Acute or Chronic? A Stressful Question

Musazzi, Laura; Tornese, Paolo; Sala, Nathalie; Popoli, Maurizio

doi:10.1016/j.tins.2017.07.002

Cited by 81 publications

(83 citation statements)

References 56 publications

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“…Here, using real-time FRET to measure spatiotemporal JNK activation by corticosterone, we find that spine-head JNK is activated within 10 min of treatment, followed by a second phase of activation after 20 min. This could be a consequence of increased glutamate efflux which occurs following corticosterone (Musazzi et al, 2010(Musazzi et al, , 2017Sanacora et al, 2012;Treccani et al, 2014), as we show that the NMDA receptor activates spine-head JNK within this timeframe. The downstream effect of corticosterone-activated JNK is the rapid removal of SEP-GluR2 from synapses which occurs by 5 min, followed by spine retraction commencing 10 min after corticosterone.…”

Section: Discussionsupporting

confidence: 58%

Optogenetic Control of Spine-Head JNK Reveals a Role in Dendritic Spine Regression

Hollós

John

Lehtonen

et al. 2020

eNeuro

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In this study, we use an optogenetic inhibitor of c-Jun NH 2-terminal kinase (JNK) in dendritic spine subcompartments of rat hippocampal neurons. We show that JNK inhibition exerts rapid (within seconds) reorganization of actin in the spine-head. Using real-time Förster resonance energy transfer (FRET) to measure JNK activity, we find that either excitotoxic insult (NMDA) or endocrine stress (corticosterone), activate spine-head JNK causing internalization of AMPARs and spine retraction. Both events are prevented upon optogenetic inhibition of JNK, and rescued by JNK inhibition even 2 h after insult. Moreover, we identify that the fast-acting anti-depressant ketamine reduces JNK activity in hippocampal neurons suggesting that JNK inhibition may be a downstream mediator of its anti-depressant effect. In conclusion, we show that JNK activation plays a role in triggering spine elimination by NMDA or corticosterone stress, whereas inhibition of JNK facilitates regrowth of spines even in the continued presence of glucocorticoid. This identifies that JNK acts locally in the spine-head to promote AMPAR internalization and spine shrinkage following stress, and reveals a protective function for JNK inhibition in preventing spine regression.

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Section: Discussionsupporting

confidence: 58%

Optogenetic Control of Spine-Head JNK Reveals a Role in Dendritic Spine Regression

Hollós

John

Lehtonen

et al. 2020

eNeuro

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“…In this sense, the Italian research group of Maurizio Popoli has established quite recently that not only chronic stress, but also acute stress of sufficient intensity may potentiate excitotoxicity in some brain regions [32,33]. Here it is pertinent to remember that hippocampus normally inhibits HPA axis, and its atrophy provoked by stress or GC excess can result in vicious cycle of higher GC and consequently, glutamate impact (a so called "death spiral") [31], perhaps even on various brain regions.…”

Section: Effects Of Exogenous Glucocorticoids On Central Nervous Systemmentioning

confidence: 99%

The Role of Stress and Glucocorticoids in Pathogeny of Age-Related Neuropsychiatric Disorders

Ivanovitch¹

2018

J Geriatr Med Gerontol

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An overview and commentary are presented on the role of stress and glucocorticoids in the pathogeny of age-related psychiatric and neurologic disorders, first of all depressive illness and Alzheimer's disease. The connections of these disorders with senescence-induced changes in bioregulation of hypothamo-pituitary-adrenal axis activity are discussed, focusing attention on biphasic glucocorticoid effects, gender differences, adverse effects of exogenous corticosteroids and the importance of stress and glucocorticoid effects on developing brain, as related to programming/imprinting and embedding phenomena. In addition, the interactions of neuropsychiatric disorders with diabetes mellitus and other chronic diseases, as well as of glucocorticoids with proinflammatory cytokines are briefly considered in relation to postnatal ontogeny and aging.

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“…Most neuropsychiatric disorders, such as depression, mood, and anxiety disorders, are stress related disorders [11]. The stress response is a physiological reaction to environmental changes that can be positive and pro-adaptive (in most cases) or negative and maladaptive [12] [13].…”

mentioning

confidence: 99%

Mood Disorders: Protection of the Hyper-Excited Brain, or a Risk Factor?

Nanobashvili¹,

Bilanishvili²,

Barbakadze³

et al. 2019

JBBS

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Emotional disturbances such as anxiety, fear, depression and aggression are often experienced by patients with temporal lobe epilepsy. These psychiatric symptoms may occur during or just after (postictal) a seizure; however, in some patients, they occur interictally (i.e. between seizures) and may profoundly change the individual's personality. Aside from confirming that a significant proportion of temporal lobe epileptics do suffer from interictal abnormal emotionality, there has been little progress to date in identifying the fundamental nature of these disturbances. There is a lack of evidences regarding the influence of activation of emotiogenic structures and emotional behavior on development of seizures. Kindling is a commonly used animal model for study of interictal emotionality and the effects of kindling and human epilepsy on emotional behavior are the primary focus of investigators and not vice versa. Respectively, the interrelation between emotional and seizure reactions was studied in Wistar albino rats. In our study we tried to elucidate: can emotional behavior evoked by stimulation of the emotiogenic zones of the hypothalamus or of induction of acute pain stress modify manifestations of generalized seizures within the period where a "full" epileptic syndrom has been stable formed earlier? Our leading hypothesis is as follow: the emotional disturbances can be considered as the emergence of instinctive behavior with an adaptive significance of defense and as a by-product of the inhibitory processes that build up to protect against the future occurrence of seizures.

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Acute or Chronic? A Stressful Question

Cited by 81 publications

References 56 publications

Optogenetic Control of Spine-Head JNK Reveals a Role in Dendritic Spine Regression

Optogenetic Control of Spine-Head JNK Reveals a Role in Dendritic Spine Regression

The Role of Stress and Glucocorticoids in Pathogeny of Age-Related Neuropsychiatric Disorders

Mood Disorders: Protection of the Hyper-Excited Brain, or a Risk Factor?

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