The domestic chick as an animal model of autism spectrum disorder: building adaptive social perceptions through prenatally formed predispositions

Matsushima, Toshiya; Izumi, Takeshi; Vallortigara, Giorgio

doi:10.3389/fnins.2024.1279947

Cited by 4 publications

(1 citation statement)

References 201 publications

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“…Rodent models of ASD developed by prenatal VPA exposure confirm behavioral abnormalities like those observed in ASD. More recently, a VPA model of ASD using domestic chicks has been proposed [128].…”

Section: Vpa and Asdmentioning

confidence: 99%

Roles of Epigenetics and Glial Cells in Drug-Induced Autism Spectrum Disorder

Csoka,

El Kouhen,

Bennani

et al. 2024

Biomolecules

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Autism spectrum disorder (ASD) is a neurodevelopmental disorder characterized by severe deficits in social communication and interaction, repetitive movements, abnormal focusing on objects, or activity that can significantly affect the quality of life of the afflicted. Neuronal and glial cells have been implicated. It has a genetic component but can also be triggered by environmental factors or drugs. For example, prenatal exposure to valproic acid or acetaminophen, or ingestion of propionic acid, can increase the risk of ASD. Recently, epigenetic influences on ASD have come to the forefront of investigations on the etiology, prevention, and treatment of this disorder. Epigenetics refers to DNA modifications that alter gene expression without making any changes to the DNA sequence. Although an increasing number of pharmaceuticals and environmental chemicals are being implicated in the etiology of ASD, here, we specifically focus on the molecular influences of the abovementioned chemicals on epigenetic alterations in neuronal and glial cells and their potential connection to ASD. We conclude that a better understanding of these phenomena can lead to more effective interventions in ASD.

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Section: Vpa and Asdmentioning

confidence: 99%

Roles of Epigenetics and Glial Cells in Drug-Induced Autism Spectrum Disorder

Csoka,

El Kouhen,

Bennani

et al. 2024

Biomolecules

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Embryonic exposure to valproic acid and neonicotinoid deteriorates the developmental GABA switch and impairs long-term potentiation in the local circuit of intermediate medial mesopallium of chick telencephalon

Matsushima,

Toji,

Wada

et al. 2024

Preprint

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Embryonic exposure to valproic acid (VPA) and imidacloprid (IMI, a neonicotinoid insecticide) impairs filial imprinting in hatchlings, and the deteriorating effects of VPA are mitigated by post-hatch injection of bumetanide, a blocker of the chloride intruder NKCC1. Here, we report that these exposures depolarized the reversal potential of local GABAergic transmission in the neurons of the intermediate medial mesopallium (IMM), the pallial region critical for imprinting. Furthermore, exposure increased field excitatory post-synaptic potentials in pre-tetanus recordings (fEPSPs) and impaired long-term potentiation by low-frequency tetanic stimulation (LTP). Bath-applied bumetanide rescued the impaired LTP in the VPA slices, whereas VU0463271, a blocker of the chloride extruder KCC2, suppressed LTP in the control slices, suggesting that hyperpolarizing GABA action is necessary for the potentiation of excitatory synaptic transmission. However, the transcriptional profiles of IMM slices did not support the expected increase in the NKCC1/KCC2 ratio, suggesting a potential modification of post-transcriptional processes. Instead, exposure to both VPA and IMI downregulated several transcriptional regulators (FOS, NR4A1, and NR4A2) and upregulated the RNA component of signal recognition particles (RN7SL1). As a limited set of response genes were shared, VPA and IMI could cause common neuronal malfunctions via distinct molecular cascades.

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Face processing in animal models: implications for autism spectrum disorder

Sgadò,

Pross,

Lamanna

et al. 2024

Front. Neurosci.

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Processing facial features is crucial to identify social partners (prey, predators, or conspecifics) and recognize and accurately interpret emotional expressions. Numerous studies in both human and non-human primates provided evidence promoting the notion of inherent mechanisms for detecting facial features. These mechanisms support a representation of faces independent of prior experiences and are vital for subsequent development in social and language domains. Moreover, deficits in processing faces are a reliable biomarker of autism spectrum disorder, appearing early and correlating with symptom severity. Face processing, however, is not only a prerogative of humans: other species also show remarkable face detection abilities. In this review, we present an overview of the current literature on face detection in vertebrate models that could be relevant to the study of autism.

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The domestic chick as an animal model of autism spectrum disorder: building adaptive social perceptions through prenatally formed predispositions

Cited by 4 publications

References 201 publications

Roles of Epigenetics and Glial Cells in Drug-Induced Autism Spectrum Disorder

Roles of Epigenetics and Glial Cells in Drug-Induced Autism Spectrum Disorder

Embryonic exposure to valproic acid and neonicotinoid deteriorates the developmental GABA switch and impairs long-term potentiation in the local circuit of intermediate medial mesopallium of chick telencephalon

Face processing in animal models: implications for autism spectrum disorder

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