Correlation of distinct behaviors to the modified expression of cerebral Shank1,3 and BDNF in two autistic animal models

Alò, Raffaella; Olivito, Ilaria; Fazzari, Gilda; Zizza, Merylin; Vito, Anna Di; Avolio, Ennio; Mandalà, Maurizio; Bruno, Rosalinda; Barni, Tullio; Canonaco, Marcello; Facciolo, Rosa Maria

doi:10.1016/j.bbr.2021.113165

Cited by 16 publications

(7 citation statements)

References 76 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…This is in parallel with other studies using PPA treatment, which also report social impairment measured more than four weeks after the initial PPA treatment [22,[49][50][51]. PPA animals also exhibited an increased immobility time compared to the control animals (Figure 2C), which might indicate an increased anxiety-like behavior, which is a behavioral feature of ASD models [27,49]. However, validated tests of anxiety need to be performed in future studies to better assess anxiety-like behavior in this model of autism.…”

Section: Discussionsupporting

confidence: 89%

“…In addition, several clinical studies have reported significantly higher levels of BDNF in the serum of autistic individuals [26]. However, others using the subcutaneous injection of PPA in rats have reported a significant reduction in the protein levels of BDNF in the hippocampus in juvenile animals [27]. Interestingly, a study using a transgenic model of autism (Shank1 knock-out) reported an increase in Bdnf transcript levels in Shank1 knock-out animals only after an object recognition task and not at baseline, and levels were negatively correlated with object recognition memory [87].…”

Section: Discussionmentioning

confidence: 99%

“…Serum BDNF levels have been reported to be higher in autistic individuals [26]. BDNF levels in the brain of animal models of autism have shown unclear results ranging from no change, increase, or decrease [27][28][29]. Interestingly, BDNF transcript levels have been shown to be regulated by gut microbiota and short-chain fatty acids [30,31].…”

Section: Introductionmentioning

confidence: 99%

See 2 more Smart Citations

Fecal Transplant and Bifidobacterium Treatments Modulate Gut Clostridium Bacteria and Rescue Social Impairment and Hippocampal BDNF Expression in a Rodent Model of Autism

et al. 2021

View full text Add to dashboard Cite

Autism is associated with gastrointestinal dysfunction and gut microbiota dysbiosis, including an overall increase in Clostridium. Modulation of the gut microbiota is suggested to improve autistic symptoms. In this study, we explored the implementation of two different interventions that target the microbiota in a rodent model of autism and their effects on social behavior: the levels of different fecal Clostridium spp., and hippocampal transcript levels. Autism was induced in young Sprague Dawley male rats using oral gavage of propionic acid (PPA) for three days, while controls received saline. PPA-treated animals were divided to receive either saline, fecal transplant from healthy donor rats, or Bifidobacterium for 22 days, while controls continued to receive saline. We found that PPA attenuated social interaction in animals, which was rescued by the two interventions. PPA-treated animals had a significantly increased abundance of fecal C. perfringens with a concomitant decrease in Clostridium cluster IV, and exhibited high hippocampal Bdnf expression compared to controls. Fecal microbiota transplantation or Bifidobacterium treatment restored the balance of fecal Clostridium spp. and normalized the level of Bdnf expression. These findings highlight the involvement of the gut–brain axis in the etiology of autism and propose possible interventions in a preclinical model of autism.

show abstract

Section: Discussionsupporting

confidence: 89%

Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

See 1 more Smart Citation

Fecal Transplant and Bifidobacterium Treatments Modulate Gut Clostridium Bacteria and Rescue Social Impairment and Hippocampal BDNF Expression in a Rodent Model of Autism

et al. 2021

View full text Add to dashboard Cite

show abstract

“…However, the decreased sociability and social preference indices observed in VPA mice, compared to control mice, suggested an impairment of their sociability and social preference, similar to previous observations (19,20). Moreover, the results from the self-grooming, open field, and light-dark tests showed that VPA mice exhibited more anxiety-like and stereotypic behaviors than control mice, which was consistent with previous studies (19,31,34). The autistic-like behaviors of VPA mice indicated the successful establishment of the VPA-treated ASD mouse model.…”

Section: Discussionsupporting

confidence: 91%

The Alteration of Salivary Immunoglobulin A in Autism Spectrum Disorders

Gong

Qiao

et al. 2021

Front. Psychiatry

View full text Add to dashboard Cite

Objectives: Autism spectrum disorders (ASD) are neurodevelopmental disorders with changes in the gut and oral microbiota. Based on the intimate relationship between the oral microbiota and oral mucosal immunity, this study aimed to investigate changes in salivary immunoglobulin A (IgA) level in ASD and the underlying mechanism for any such changes.Methods: We recruited 36 children diagnosed with ASD and 35 normally developing children and measured their salivary IgA content using enzyme-linked immunosorbent assay (ELISA). The valproate (VPA) -treated ASD mouse model was established by prenatal exposure to valproate and mouse salivary IgA content was also quantified by ELISA. The submandibular glands of VPA and control mice were isolated and analyzed using qRT-PCR, immunofluorescence staining, and flow cytometry. ASD-related Streptococci were co-incubated with the human salivary gland (HSG) cell line, and western blotting was used to detect the levels of relevant proteins.Results: We found that salivary IgA content was significantly decreased in patients with ASD and had a significant ASD diagnostic value. The salivary IgA content also decreased in VPA mice and was significantly correlated with autistic-like behaviors among them. The mRNA and protein levels of the polymeric immunoglobulin receptor (Pigr) were downregulated in the submandibular glands of VPA mice and the Pigr mRNA level was positively correlated with mouse salivary IgA content. HSG cells treated with ASD-related Streptococci had reduced PIGR protein level.Conclusion: Therefore, protective IgA levels were reduced in the saliva of individuals with ASD, which correlated with the bacteria-induced downregulation of Pigr in salivary glands. This study suggests a new direction for ASD diagnosis and prevention of oral diseases in ASD cohorts and provides evidence for the ASD mucosal immunophenotype in the oral cavity.

show abstract

“…Furthermore, expression levels of BDNF, proBDNF, and its intrinsic receptor, TrkB, are reduced in the cerebella of patients with neuropsychiatric disorders, including schizophrenia, bipolar disorder (BPD), and major depressive disorder (MDD) as well as in a rodent model for ASD (Soontornniyomkij et al, 2011;Yang et al, 2017;Alò et al, 2021). Additionally, CAPS2-deficient mice that show reduced secretion of BDNF from CGNs exhibit developmental deficits around the cerebellar vermis, such as increased CGN apoptosis and impaired PC dendritogenesis.…”

Section: Bdnf In Cerebellar-related Neurodevelopmental Disordersmentioning

confidence: 99%

Building better brains: the pleiotropic function of neurotrophic factors in postnatal cerebellar development

Boxy,

Nykjær,

Kisiswa

2023

Front. Mol. Neurosci.

View full text Add to dashboard Cite

The cerebellum is a multifunctional brain region that controls diverse motor and non-motor behaviors. As a result, impairments in the cerebellar architecture and circuitry lead to a vast array of neuropsychiatric and neurodevelopmental disorders. Neurotrophins and neurotrophic growth factors play essential roles in the development as well as maintenance of the central and peripheral nervous system which is crucial for normal brain function. Their timely expression throughout embryonic and postnatal stages is important for promoting growth and survival of both neurons and glial cells. During postnatal development, the cerebellum undergoes changes in its cellular organization, which is regulated by a variety of molecular factors, including neurotrophic factors. Studies have shown that these factors and their receptors promote proper formation of the cerebellar cytoarchitecture as well as maintenance of the cerebellar circuits. In this review, we will summarize what is known on the neurotrophic factors’ role in cerebellar postnatal development and how their dysregulation assists in developing various neurological disorders. Understanding the expression patterns and signaling mechanisms of these factors and their receptors is crucial for elucidating their function within the cerebellum and for developing therapeutic strategies for cerebellar-related disorders.

show abstract

Correlation of distinct behaviors to the modified expression of cerebral Shank1,3 and BDNF in two autistic animal models

Cited by 16 publications

References 76 publications

Fecal Transplant and Bifidobacterium Treatments Modulate Gut Clostridium Bacteria and Rescue Social Impairment and Hippocampal BDNF Expression in a Rodent Model of Autism

Fecal Transplant and Bifidobacterium Treatments Modulate Gut Clostridium Bacteria and Rescue Social Impairment and Hippocampal BDNF Expression in a Rodent Model of Autism

The Alteration of Salivary Immunoglobulin A in Autism Spectrum Disorders

Building better brains: the pleiotropic function of neurotrophic factors in postnatal cerebellar development

Contact Info

Product

Resources

About