The expression of plasticity-related genes in an acute model of stress is modulated by chronic desipramine in a time-dependent manner within medial prefrontal cortex

Nava, Nicoletta; Treccani, Giulia; Müller, Heidi Kaastrup; Popoli, Maurizio; Wegener, Gregers; Elfving, Betina

doi:10.1016/j.euroneuro.2016.11.010

Cited by 14 publications

(11 citation statements)

References 36 publications

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“…Interference of adhesion molecules that anchor glutamate receptors at the synaptic surface abolishes the acute stress-induced enhancement of GluR2 membrane trafficking and memory facilitation ( Conboy and Sandi, 2010 ). In addition, acute footshock stress induces both rapid and sustained alterations of the expression of key genes involved in synaptic plasticity and spine structure, such as Homer , Shank , Spinophilin , Rac1 , and downstream target genes Limk1 , Cofilin1 , and Rock1 ( Nava et al, 2017b ). Overall, acute stress facilitates postsynaptic signaling molecules or adhesion/cytoskeleton networks that support the synaptic trafficking of glutamate receptors.…”

Section: Introductionmentioning

confidence: 99%

Molecular and Epigenetic Mechanisms for the Complex Effects of Stress on Synaptic Physiology and Cognitive Functions

Yuen

Wei

Zhang³

2017

International Journal of Neuropsychopharmacology

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Evidence over the past decades has found that stress, particularly through the corticosterone stress hormones, produces complex changes in glutamatergic signaling in prefrontal cortex, which leads to the alteration of cognitive processes medicated by this brain region. Interestingly, the effects of stress on glutamatergic transmission appear to be “U-shaped,” depending upon the duration and severity of the stressor. These biphasic effects of acute vs chronic stress represent the adaptive vs maladaptive responses to stressful stimuli. Animal studies suggest that the stress-induced modulation of excitatory synaptic transmission involves changes in presynaptic glutamate release, postsynaptic glutamate receptor membrane trafficking and degradation, spine structure and cytoskeleton network, and epigenetic control of gene expression. This review will discuss current findings on the key molecules involved in the stress-induced regulation of prefrontal cortex synaptic physiology and prefrontal cortex-mediated functions. Understanding the molecular and epigenetic mechanisms that underlie the complex effects of stress will help to develop novel strategies to cope with stress-related mental disorders.

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Section: Introductionmentioning

confidence: 99%

Molecular and Epigenetic Mechanisms for the Complex Effects of Stress on Synaptic Physiology and Cognitive Functions

Yuen

Wei

Zhang³

2017

International Journal of Neuropsychopharmacology

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“…Some TCAs also display a significant affinity for specific subtypes of serotonin receptors, which may contribute to their antidepressant effects [ 105 , 109 ]. Subsequently, in line with the evolution of MDD pathogenic hypotheses, various evidence, obtained both in experimental animal models and in humans, has shown that some TCAs are capable of regulating the expression of different genes, including neurotrophic factors, such as BDNF, and genes encoding for key components of the synapses, crucial for synaptic plasticity, inducing functional and structural changes in the CNS [ 105 , 110 , 111 ]. As well as for the majority of classical ADs, for TCAs evidence was also provided for a modulation of glutamatergic transmission; for example, chronic treatment with imipramine was shown to reduce glutamate-based excitatory neurotransmission [ 112 ], whereas chronic treatment with desipramine was shown to significantly reduce the release of glutamate from synaptosomes (isolated synaptic terminals prepared from neurons for experimental purposes) [ 113 ] and to block the release of glutamate induced by stress in rats [ 114 ].…”

Section: Molecular Mechanisms Of Pharmacological Treatments For MDmentioning

confidence: 99%

Blues in the Brain and Beyond: Molecular Bases of Major Depressive Disorder and Relative Pharmacological and Non-Pharmacological Treatments

Maffioletti

Minelli

Tardito

et al. 2020

Genes

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Despite the extensive research conducted in recent decades, the molecular mechanisms underlying major depressive disorder (MDD) and relative evidence-based treatments remain unclear. Various hypotheses have been successively proposed, involving different biological systems. This narrative review aims to critically illustrate the main pathogenic hypotheses of MDD, ranging from the historical ones based on the monoaminergic and neurotrophic theories, through the subsequent neurodevelopmental, glutamatergic, GABAergic, inflammatory/immune and endocrine explanations, until the most recent evidence postulating a role for fatty acids and the gut microbiota. Moreover, the molecular effects of established both pharmacological and non-pharmacological approaches for MDD are also reviewed. Overall, the existing literature indicates that the molecular mechanisms described in the context of these different hypotheses, rather than representing alternative ones to each other, are likely to contribute together, often with reciprocal interactions, to the development of MDD and to the effectiveness of treatments, and points at the need for further research efforts in this field.

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“…The results were in accordance with their hypothesis that DMI activates this projection, which may thus play a part in the regulation of emotion and antidepressant effects of the antidepressants [ 74 ]. DMI exerts significant short-term and long-term effects on the mRNA levels of genes involved in spine plasticity within mPFC [ 141 ].…”

Section: Effects Of Typical Antidepressant Drugs On Pfc Synaptogenesimentioning

confidence: 99%

Targeting the Neuronal Activity of Prefrontal Cortex: New Directions for the Therapy of Depression

Zhou

Bao

Liú

et al. 2020

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Depression is one of the prevalent psychiatric illnesses with a comprehensive performance such as low self-esteem, lack of motivation, anhedonia, poor appetite, low energy, and uncomfortableness without a specific cause. So far, the cause of depression is not very clear, but it is certain that many aspects of biological psychological and social environment are involved in the pathogenesis of depression. Recently, the prefrontal cortex (PFC) has been indicated to be a pivotal brain region in the pathogenesis of depression. And increasing evidence showed that the abnormal activity of the PFC neurons is linked with depressive symptoms. Unveiling the molecular and cellular, as well as the circuit properties of the PFC neurons will help to find out how abnormalities in PFC neuronal activity are associated with depressive disorders. In addition, concerning many antidepressant drugs, in this review, we concluded the effect of several antidepressants on PFC neuronal activity to better understand its association with depression.

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The expression of plasticity-related genes in an acute model of stress is modulated by chronic desipramine in a time-dependent manner within medial prefrontal cortex

Cited by 14 publications

References 36 publications

Molecular and Epigenetic Mechanisms for the Complex Effects of Stress on Synaptic Physiology and Cognitive Functions

Molecular and Epigenetic Mechanisms for the Complex Effects of Stress on Synaptic Physiology and Cognitive Functions

Blues in the Brain and Beyond: Molecular Bases of Major Depressive Disorder and Relative Pharmacological and Non-Pharmacological Treatments

Targeting the Neuronal Activity of Prefrontal Cortex: New Directions for the Therapy of Depression

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