Antidepressant activities of escitalopram and blonanserin on prenatal and adolescent combined stress-induced depression model: Possible role of neurotrophic mechanism change in serum and nucleus accumbens

Furuse, Kengo; Ukai, Wataru; Hashimoto, Eri; Hashiguchi, Hanako; Kigawa, Yoshiyasu; Ishii, Takao; Tayama, Masaya; Deriha, Kenta; Shiraishi, Masaki; Kawanishi, Chiaki

doi:10.1016/j.jad.2019.01.007

Cited by 15 publications

(9 citation statements)

References 65 publications

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“…As an example, treatment with olanzapine during adolescence tends to counteract some of the alterations produced by early maternal deprivation (MD), including the reduction in body weight, corticosterone responses, and the reduced expression of the cannabinoid CB1 receptor [ 126 ]. In addition, the AAPD blonanserin can ameliorate social deficits, assessed in the social interaction test, produced following a combination of prenatal and adolescent stressors [ 127 ]. Treatments with AAPDs are also able to normalize cognitive performances in adolescent rats: for instance, risperidone can revert some of the cognitive deficits that follow adolescent social isolation [ 128 ], while quetiapine and olanzapine normalize the deficits observed in pre-pulse inhibition [ 129 ].…”

Section: Atypical Antipsychotic Drugs and Stress-related Mechanismmentioning

confidence: 99%

Anti-stress Properties of Atypical Antipsychotics

Sanson

Riva

2020

Pharmaceuticals

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Stress exposure represents a major environmental risk factor for schizophrenia and other psychiatric disorders, as it plays a pivotal role in the etiology as well as in the manifestation of disease symptomatology. It may be inferred that pharmacological treatments must be able to modulate the behavioral, functional, and molecular alterations produced by stress exposure to achieve significant clinical outcomes. This review aims at examining existing clinical and preclinical evidence that supports the ability of atypical antipsychotic drugs (AAPDs) to modulate stress-related alterations. Indeed, while the pharmacodynamic differences between AAPDs have been extensively characterized, less is known on their ability to regulate downstream mechanisms that are critical for functional recovery and patient stabilization. We will discuss stress-related mechanisms, spanning from neuroendocrine function to inflammation and neuronal plasticity, which are relevant for the manifestation of schizophrenic symptomatology, and we will discuss if and how AAPDs may interfere with such mechanisms. Considering the impact of stress in everyday life, we believe that a better understanding of the potential effects of AAPDs on stress-related mechanisms may provide novel and important insights for improving therapeutic strategies aimed at promoting coping mechanisms and enhancing the quality of life of patients affected by psychiatric disorders.

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Section: Atypical Antipsychotic Drugs and Stress-related Mechanismmentioning

confidence: 99%

Anti-stress Properties of Atypical Antipsychotics

Sanson

Riva

2020

Pharmaceuticals

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“…Several antidepressants were shown to increase serum/plasma BDNF levels in MDD persons compared to pre-treatment levels, including agomelatine ( 41 ), duloxetine ( 27 ), escitalopram ( 27 , 43 , 44 ), fluoxetine ( 41 , 45 ), milnacipran ( 36 ), paroxetine ( 36 , 38 , 44 ), sertraline ( 44 ), venlafaxine ( 44 ), and vortioxetine ( 17 , 46 ). However, recent works have shown that not all antidepressants increase BDNF concentrations ( 47 ), and antidepressant-induced rise in BDNF concentrations are more substantial in responders compared to non-responders ( 48 – 51 ). Moreover, it was demonstrated that high-intensity exercises ( 52 ), electroconvulsive therapy ( 15 , 18 , 19 , 53 ), and deep brain stimulation ( 54 ) also increase BDNF levels.…”

Section: Discussionmentioning

confidence: 99%

The Diagnostic Value of the Combination of Serum Brain-Derived Neurotrophic Factor and Insulin-Like Growth Factor-1 for Major Depressive Disorder Diagnosis and Treatment Efficacy

Troyan

2020

Front. Psychiatry

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Background: Last decades of psychiatric investigations have been marked by a search for biological markers that can clarify etiology and pathogenesis, confirm the diagnosis, screen individuals at risk, define the severity, and predict the course of mental disorders. In our study, we aimed to evaluate if BDNF and IGF-1 serum concentrations separately and in combination might be used as biomarkers for major depressive disorder (MDD) diagnosis and treatment efficacy and to evaluate the relationships among those proteins and clinical parameters of MDD. Methods: Forty-one MDD patients (according to DSM-5) and 32 healthy controls (HC) were included in this study. BDNF and IGF-1 serum concentrations, psychopathological (MADRS, CGI) and neuropsychological parameters (PDQ-5, RAVLT, TMT-B, DSST), functioning according to Sheehan Disability Scale were analyzed in all subjects at admission and 30 MDD patients after 8 weeks of vortioxetine treatment. Correlational analyses were performed to explore relationships between BDNF and IGF-1 and clinical characteristics. AUC-ROCs were calculated to determine if the value of serum BDNF and IGF-1 levels could serve for MDD diagnosis. Results: MDD patients had significantly lower serum BDNF (727.6 ± 87.9 pg/ml vs. 853.0 ± 93.9 pg/ml) and higher serum IGF-1 levels (289.15 ± 125.3 ng/ml vs. 170.2 ± 58.2 ng/ ml) compared to HC. Significant correlations were obtained between BDNF levels and MDD status, depressive episode (DE) severity, precipitating factors, executive functions disruption (TMT-B, RAVLT immediate recall scores) and all subdomains of functioning. As for IGF-1, correlations were found between IGF-1 level and MDD status, DE severity, number and duration of DE, parameters of subjective and objective cognitive functioning (PDQ-5, RAVLT, TMT-B, DSST scores), and all subdomains of functioning. The associations between IGF-1 concentrations and cognitive tests' performance were stronger than those of BDNF. Separately both BDNF and IGF-1 demonstrated good

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“…In our previous study, we have shown that pre-gestational maternal stress may affect hippocampus at the time of birth by increasing the resting membrane potential, suppressing depolarization-activated action potential firing, and increasing the spontaneous activity of hippocampal cells from newborn rat offspring (28), but pre-gestational stress induced changes in different subregions of hippocampus are not thoroughly known. However, antidepressant treatment may facilitate the challenged neurogenesis by, upregulating the hippocampal concentration of glucocorticoid receptors, which help to attenuate the hyperactivity of the HPA axis and inducing morphological changes in the neuronal network (11,27,29). Some studies suggest that developmental fluoxetine (SSRI) exposure of prenatally stressed male and female offspring reversed the effect of stress on the number of immature neurons in the dentate gyrus (DG), with effects being more prevalent in adult male offspring (30,31).…”

Section: Introductionmentioning

confidence: 99%

“…Theoretical work, as well as anatomical, physiological, and behavioral experiments support the idea that the DG-CA3 system performs the pattern separation and the pattern completion of the inputs to the hippocampus, operations needed for memory encoding and retrieval (26). Purpose of the hippocampus happens to be severely affected by early life stress, predisposing the individual to an impaired reactivity when exposed to adverse environmental stimuli (27). In our previous study, we have shown that pre-gestational maternal stress may affect hippocampus at the time of birth by increasing the resting membrane potential, suppressing depolarization-activated action potential firing, and increasing the spontaneous activity of hippocampal cells from newborn rat offspring (28), but pre-gestational stress induced changes in different subregions of hippocampus are not thoroughly known.…”

Section: Introductionmentioning

confidence: 99%

Sex- and age- dependent effect of pre-gestational chronic stress and mirtazapine treatment on neurobehavioral development of offspring

Viñas-Noguera

Csatlósová

Šimončičová

et al. 2021

Preprint

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Hormonal fluctuations, such as the perinatal period, may increase susceptibility of women to depression, which in turn exert a negative impact on child’s neurodevelopment, becoming a risk factor in development of neuropsychiatric disorders. Moreover, the use of antidepressants during this critical period presents a serious health concern for both the mother and the child, due to the consequences of treatment in terms of the reliability and safety for the proper neurodevelopment of the organism being not well known. Atypical antidepressants, such as mirtazapine, that targets both serotonergic and noradrenergic systems in the central nervous system (CNS), represent a novel focus of research due to its unique pharmacological profile. The aim of this work was to study the effects of maternal depression and/or perinatal antidepressant mirtazapine treatment on the neurobehavioral development of the offspring. Pre-gestationally chronically stressed or non-stressed Wistar rat dams were treated with either mirtazapine (10 mg/kg/day) or vehicle during pregnancy and lactation followed by analysis of offspring’s behavior at juvenile and adolescent age. We found mirtazapine induced alterations of nursing behavior. In offspring, pregestational stress (PS) had an anxiogenic effect on adolescent males and increased their active behavior in forced swim test. Interaction between pregestational stress and mirtazapine treatment variously induced anxiolytic changes of juvenile and adolescent females and impairment of spatial memory in adolescent females as well. Hippocampal density of synaptophysin, pre-synaptic protein marker, was decreased mainly by mirtazapine treatment. In conclusion, our results show mirtazapine induced alterations in maternal behavior and several sex- and age-dependent changes in neurobehavioral development of offspring caused by both prenatal mirtazapine treatment and/or chronic pregestational stress.

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Antidepressant activities of escitalopram and blonanserin on prenatal and adolescent combined stress-induced depression model: Possible role of neurotrophic mechanism change in serum and nucleus accumbens

Cited by 15 publications

References 65 publications

Anti-stress Properties of Atypical Antipsychotics

Anti-stress Properties of Atypical Antipsychotics

The Diagnostic Value of the Combination of Serum Brain-Derived Neurotrophic Factor and Insulin-Like Growth Factor-1 for Major Depressive Disorder Diagnosis and Treatment Efficacy

Sex- and age- dependent effect of pre-gestational chronic stress and mirtazapine treatment on neurobehavioral development of offspring

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