scholarly journals Hyperoxygenation Ameliorates Stress-induced Neuronal and Behavioral Deficits

2021 ◽  
Vol 30 (6) ◽  
pp. 415-429
Author(s):  
Juli Choi ◽  
Hye-Jin Kwon ◽  
Ju-Young Seoh ◽  
Pyung-Lim Han
Keyword(s):  
Behavioral Deficits

Consideration of the Federal Guidelines for Academic Services for Student-Athletes with Sports-Related Concussion

2012 ◽  
Vol 13 (3) ◽  
pp. 70-78 ◽  
Author(s):  
Bess Sirmon-Taylor ◽  
Anthony P. Salvatore
Keyword(s):  
Student Athletes ◽  
Section 504 ◽  
Return To Play ◽  
Behavioral Deficits ◽  
Prevention Education ◽  
Concussion Management ◽  
School Settings ◽  
Definition Of ◽  
Federal Guidelines ◽  
Academic Services

Abstract Purpose: Federal regulations should be implemented to provide appropriate services for student-athletes who have sustained a concussion, which can result in impaired function in the academic setting. Eligibility guidelines for special education services do not specifically address the significant, but sometimes transient, impairments that can manifest after concussion, which occur in up to 10% of student-athletes. Method: We provide a definition of the word concussion and discuss the eligibility guidelines for traumatic brain injury and other health-impaired under IDEA, as is the use of Section 504. Results: The cognitive-linguistic and behavioral deficits that can occur after concussion can have a significant impact on academic function. We draw comparisons between the clinical presentation of concussion and the eligibility indicators in IDEA and Section 504. Conclusion: Speech-language pathologists are well-positioned to serve on concussion management teams in school settings, providing services including collection of baseline data, intervention and reassessment after a concussion has occurred, prevention education, and legislative advocacy. Until the cultural perception of concussion changes, with increased recognition of the potential consequences, student-athletes are at risk and appropriate implementation of the existing guidelines can assist in preservation of brain function, return to the classroom, and safe return to play.

Riluzole Exhibits No Therapeutic Efficacy on a Transgenic Rat model of Amyotrophic Lateral Sclerosis

2020 ◽  
Vol 17 (3) ◽  
pp. 275-285 ◽  
Author(s):  
Si Chen ◽  
Qiao Liao ◽  
Ke Lu ◽  
Jinxia Zhou ◽  
Cao Huang ◽  
...  
Keyword(s):  
Amyotrophic Lateral Sclerosis ◽  
Motor Neurons ◽  
Rat Model ◽  
Microglial Activation ◽  
Transgenic Rat ◽  
Intragastric Administration ◽  
Behavioral Deficits ◽  
Als Patients ◽  
Lateral Sclerosis ◽  
Transgenic Rat Model

Background: Amyotrophic lateral sclerosis (ALS) is a neurological disorder clinically characterized by motor system dysfunction, with intraneuronal accumulation of the TAR DNAbinding protein 43 (TDP-43) being a pathological hallmark. Riluzole is a primarily prescribed medicine for ALS patients, while its therapeutical efficacy appears limited. TDP-43 transgenic mice are existing animal models for mechanistic/translational research into ALS. Methods: We developed a transgenic rat model of ALS expressing a mutant human TDP-43 transgene (TDP-43M337V) and evaluated the therapeutic effect of Riluzole on this model. Relative to control, rats with TDP-43M337V expression promoted by the neurofilament heavy subunit (NEF) gene or specifically in motor neurons promoted by the choline acetyltransferase (ChAT) gene showed progressive worsening of mobility and grip strength, along with loss of motor neurons, microglial activation, and intraneuronal accumulation of TDP-43 and ubiquitin aggregations in the spinal cord. Results: Compared to vehicle control, intragastric administration of Riluzole (30 mg/kg/d) did not mitigate the behavioral deficits nor alter the neuropathologies in the transgenics. Conclusion: These findings indicate that transgenic rats recapitulate the basic neurological and neuropathological characteristics of human ALS, while Riluzole treatment can not halt the development of the behavioral and histopathological phenotypes in this new transgenic rodent model of ALS.

scholarly journals Intranasal oxytocin administration ameliorates social behavioral deficits in a POGZWT/Q1038R mouse model of autism spectrum disorder

2021 ◽  
Vol 14 (1) ◽  
Author(s):  
Kohei Kitagawa ◽  
Kensuke Matsumura ◽  
Masayuki Baba ◽  
Momoka Kondo ◽  
Tomoya Takemoto ◽  
...  
Keyword(s):  
Autism Spectrum Disorder ◽  
Social Behavior ◽  
Mouse Model ◽  
Mouse Models ◽  
De Novo ◽  
Neurodevelopmental Disorder ◽  
Autism Spectrum ◽  
Spectrum Disorder ◽  
De Novo Mutation ◽  
Behavioral Deficits

AbstractAutism spectrum disorder (ASD) is a highly prevalent neurodevelopmental disorder characterized by core symptoms of impaired social behavior and communication. Recent studies have suggested that the oxytocin system, which regulates social behavior in mammals, is potentially involved in ASD. Mouse models of ASD provide a useful system for understanding the associations between an impaired oxytocin system and social behavior deficits. However, limited studies have shown the involvement of the oxytocin system in the behavioral phenotypes in mouse models of ASD. We have previously demonstrated that a mouse model that carries the ASD patient-derived de novo mutation in the pogo transposable element derived with zinc finger domain (POGZWT/Q1038R mice), showed ASD-like social behavioral deficits. Here, we have explored whether oxytocin (OXT) administration improves impaired social behavior in POGZWT/Q1038R mice and found that intranasal oxytocin administration effectively restored the impaired social behavior in POGZWT/Q1038R mice. We also found that the expression level of the oxytocin receptor gene (OXTR) was low in POGZWT/Q1038R mice. However, we did not detect significant changes in the number of OXT-expressing neurons between the paraventricular nucleus of POGZWT/Q1038R mice and that of WT mice. A chromatin immunoprecipitation assay revealed that POGZ binds to the promoter region of OXTR and is involved in the transcriptional regulation of OXTR. In summary, our study demonstrate that the pathogenic mutation in the POGZ, a high-confidence ASD gene, impairs the oxytocin system and social behavior in mice, providing insights into the development of oxytocin-based therapeutics for ASD.

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