ArticleThe international journal of neuropsychopharmacology2014
Chronic desipramine prevents acute stress-induced reorganization of medial prefrontal cortex architecture by blocking glutamate vesicle accumulation and excitatory synapse increase.
Article in The international journal of neuropsychopharmacology, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.
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17 citing papers in PubMed, 33 citations in OpenAlex.
- Challenges and rewards of in vivo synaptic density imaging, and its application to the study of depression.Neuropsychopharmacology : official publication of the American College of Neuropsychopharmacology · 2024Review
- Stress-related cellular pathophysiology as a crosstalk risk factor for neurocognitive and psychiatric disorders.BMC neuroscience · 2023Review
- Changes at glutamate tripartite synapses in the prefrontal cortex of a new animal model of resilience/vulnerability to acute stress.Translational psychiatry · 2023Article
- Involvement of miR-135a-5p Downregulation in Acute and Chronic Stress Response in the Prefrontal Cortex of Rats.International journal of molecular sciences · 2023Article
- The stressed synapse 2.0: pathophysiological mechanisms in stress-related neuropsychiatric disorders.Nature reviews. Neuroscience · 2022Review
- Mechanisms of synaptic transmission dysregulation in the prefrontal cortex: pathophysiological implications.Molecular psychiatry · 2022Review
- Morphological Responses of Excitatory Prelimbic and Orbitofrontal Cortical Neurons to Excess Corticosterone in Adolescence and Acute Stress in Adulthood.Frontiers in neuroanatomy · 2020Article
- What Acute Stress Protocols Can Tell Us About PTSD and Stress-Related Neuropsychiatric Disorders.Frontiers in pharmacology · 2018Review
- Reduced Synapse and Axon Numbers in the Prefrontal Cortex of Rats Subjected to a Chronic Stress Model for Depression.Frontiers in cellular neuroscience · 2018Article
- Molecular and Epigenetic Mechanisms for the Complex Effects of Stress on Synaptic Physiology and Cognitive Functions.The international journal of neuropsychopharmacology · 2017Review
- Acute stress is not acute: sustained enhancement of glutamate release after acute stress involves readily releasable pool size and synapsin I activation.Molecular psychiatry · 2017Article
- Modulation of the activity ofNeuropsychiatric disease and treatment · 2017Review
- Long-Term Citalopram Treatment Alters the Stress Responses of the Cortical Dopamine and Noradrenaline Systems: the Role of Cortical 5-HT1A Receptors.The international journal of neuropsychopharmacology · 2016Article
- Dendritic Spines in Depression: What We Learned from Animal Models.Neural plasticity · 2016Review
- Stress Response and Perinatal Reprogramming: Unraveling (Mal)adaptive Strategies.Neural plasticity · 2016Review
- Acute Footshock Stress Induces Time-Dependent Modifications of AMPA/NMDA Protein Expression and AMPA Phosphorylation.Neural plasticity · 2016Article
- Functional and structural remodeling of glutamate synapses in prefrontal and frontal cortex induced by behavioral stress.Frontiers in psychiatry · 2015Review
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Authors and funding
7 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundAlthough a clear negative influence of chronic exposure to stressful experiences has been repeatedly demonstrated, the outcome of acute stress on key brain regions has only just started to be elucidated. Although it has been proposed that acute stress may produce enhancement of brain plasticity and that antidepressants may prevent such changes, we still lack ultrastructural evidence that acute stress-induced changes in neurotransmitter physiology are coupled with structural synaptic modifications.
methodsRats were pretreated chronically (14 days) with desipramine (10mg/kg) and then subjected to acute foot-shock stress. By means of serial section electron microscopy, the structural remodeling of medial prefrontal cortex glutamate synapses was assessed soon after acute stressor cessation and stress hormone levels were measured.
resultsFoot-shock stress induced a remarkable increase in the number of docked vesicles and small excitatory synapses, partially and strongly prevented by desipramine pretreatment, respectively. Acute stress-induced corticosterone elevation was not affected by drug treatment.
conclusionsSince desipramine pretreatment prevented the stress-induced structural plasticity but not the hormone level increase, we hypothesize that the preventing action of desipramine is located on pathways downstream of this process and/or other pathways. Moreover, because enhancement of glutamate system remodeling may contribute to overexcitation dysfunctions, this aspect could represent a crucial component in the pathophysiology of stress-related disorders.
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