Memantine rescues prenatal citalopram exposure-induced striatal and social abnormalities in mice

Zahra, Aqeela; Jiang, Jinxiang; Chen, Yunan; Long, Cheng

doi:10.1016/j.expneurol.2018.06.003

Cited by 19 publications

(8 citation statements)

References 68 publications

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“…At the behavioral level, fluoxetine administration in mice that began before pregnancy or from early gestation to late-gestation or delivery produced ASD-like behavioral deficits in offspring, decreased USVs in pups, disrupted social interaction, enhanced social dominance, and increased tactile hypersensitivity (135)(136)(137). Citalopram, an SSRI with particularly high specificity for blocking SERT compared with dopamine and norepinephrine transporters, also altered behavior in mouse offspring, decreased sociability, decreased social preference, decreased locomotor activity, and increased anxiety-related behavior when given during late gestation (138). In fetal brains that were exposed to fluoxetine, neurons in the prefrontal cortex exhibited a reduction of the frequency of inhibitory synaptic currents, and interneurons exhibited an increase in intrinsic and serotonininduced excitability (136).…”

Section: Ssris Serotonin Metabolism and Asd In Animal Modelsmentioning

confidence: 99%

“…Prefrontal cortex tissue from the fluoxetine-exposed brain exhibited high mRNA levels of 5-HT 2A receptor ( 136 ). Striatal extracts from mice that were prenatally exposed to citalopram expressed higher levels of NMDAR1 and CaMKIIα, which were associated with morphological changes in the striatal neurons and decreases in dendritic length, number, and branch patterns ( 138 ). Prenatal exposure to SSRIs is suggested to result in excessive 5-HT signaling and altered E/I balance.…”

Section: Prenatal Exposure To Drugsmentioning

confidence: 99%

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Influence of Prenatal Drug Exposure, Maternal Inflammation, and Parental Aging on the Development of Autism Spectrum Disorder

et al. 2022

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Autism spectrum disorder (ASD) affects reciprocal social interaction and produces abnormal repetitive, restrictive behaviors and interests. The diverse causes of ASD are divided into genetic alterations and environmental risks. The prevalence of ASD has been rising for several decades, which might be related to environmental risks as it is difficult to consider that the prevalence of genetic disorders related to ASD would increase suddenly. The latter includes (1) exposure to medications, such as valproic acid (VPA) and selective serotonin reuptake inhibitors (SSRIs) (2), maternal complications during pregnancy, including infection and hypertensive disorders of pregnancy, and (3) high parental age. Epidemiological studies have indicated a pathogenetic role of prenatal exposure to VPA and maternal inflammation in the development of ASD. VPA is considered to exert its deleterious effects on the fetal brain through several distinct mechanisms, such as alterations of γ-aminobutyric acid signaling, the inhibition of histone deacetylase, the disruption of folic acid metabolism, and the activation of mammalian target of rapamycin. Maternal inflammation that is caused by different stimuli converges on a higher load of proinflammatory cytokines in the fetal brain. Rodent models of maternal exposure to SSRIs generate ASD-like behavior in offspring, but clinical correlations with these preclinical findings are inconclusive. Hypertensive disorders of pregnancy and advanced parental age increase the risk of ASD in humans, but the mechanisms have been poorly investigated in animal models. Evidence of the mechanisms by which environmental factors are related to ASD is discussed, which may contribute to the development of preventive and therapeutic interventions for ASD.

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Section: Ssris Serotonin Metabolism and Asd In Animal Modelsmentioning

confidence: 99%

Section: Prenatal Exposure To Drugsmentioning

confidence: 99%

Influence of Prenatal Drug Exposure, Maternal Inflammation, and Parental Aging on the Development of Autism Spectrum Disorder

et al. 2022

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“…As such, GluN2B subunits predominate in the fetal brain and generally decline throughout development, whereas the expression of GluN2A subunits increases after birth and predominates over GluN2B in the cortex, hippocampus and cerebellum by postnatal days 14-21 in rats and mice [8,9,10,11,12]. Interestingly, the NMDA receptor antagonists 1-amino-3,5-dimethyladamantane hydrochloride (memantine) reduced the social interaction deficits in mice prenatally treated with citalopram [74]. These effects of memantine, however, are not so surprising given that prenatal citalopram treatment increased GluN1 expression in the striatum [74].…”

Section: Role Of the Nmda Receptors In Social Interactionmentioning

confidence: 99%

“…Interestingly, the NMDA receptor antagonists 1-amino-3,5-dimethyladamantane hydrochloride (memantine) reduced the social interaction deficits in mice prenatally treated with citalopram [74]. These effects of memantine, however, are not so surprising given that prenatal citalopram treatment increased GluN1 expression in the striatum [74]. Similarly, memantine reduced the social interaction deficits in IRSp53 knock-out mice [75] which show increased NMDA receptor function in the hippocampus [76], suggesting that deviations in NMDA receptor functioning in either direction (see also Section 2.3.)…”

Section: Role Of the Nmda Receptors In Social Interactionmentioning

confidence: 99%

The Role of the N-Methyl-D-Aspartate Receptors in Social Behavior in Rodents

Zoicas

Kornhuber

2019

IJMS

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The appropriate display of social behaviors is essential for the well-being, reproductive success and survival of an individual. Deficits in social behavior are associated with impaired N-methyl-D-aspartate (NMDA) receptor-mediated neurotransmission. In this review, we describe recent studies using genetically modified mice and pharmacological approaches which link the impaired functioning of the NMDA receptors, especially of the receptor subunits GluN1, GluN2A and GluN2B, to abnormal social behavior. This abnormal social behavior is expressed as impaired social interaction and communication, deficits in social memory, deficits in sexual and maternal behavior, as well as abnormal or heightened aggression. We also describe the positive effects of pharmacological stimulation of the NMDA receptors on these social deficits. Indeed, pharmacological stimulation of the glycine-binding site either by direct stimulation or by elevating the synaptic glycine levels represents a promising strategy for the normalization of genetically-induced, pharmacologically-induced or innate deficits in social behavior. We emphasize on the importance of future studies investigating the role of subunit-selective NMDA receptor ligands on different types of social behavior to provide a better understanding of the underlying mechanisms, which might support the development of selective tools for the optimized treatment of disorders associated with social deficits.

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“…To examine whether various parameters of stained neurons could be quantified, two parameters (total dendritic length and neural spine density) were analyzed using ImageJ (NIH, USA). Neural spine density, the number of dendrites, and dendritic intersections were analyzed by the concentric circle method reported by Sholl (Sholl, 1953 ; Zahra et al, 2018 ). The number of branches and intersections were counted up to a distance of 140 μm from the soma.…”

Section: Methodsmentioning

confidence: 99%

Optimized Golgi-Cox Staining Validated in the Hippocampus of Spared Nerve Injury Mouse Model

et al. 2020

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Memantine rescues prenatal citalopram exposure-induced striatal and social abnormalities in mice

Cited by 19 publications

References 68 publications

Influence of Prenatal Drug Exposure, Maternal Inflammation, and Parental Aging on the Development of Autism Spectrum Disorder

Influence of Prenatal Drug Exposure, Maternal Inflammation, and Parental Aging on the Development of Autism Spectrum Disorder

The Role of the N-Methyl-D-Aspartate Receptors in Social Behavior in Rodents

Optimized Golgi-Cox Staining Validated in the Hippocampus of Spared Nerve Injury Mouse Model

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