scholarly journals Disrupted copper homeostasis: Pathogenic factor in autism spectrum disorder and side effect of valproic acid

2021 ◽  
Vol 29-30 ◽  
pp. 100087
Author(s):  
Stephen I. Deutsch ◽  
David R. Spiegel ◽  
Jessica A. Burket
Keyword(s):  
Autism Spectrum Disorder ◽  
Valproic Acid ◽  
Side Effect ◽  
Copper Homeostasis ◽  
Autism Spectrum ◽  
Spectrum Disorder ◽  
Pathogenic Factor

scholarly journals Preliminary Results Regarding Sleep in a Zebrafish Model of Autism Spectrum Disorder

2021 ◽  
Vol 11 (5) ◽  
pp. 556
Author(s):  
Madalina Andreea Robea ◽  
Alin Ciobica ◽  
Alexandrina-Stefania Curpan ◽  
Gabriel Plavan ◽  
Stefan Strungaru ◽  
...  
Keyword(s):  
Autism Spectrum Disorder ◽  
Valproic Acid ◽  
Social Behavior ◽  
Antiepileptic Drug ◽  
Alternative Model ◽  
Neurological Diseases ◽  
Autism Spectrum ◽  
Spectrum Disorder ◽  
Zebrafish Model ◽  
Developmental Defects

Autism spectrum disorder (ASD) is one of the most salient developmental neurological diseases and remarkable similarities have been found between humans and model animals of ASD. A common method of inducing ASD in zebrafish is by administrating valproic acid (VPA), which is an antiepileptic drug that is strongly linked with developmental defects in children. In the present study we replicated and extended the findings of VPA on social behavior in zebrafish by adding several sleep observations. Juvenile zebrafish manifested hyperactivity and an increase in ASD-like social behaviors but, interestingly, only exhibited minimal alterations in sleep. Our study confirmed that VPA can generate specific ASD symptoms, indicating that the zebrafish is an alternative model in this field of research.

scholarly journals Valproic Acid in Autism Spectrum Disorder: From an Environmental Risk Factor to a Reliable Animal Model

10.5772/54824 ◽  
2013 ◽  
Author(s):  
Carmem Gottfried ◽  
Victorio Bambini-Junior ◽  
Diego Baronio ◽  
Geancarlo Zanatta ◽  
Roberta Bristot ◽  
...  
Keyword(s):  
Autism Spectrum Disorder ◽  
Valproic Acid ◽  
Animal Model ◽  
Risk Factor ◽  
Environmental Risk ◽  
Autism Spectrum ◽  
Spectrum Disorder ◽  
Environmental Risk Factor

scholarly journals What We Have Learned about Autism Spectrum Disorder from Valproic Acid

2013 ◽  
Vol 2013 ◽  
pp. 1-8 ◽  
Author(s):  
Taylor Chomiak ◽  
Nathanael Turner ◽  
Bin Hu
Keyword(s):  
Autism Spectrum Disorder ◽  
Valproic Acid ◽  
Animal Model ◽  
Neurodevelopmental Disorders ◽  
Significant Risk ◽  
Autism Spectrum ◽  
Research Literature ◽  
Spectrum Disorder ◽  
Epidemiological Evidence ◽  
Growing Body

Two recent epidemiological investigations in children exposed to valproic acid (VPA) treatment in utero have reported a significant risk associated with neurodevelopmental disorders and autism spectrum disorder (ASD) in particular. Parallel to this work, there is a growing body of animal research literature using VPA as an animal model of ASD. In this focused review we first summarize the epidemiological evidence linking VPA to ASD and then comment on two important neurobiological findings linking VPA to ASD clinicopathology, namely, accelerated or early brain overgrowth and hyperexcitable networks. Improving our understanding of how the drug VPA can alter early development of neurological systems will ultimately improve our understanding of ASD.

Neurobiological substrates underlying corpus callosum hypoconnectivity and brain metabolic patterns in the valproic acid rat model of autism spectrum disorder

2021 ◽  
Author(s):  
Nonthué Alejandra Uccelli ◽  
Martín Gabriel Codagnone ◽  
Marianela Evelyn Traetta ◽  
Nadia Levanovich ◽  
María Victoria Rosato Siri ◽  
...  
Keyword(s):  
Autism Spectrum Disorder ◽  
Valproic Acid ◽  
Corpus Callosum ◽  
Rat Model ◽  
Autism Spectrum ◽  
Spectrum Disorder ◽  
Neurobiological Substrates

scholarly journals Long-Lasting Changes in Glial Cells Isolated From Rats Subjected to the Valproic Acid Model of Autism Spectrum Disorder

2021 ◽  
Vol 12 ◽  
Author(s):  
Marianela Evelyn Traetta ◽  
Nonthué Alejandra Uccelli ◽  
Sandra Cristina Zárate ◽  
Dante Gómez Cuautle ◽  
Alberto Javier Ramos ◽  
...  
Keyword(s):  
Autism Spectrum Disorder ◽  
Valproic Acid ◽  
Cortical Neurons ◽  
Primary Cultures ◽  
Autism Spectrum ◽  
Spectrum Disorder ◽  
Saline Control ◽  
Synaptic Changes

Synaptic alterations concomitant with neuroinflammation have been described in patients and experimental models of autism spectrum disorder (ASD). However, the role of microglia and astroglia in relation to synaptic changes is poorly understood. Male Wistar rats prenatally exposed to valproic acid (VPA, 450 mg/kg, i.p.) or saline (control) at embryonic day 10.5 were used to study synapses, microglia, and astroglia in the prefrontal cortex (PFC) at postnatal days 3 and 35 (PND3 and PND35). Primary cultures of cortical neurons, microglia, and astroglia isolated from control and VPA animals were used to study each cell type individually, neuron-microglia and microglia-astroglia crosstalk. In the PFC of VPA rats, synaptic changes characterized by an increase in the number of excitatory synapses were evidenced at PND3 and persisted until PND35. At PND3, microglia and astroglia from VPA animals were morphologically similar to those of age-matched controls, whereas at PND35, reactive microgliosis and astrogliosis were observed in the PFC of VPA animals. Cortical neurons isolated from VPA rats mimicked in vitro the synaptic pattern seen in vivo. Cortical microglia and astroglia isolated from VPA animals exhibited reactive morphology, increased pro-inflammatory cytokines, and a compromised miRNA processing machinery. Microglia from VPA animals also showed resistance to a phagocytic challenge. In the presence of neurons from VPA animals, microglia isolated from VPA rats revealed a non-reactive morphology and promoted neurite outgrowth, while microglia from control animals displayed a reactive profile and promoted dendritic retraction. In microglia-astroglia co-cultures, microglia from VPA animals displayed a reactive profile and exacerbated astrocyte reactivity. Our study indicates that cortical microglia from VPA animals are insensitive or adapted to neuronal cues expressed by neurons from VPA animals. Further, long-term in vivo microgliosis could be the result of altered microglia-astroglia crosstalk in VPA animals. Thus, our study highlights cortical microglia-astroglia communication as a new mechanism implicated in neuroinflammation in ASD; consequently, we propose that this crosstalk is a potential target for interventions in this disorder.

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