. Apart from BDNF, other neurotrophic factors such as nerve growth factor, glial cell-derived growth factor, vascular endothelial growth factor (VEGF), neurotrophin-3 (NT), and NT-4/5 are responsible for maintaining a favourable microenvironment for the nourishment of neurons and for balancing the glial ratio [27].…”

Section: Hippocampusmentioning

confidence: 99%

“…Studies have shown the development of anxiety-like behaviour after chronic stress exposure [34]. This was signified with retraction of the spines in the medial nucleus of the amygdala facilitated by molecular changes like overexpression of serine protease tissue-plasminogen activator in the amygdala, and BDNF [21]. Furthermore, transgenic overexpression of the neurotrophin BDNF has also revealed an initiator effect on anxiety-like behaviour due to increased spinogenesis in the basolateral amygdala.…”

Section: Amygdalamentioning

confidence: 99%

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Glial pathology in neuropsychiatric disorders: a brief review

Mayegowda

Thomas

2019

Journal of Basic and Clinical Physiology and Pharmacology

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Neurons have been considered the major functional entities of the nervous system that are responsible for most of the functions even though glial cells largely outnumber them. However, recent reports have proved that glial cells do not function just like glue in the nervous system but also substantially affect neuronal function and activities, and are significantly involved in the underlying pathobiology of various psychiatric disorders. Dysfunctional astrocytes and degeneration of glial cells are postulated to be critical factors contributing to the aggravation of depressive-like symptoms in humans, which was proved using animal models. Alteration in glial cell function predominantly targets three main brain regions – the prefrontal cortex, limbic areas including the hippocampus, and the amygdala, which have been extensively studied by various researchers across the globe. These studies have postulated that failure in adopting to the changing neurophysiology due to stress will lead to regressive plasticity in the hippocampus and prefrontal cortex, but to progressive plasticity in the amygdala. In this present review, an effort has been made to understand the different alterations in chronic stress models in correlation with clinical conditions, providing evidence on the defective maintenance of glial function and its potential role in the precipitation of neuropsychiatric disorders.

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Section: Amygdalamentioning

confidence: 95%

Section: Hippocampusmentioning

confidence: 99%

Section: Hippocampusmentioning

confidence: 99%

Section: Amygdalamentioning

confidence: 99%

See 2 more Smart Citations

Glial pathology in neuropsychiatric disorders: a brief review

Mayegowda

Thomas

2019

Journal of Basic and Clinical Physiology and Pharmacology

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“…Furthermore, glial cells can regulate the structure and function of synapses [30], the synapse formation, the stable maintenance of synaptic connections, and the process of synapse elimination through some adhesion molecules and cytokines [31]. In addition, glial cells play an important role in neuronal differentiation and loop formation, and most of these effects are mediated by GDNF [32]. The growth of astrocytes is closely related to the function of neurons.…”

Section: Effects Of Gc/gr/glucocorticoid Receptor Interacting Proteinmentioning

confidence: 99%

The brain development of infants with intrauterine growth restriction: role of glucocorticoids

Ding

Cui

2019

Hormone Molecular Biology and Clinical Investigation

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Brain injury is a serious complication of intrauterine growth restriction (IUGR), but the exact mechanism remains unclear. While glucocorticoids (GCs) play an important role in intrauterine growth and development, GCs also have a damaging effect on microvascular endothelial cells. Moreover, intrauterine adverse environments lead to fetal growth restriction and the hypothalamus-pituitary-adrenal (HPA) axis resetting. In addition, chronic stress can cause a decrease in the number and volume of astrocytes in the hippocampus and glial cells play an important role in neuronal differentiation. Therefore, it is speculated that the effect of GCs on cerebral neurovascular units under chronic intrauterine stimulation is an important mechanism leading to brain injury in infants with growth restrictions.

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Enrichment Protocol for Rat Models

et al. 2021

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An environmental enrichment (EE) cage consisting of a broad living area and various stimulators triggers social, cognitive, and physical activities. EE has been utilized in a wide range of neurological and non-neurological studies. However, the details of the environmental enrichment protocol were not well described in these studies. This has resulted in uncertainty and inconsistency in methodology, which may thus fail to replicate environmental enrichment effects, influencing the study outcome. Here we describe the basic guidelines and present an easy-to-follow protocol for environmental enrichment in rat models.

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Environmental enrichment ameliorates chronic immobilisation stress-induced spatial learning deficits and restores the expression of BDNF, VEGF, GFAP and glucocorticoid receptors

Cited by 94 publications

References 109 publications

Glial pathology in neuropsychiatric disorders: a brief review

Glial pathology in neuropsychiatric disorders: a brief review

The brain development of infants with intrauterine growth restriction: role of glucocorticoids

Enrichment Protocol for Rat Models

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