Stress-Induced Functional Alterations in Amygdala: Implications for Neuropsychiatric Diseases

Zhang, Xin; Ge, Tongtong; Yin, Guanghao; Cui, Ranji; Zhao, Guangyao; Yang, Wei

doi:10.3389/fnins.2018.00367

Cited by 83 publications

(54 citation statements)

References 102 publications

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“…At 7/8 DPI or 28/29 DPI, injured and sham rats underwent OFT between 07:00 and 09:00, immediately followed by in vivo amperometric recordings by the handling investigator. Time of day and timing between OFT and recordings were held constant throughout all experiments to account for any potential influence of diurnal corticosterone levels and lasting molecular and structural influences from behavior (OFT)-induced stress responses (Zhang et al, 2018). For the remainder of the manuscript, DPI for the amperometric and behavioral outcome measures at 7/8 and 28/29 DPI will be abbreviated as 7 DPI and 28 DPI.…”

Section: Animalsmentioning

confidence: 99%

Experimental Traumatic Brain Injury Induces Chronic Glutamatergic Dysfunction in Amygdala Circuitry Known to Regulate Anxiety-Like Behavior

et al. 2020

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Up to 50% of traumatic brain injury (TBI) survivors demonstrate persisting and late-onset anxiety disorders indicative of limbic system dysregulation, yet the pathophysiology underlying the symptoms is unclear. We hypothesize that the development of TBIinduced anxiety-like behavior in an experimental model of TBI is mediated by changes in glutamate neurotransmission within the amygdala. Adult, male Sprague-Dawley rats underwent midline fluid percussion injury or sham surgery. Anxiety-like behavior was assessed at 7 and 28 days post-injury (DPI) followed by assessment of real-time glutamate neurotransmission in the basolateral amygdala (BLA) and central nucleus of the amygdala (CeA) using glutamate-selective microelectrode arrays. The expression of anxiety-like behavior at 28 DPI coincided with decreased evoked glutamate release and slower glutamate clearance in the CeA, not BLA. Numerous factors contribute to the changes in glutamate neurotransmission over time. In two additional animal cohorts, protein levels of glutamatergic transporters (Glt-1 and GLAST) and presynaptic modulators of glutamate release (mGluR2, TrkB, BDNF, and glucocorticoid receptors) were quantified using automated capillary western techniques at 28 DPI. Astrocytosis and microglial activation have been shown to drive maladaptive glutamate signaling and were histologically assessed over 28 DPI. Alterations in glutamate neurotransmission could not be explained by changes in protein levels for glutamate transporters, mGluR2 receptors, astrocytosis, and microglial activation. Presynaptic modulators, BDNF and TrkB, were significantly decreased at 28 DPI in the amygdala. Dysfunction in presynaptic regulation of glutamate neurotransmission may contribute to anxiety-related behavior and serve as a therapeutic target to improve circuit function.

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Section: Animalsmentioning

confidence: 99%

Experimental Traumatic Brain Injury Induces Chronic Glutamatergic Dysfunction in Amygdala Circuitry Known to Regulate Anxiety-Like Behavior

et al. 2020

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“…Proper balance of excitatory and inhibitory neurotransmission is crucial for preventing amygdala hyperactivity, a neurological feature often noted in patients suffering from depression and anxiety disorders (Tzanoulinou et al, 2014;Zhang et al, 2018). The complex pattern of changes in genes associated with synaptic transmission detected in our study could be affecting the balance of excitatory and inhibitory transmission within the amygdala and resulting in the behavioral abnormalities observed in PS males.…”

Section: Discussionmentioning

confidence: 61%

“…The amygdala undergoes dramatic structural and functional modifications as a result of stress (Schulkin, 2017;Zhang et al, 2018). Here, we examined amygdalar transcriptional responses following psychosocial PS.…”

Section: Discussionmentioning

confidence: 99%

Prenatal psychosocial stress-induced behavioral and neuroendocrine abnormalities are associated with sex-specific alterations in synaptic transmission and differentially modulated by maternal environment

Williams

Hoseus

et al. 2020

Preprint

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Louis.Muglia@cchmc.org, phone: (513) 803-8040, fax: (513) 803-5009 3 ABSTRACT Prenatal stress (PS) is associated with increased vulnerability to affective disorders.Transplacental glucocorticoid passage and stress-induced maternal environment alterations are recognized as potential routes of transmission that can fundamentally alter neurodevelopment.However, molecular mechanisms underlying aberrant emotional outcomes or the individual contributions intrauterine stress versus maternal environment play in shaping these mechanisms remain unknown. Here, we report anxiogenic behaviors, anhedonia, and female hypothalamic-pituitary-adrenal axis hyperactivity as a consequence of psychosocial PS in mice.Sex-specific placental responses to stress and evidence of fetal amygdala programming precede these abnormalities. In adult offspring, we observe amygdalar transcriptional changes demonstrating sex-specific dysfunction in synaptic transmission and neurotransmitter systems.We find these abnormalities are primarily driven by in-utero stress exposure. Importantly, maternal care changes postnatally reverse anxiety-related behaviors and partially rescue gene alterations associated with neurotransmission. Our data demonstrate the influence maternal environment exerts in shaping offspring emotional development despite deleterious effects of intrauterine stress.

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“…The amygdala facilitates the encoding of emotional memories by coordination with other brain areas particularly the prefrontal cortex and hippocampus. 8 The amygdala through interacting with other brain structures obviously regulates stress response and plays a key role in emotional and stress-related behavior. 9 Exposure to acute or chronic stress can induce morphological and functional changes in the amygdala and these changes play an important role in stress-induced neuropsychiatric disorders.…”

Section: Introductionmentioning

confidence: 99%

<p>Therapeutic Effects of <em>Spirulina platensis</em> Against Adolescent Stress-Induced Oxidative Stress, Brain-Derived Neurotrophic Factor Alterations and Morphological Remodeling in the Amygdala of Adult Female Rats</p>

Kor¹,

Ghanbari²,

Rashidipour³

et al. 2020

JEP

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Objective: The amygdala structural and functional abnormalities have been implicated in numerous neuropsychiatric and neurodevelopmental disorders. Given the important role of the amygdala in stress responses and the susceptibility of the females to adolescent stress, the present study investigated the beneficial effects of Spirulina platensis microalgae (SP) as a neuroprotective supplement against adolescent stress-induced oxidative stress, brainderived neurotrophic factor (BDNF) alterations, molecular and morphological remodeling in the basolateral amygdala (BLA) of adult female rats. Methods: During the adolescent period (PNDs 30-40) rats were subjected to restraint stress (2 h/day for 10 days). Then, the animals were subjected to 15 days treatment (PNDs 41-55) with SP (200 mg/kg/day) followed by biochemical (BDNF and stress oxidative markers), molecular (BDNF and its receptor tropomyosin receptor kinase B [TrkB] mRNA expression), and morphological (dendritic length and spines) assessments in the BLA. Results: The study revealed that adolescent stress decreased BDNF levels and reduced apical dendritic length and branch points of pyramidal neurons in the BLA. In addition, chronic stress significantly increased oxidative stress parameters and decreased BDNF and TrkB mRNA expression in the BLA. Treatment with SP alleviated both biochemical, molecular, and neuroanatomical deficits that induced by adolescent stress. Conclusion: Our findings provide important evidence that SP as a non-pharmacological intervention during adolescent period can protect against chronic stress-induced neuroanatomical biochemical, and molecular deficits in adulthood, and thus, reduce stress-related disorders.

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Stress-Induced Functional Alterations in Amygdala: Implications for Neuropsychiatric Diseases

Cited by 83 publications

References 102 publications

Experimental Traumatic Brain Injury Induces Chronic Glutamatergic Dysfunction in Amygdala Circuitry Known to Regulate Anxiety-Like Behavior

Experimental Traumatic Brain Injury Induces Chronic Glutamatergic Dysfunction in Amygdala Circuitry Known to Regulate Anxiety-Like Behavior

Prenatal psychosocial stress-induced behavioral and neuroendocrine abnormalities are associated with sex-specific alterations in synaptic transmission and differentially modulated by maternal environment

<p>Therapeutic Effects of <em>Spirulina platensis</em> Against Adolescent Stress-Induced Oxidative Stress, Brain-Derived Neurotrophic Factor Alterations and Morphological Remodeling in the Amygdala of Adult Female Rats</p>

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