Fluoxetine ameliorates adult hippocampal injury in rats after early maternal separation. A biochemical, histological and immunohistochemical study

Arafat, Eetmad A.; Shabaan, Dalia A.

doi:10.1080/10520295.2019.1637021

Cited by 5 publications

(3 citation statements)

References 60 publications

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“…Although the number of the astrocytes was lower in the MSG group than in the FLX/MSG one, there was no statistical difference between both groups, as kainic acid-induced gliosis in rodents was suppressed by FLX administration because of its anti-inflammatory effect [ 38 ]. FLX prevents the infiltration of macrophages and inhibits the messenger ribonucleic acid (mRNA) expression of inflammatory mediators after an injury resulting in a decrease in activation of microglia and astrocyte in hippocampal regions [ 12 , 39 ].…”

Section: ⧉ Discussionmentioning

confidence: 99%

“…FLX treatment in rodents promotes neuroplasticity, especially in the hippocampus, by inducing neuronal proliferation, increasing survival of the newly formed cell, accelerating neuronal maturation, and increasing both dendritic arborization and length in the dentate gyrus (DG) [ 11 ]. Nevertheless, it has a wide range of common side effects, such as headache, agitation, anorexia, insomnia, sexual dysfunctions, bleeding, and hyperprolactinemia [ 12 ].…”

Section: ⧉ Introductionmentioning

confidence: 99%

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Protective effects of Rosemary extract and/or Fluoxetine on Monosodium Glutamate-induced hippocampal neurotoxicity in rat

Atef

Fattah

Mahmoud³

et al. 2021

Rom J Morphol Embryol

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The use of Monosodium Glutamate (MSG) as a food flavor enhancer is increasing worldwide despite its neurotoxic effects. Fluoxetine (FLX) and Rosemary extract (RE) are known to have beneficial neuroprotective properties. Rats were divided into five groups: control group; MSG group, rats received 2 g/kg/day intraperitoneal (i.p.) injections of MSG for seven days; RE/MSG group, rats received 50 mg/kg/day of oral RE for 28 days starting prior to MSG; FLX/MSG group, rats received 10 mg/kg/day of oral FLX for 28 days beginning before MSG; and RE/FLX/MSG group, received combined treatments as mentioned above. Rats underwent the Barnes maze test, in addition to histopathological, immunohistochemical, morphometric and ultrastructural evaluations for their hippocampi. MSG increased the number of errors and escaped latency in the Barnes maze test that was significantly minimized in the three treatment groups. The MSG group exhibited pyramidal cell (PC) degeneration, shrunken glial cells and massive vascular dilatation that were improved with RE and/or FLX treatment. The number of glial fibrillary acidic protein (GFAP)-immunopositive cells were increased, and the number of PCs was decreased in the MSG group, while these values were significantly reversed with the three treatment groups with the most significant improvement at RE/FLX/MSG one. Ultrastructurally, PCs were shrunken with degenerated nuclei, dilated endoplasmic reticulum, swollen mitochondria, and vacuolations in the MSG group that were improved with RE and/or FLX. In conclusion, the combined RE and FLX treatment can ameliorate the toxic effect of MSG on rat hippocampus probably through its antioxidant and anti-inflammatory effects.

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Section: ⧉ Discussionmentioning

confidence: 99%

Section: ⧉ Introductionmentioning

confidence: 99%

Protective effects of Rosemary extract and/or Fluoxetine on Monosodium Glutamate-induced hippocampal neurotoxicity in rat

Atef

Fattah

Mahmoud³

et al. 2021

Rom J Morphol Embryol

View full text Add to dashboard Cite

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“…showed that fluoxetine treatment (18 mg/kg) reduced ROS production in skeletal muscle [277], and Garabadu et al showed that paroxetine (10 mg/kg) treatment rescued stressinduced oxidative damage in the brain [278]. Interestingly, publications by Arafat and Shabaan [279] and Shu et al [280] both showed that fluoxetine treatment rescued ultrastructural changes to mitochondria in the hippocampus resulting from stress-based paradigms, suggesting that the effect of SSRIs on mitochondrial health and function is broad.…”

Section: Animal Studiesmentioning

confidence: 99%

Mitochondrial abundance and function in the serotonin transporter knockout model: a sexually dimorphic association

Thorne¹

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Neuropsychiatric and neurodevelopmental disorders such as major depressive disorder (MDD) and autism spectrum disorder (ASD) are complex conditions that can be attributed to a variety of genetic and environmental factors. Altered serotonergic signalling and mitochondrial dysfunction are two factors that are strongly implicated in the pathophysiology of these conditions. Furthermore, there is also a growing body of evidence to suggest a connection between these two factors, as studies have shown that signalling through specific serotonin (5-HT) receptors stimulates mitochondrial biogenesis. The serotonin transporter (SERT) is important in these disorders as it functions to regulate synaptic 5-HT, therefore having a significant influence over serotonergic signalling. Human allelic variants of the serotonin transporter-linked polymorphic region (5-HTTLPR) are associated with reduced SERT expression and increased susceptibility for developing neuropsychiatric disorders. This genetic association is modelled with the heterozygous variant (HET) of the SERT knockout rat, which shows a reduction in SERT expression similar to that of low-expressing human 5 HTTLPR variants. This thesis explores mitochondrial biogenesis and respiratory chain activity in the brains of rats with reduced SERT expression, demonstrating that mitochondrial mRNA and protein expression and respiratory chain activity are altered in the brain in a sexually dimorphic manner. While expression and activity are increased in the frontal cortex of male HETs relative to their wild-type counterparts, the opposite trend is seen in females, suggesting that the response to reduced SERT expression differs substantially between males and females. The sex differences identified throughout this thesis are particularly significant as neuropsychiatric and neurodevelopmental disorders differ between males and females in many aspects, with depressive and anxiety disorders being more common in women, and ASD more common in boys. Sex differences are also evident across symptoms, risk factors, and treatment efficacy. Despite this, consideration of sex as a biological variable in preclinical studies of these disorders is poor, and studies continue to restrict their cohorts to male animals. The findings presented in this thesis suggest that the relationship between serotonergic signalling and mitochondrial function may be important for both understanding the pathophysiology of neuropsychiatric and neurodevelopmental disorders, and for inspiring the development of new effective treatments. The prevalence of these disorders is increasing worldwide, significantly impacting the quality of life and life expectancy of those affected, while also generating a substantial economic cost for society. As such, there is a critical need for new research exploring the multitude of genetic and environmental factors associated with these disorders. However, successfully pursuing this line of research is contingent on continued efforts to address sex as a biological variable.

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Maternal separation increases pain sensitivity by reducing the activity of serotonergic neurons in the dorsal raphe nucleus and noradrenergic neurons in locus coeruleus

Vilela

Vieira

Kalil-Cutti

et al. 2021

Neuroscience Letters

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Fluoxetine ameliorates adult hippocampal injury in rats after early maternal separation. A biochemical, histological and immunohistochemical study

Cited by 5 publications

References 60 publications

Protective effects of Rosemary extract and/or Fluoxetine on Monosodium Glutamate-induced hippocampal neurotoxicity in rat

Protective effects of Rosemary extract and/or Fluoxetine on Monosodium Glutamate-induced hippocampal neurotoxicity in rat

Mitochondrial abundance and function in the serotonin transporter knockout model: a sexually dimorphic association

Maternal separation increases pain sensitivity by reducing the activity of serotonergic neurons in the dorsal raphe nucleus and noradrenergic neurons in locus coeruleus

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