Jens Randel Nyengaard

Synaptic stress, changes in glutamate transmission and circuitry, and psychopathology

Research output: Contribution to book/anthology/report/proceedingBook chapterResearchpeer-review

Standard

Synaptic stress, changes in glutamate transmission and circuitry, and psychopathology. / Musazzi, Laura; Treccani, Giulia; Perego, Carla; Nava, Nicoletta; Nyengaard, Jens R.; Popoli, Maurizio.

Synaptic Stress and Pathogenesis of Neuropsychiatric Disorders. Springer New York, 2014. p. 33-52.

Research output: Contribution to book/anthology/report/proceedingBook chapterResearchpeer-review

Harvard

Musazzi, L, Treccani, G, Perego, C, Nava, N, Nyengaard, JR & Popoli, M 2014, Synaptic stress, changes in glutamate transmission and circuitry, and psychopathology. in Synaptic Stress and Pathogenesis of Neuropsychiatric Disorders. Springer New York, pp. 33-52. https://doi.org/10.1007/978-1-4939-1056-4_3

APA

Musazzi, L., Treccani, G., Perego, C., Nava, N., Nyengaard, J. R., & Popoli, M. (2014). Synaptic stress, changes in glutamate transmission and circuitry, and psychopathology. In Synaptic Stress and Pathogenesis of Neuropsychiatric Disorders (pp. 33-52). Springer New York. https://doi.org/10.1007/978-1-4939-1056-4_3

CBE

Musazzi L, Treccani G, Perego C, Nava N, Nyengaard JR, Popoli M. 2014. Synaptic stress, changes in glutamate transmission and circuitry, and psychopathology. In Synaptic Stress and Pathogenesis of Neuropsychiatric Disorders. Springer New York. pp. 33-52. https://doi.org/10.1007/978-1-4939-1056-4_3

MLA

Musazzi, Laura et al. "Synaptic stress, changes in glutamate transmission and circuitry, and psychopathology". Synaptic Stress and Pathogenesis of Neuropsychiatric Disorders. Springer New York. 2014, 33-52. https://doi.org/10.1007/978-1-4939-1056-4_3

Vancouver

Musazzi L, Treccani G, Perego C, Nava N, Nyengaard JR, Popoli M. Synaptic stress, changes in glutamate transmission and circuitry, and psychopathology. In Synaptic Stress and Pathogenesis of Neuropsychiatric Disorders. Springer New York. 2014. p. 33-52 https://doi.org/10.1007/978-1-4939-1056-4_3

Author

Musazzi, Laura ; Treccani, Giulia ; Perego, Carla ; Nava, Nicoletta ; Nyengaard, Jens R. ; Popoli, Maurizio. / Synaptic stress, changes in glutamate transmission and circuitry, and psychopathology. Synaptic Stress and Pathogenesis of Neuropsychiatric Disorders. Springer New York, 2014. pp. 33-52

Bibtex

@inbook{5f26060eb1b74e2ab6998d96bb44e721,
title = "Synaptic stress, changes in glutamate transmission and circuitry, and psychopathology",
abstract = "Dysfunction of the glutamate system is increasingly considered a core feature of stress-dependent neuropsychiatric disorders. Clinical neuroimaging studies have shown consistent volumetric changes in limbic and cortical areas, while preclinical studies with stress protocols in rodents found dendritic remodeling and reduction of synapses in the same areas, suggesting that destabilization of glutamate release/transmission, in turn induced by stress and glucocorticoids, is crucial for cognitive function and neural architecture. We found that acute stress rapidly enhances depolarization-evoked glutamate release/transmission in prefrontal and frontal cortex (PFC/FC), an effect mediated by stimulation of synaptic corticosterone receptors. Corticosterone rapidly increases the readily releasable pool of glutamate vesicles, through activation of synaptic receptor-mediated nongenomic mechanisms in PFC/FC. Moreover, we have shown that chronic antidepressants are able to prevent the enhancement of glutamate release induced by acute stressors in these areas.",
author = "Laura Musazzi and Giulia Treccani and Carla Perego and Nicoletta Nava and Nyengaard, {Jens R.} and Maurizio Popoli",
year = "2014",
month = jan,
day = "1",
doi = "10.1007/978-1-4939-1056-4_3",
language = "English",
isbn = "9781493910557",
pages = "33--52",
booktitle = "Synaptic Stress and Pathogenesis of Neuropsychiatric Disorders",
publisher = "Springer New York",
address = "United States",

}

RIS

TY - CHAP

T1 - Synaptic stress, changes in glutamate transmission and circuitry, and psychopathology

AU - Musazzi, Laura

AU - Treccani, Giulia

AU - Perego, Carla

AU - Nava, Nicoletta

AU - Nyengaard, Jens R.

AU - Popoli, Maurizio

PY - 2014/1/1

Y1 - 2014/1/1

N2 - Dysfunction of the glutamate system is increasingly considered a core feature of stress-dependent neuropsychiatric disorders. Clinical neuroimaging studies have shown consistent volumetric changes in limbic and cortical areas, while preclinical studies with stress protocols in rodents found dendritic remodeling and reduction of synapses in the same areas, suggesting that destabilization of glutamate release/transmission, in turn induced by stress and glucocorticoids, is crucial for cognitive function and neural architecture. We found that acute stress rapidly enhances depolarization-evoked glutamate release/transmission in prefrontal and frontal cortex (PFC/FC), an effect mediated by stimulation of synaptic corticosterone receptors. Corticosterone rapidly increases the readily releasable pool of glutamate vesicles, through activation of synaptic receptor-mediated nongenomic mechanisms in PFC/FC. Moreover, we have shown that chronic antidepressants are able to prevent the enhancement of glutamate release induced by acute stressors in these areas.

AB - Dysfunction of the glutamate system is increasingly considered a core feature of stress-dependent neuropsychiatric disorders. Clinical neuroimaging studies have shown consistent volumetric changes in limbic and cortical areas, while preclinical studies with stress protocols in rodents found dendritic remodeling and reduction of synapses in the same areas, suggesting that destabilization of glutamate release/transmission, in turn induced by stress and glucocorticoids, is crucial for cognitive function and neural architecture. We found that acute stress rapidly enhances depolarization-evoked glutamate release/transmission in prefrontal and frontal cortex (PFC/FC), an effect mediated by stimulation of synaptic corticosterone receptors. Corticosterone rapidly increases the readily releasable pool of glutamate vesicles, through activation of synaptic receptor-mediated nongenomic mechanisms in PFC/FC. Moreover, we have shown that chronic antidepressants are able to prevent the enhancement of glutamate release induced by acute stressors in these areas.

UR - http://www.scopus.com/inward/record.url?scp=84930655298&partnerID=8YFLogxK

U2 - 10.1007/978-1-4939-1056-4_3

DO - 10.1007/978-1-4939-1056-4_3

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SN - 9781493910557

SP - 33

EP - 52

BT - Synaptic Stress and Pathogenesis of Neuropsychiatric Disorders

PB - Springer New York

ER -