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Synaptic Stress and Pathogenesis of Neuropsychiatric Disorders pp 33–52Cite as

Synaptic Stress, Changes in Glutamate Transmission and Circuitry, and Psychopathology

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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.

While the predominant effect of acute stress is an enhancement of synaptic transmission, repeated exposure to stress brings about atrophy and remodeling of dendrites, loss of synapses, and reduction of synaptic transmission (except perhaps in amygdala). Understanding the mechanisms and effectors involved in this biphasic action of stress is essential to the development of new diagnostic and therapeutic means for stress-related disorders. Select brain-derived neurotrophic factor (BDNF) transcripts and their translation at synapses could be among these key effectors.

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Authors and Affiliations

  1. Laboratory of Neuropsychopharmacology and Functional Neurogenomics—Dipartimento di Scienze Farmacologiche e Biomolecolari and CEND, Università di Milano, 20133, Milano, Italy

    Laura Musazzi, Giulia Treccani & Maurizio Popoli

  2. Laboratory of Cell Physiology—Dipartimento di Scienze Farmacologiche e Biomolecolari, Università di Milano, 20133, Milano, Italy

    Carla Perego

  3. Stereology and Electron Microscopy Laboratory, Centre for Stochastic Geometry and Advanced Bioimaging, Aarhus University Hospital, 8000, Aarhus C, Denmark

    Nicoletta Nava & Jens R Nyengaard

Authors
  1. Laura Musazzi
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  2. Giulia Treccani
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  3. Carla Perego
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  4. Nicoletta Nava
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  5. Jens R Nyengaard
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  6. Maurizio Popoli
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Correspondence to Maurizio Popoli .

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Editors and Affiliations

  1. Department of Pharmacological and Biomolecular Sciences, University of Milano, Milano, Italy

    Maurizio Popoli

  2. Department of Psychology, University of South Florida, Tampa, Florida, USA

    David Diamond

  3. Psychiatry Depression Research Program, Yale School of Medicine, New Haven, Connecticut, USA

    Gerard Sanacora

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Musazzi, L., Treccani, G., Perego, C., Nava, N., Nyengaard, J., Popoli, M. (2014). Synaptic Stress, Changes in Glutamate Transmission and Circuitry, and Psychopathology. In: Popoli, M., Diamond, D., Sanacora, G. (eds) Synaptic Stress and Pathogenesis of Neuropsychiatric Disorders. Springer, New York, NY. https://doi.org/10.1007/978-1-4939-1056-4_3

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