Effects of Boron on Learning and Behavioral Disorders in Rat Autism Model Induced by Intracerebroventricular Propionic Acid

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dc.authoridCoskun, Devran/0000-0003-1151-1861
dc.contributor.authorAlacabey, Nur Akman
dc.contributor.authorCoskun, Devran
dc.contributor.authorAtessahin, Ahmet
dc.date.accessioned2024-12-24T19:24:54Z
dc.date.available2024-12-24T19:24:54Z
dc.date.issued2024
dc.departmentSiirt Üniversitesi
dc.description.abstractAutism spectrum disorder is a neurodevelopmental disorder in which learning, communication, and social interaction are impaired. Research has sought to minimize the neural impairments associated with autism spectrum disorder and improve the quality of life. Recent studies suggest that boron may benefit nerve cells, with effects varying depending on the dosage. This study explored the impact of boron, administered as boric acid, on behavioral, biochemical, and histopathological parameters in a rat model of autism induced by propionic acid (PPA). Thirty-two male Sprague-Dawley rats were divided into control, autism model, and boron-treated groups. Behavioral tests were conducted pre- and post-PPA induction, with brain tissue analyzed post-euthanasia. Proinflammatory cytokines (tumor necrosis factor alpha (TNF-alpha), interleukin 1 beta (IL-1 beta), interleukin 6 (IL-6)) and brain-derived neurotrophic factor (BDNF) levels were assessed in the hippocampus. Histopathological evaluations were conducted on the hippocampus and cerebellum. Autism model rats displayed impaired learning, elevated BDNF and cytokine levels, microglial and astrocytic activation, and decreased Purkinje cell count. The boron-treated groups showed improvements, particularly with the 4 mg/kg dose. This dose enhanced learning and social interaction, reduced proinflammatory cytokine levels, prevented microglial and astrocytic activation, and increased Purkinje cell count. Boron treatment exhibited neuroprotective potential, ameliorating autism spectrum disorder deficits by modulating cytokines, BDNF, microglia, and astrocytes, with low doses yielding pronounced effects.
dc.description.sponsorshipScientific Research Projects Coordination Unit of Fimath;rat University; AAN: Formal analysis, investigation
dc.description.sponsorshipAAN: Formal analysis, investigation, methodology, writing-original draft, writing-review and editing.
dc.identifier.doi10.1007/s12011-024-04417-9
dc.identifier.issn0163-4984
dc.identifier.issn1559-0720
dc.identifier.pmid39397138
dc.identifier.scopus2-s2.0-85206375485
dc.identifier.scopusqualityQ1
dc.identifier.urihttps://doi.org/10.1007/s12011-024-04417-9
dc.identifier.urihttps://hdl.handle.net/20.500.12604/6190
dc.identifier.wosWOS:001336682500002
dc.identifier.wosqualityN/A
dc.indekslendigikaynakWeb of Science
dc.indekslendigikaynakScopus
dc.indekslendigikaynakPubMed
dc.language.isoen
dc.publisherSpringernature
dc.relation.ispartofBiological Trace Element Research
dc.relation.publicationcategoryMakale - Uluslararası Hakemli Dergi - Kurum Öğretim Elemanı
dc.rightsinfo:eu-repo/semantics/closedAccess
dc.snmzKA_20241222
dc.subjectAutism model
dc.subjectBehavioral deficits
dc.subjectBoron
dc.subjectLearning impairments
dc.subjectNeuroprotective action
dc.titleEffects of Boron on Learning and Behavioral Disorders in Rat Autism Model Induced by Intracerebroventricular Propionic Acid
dc.typeArticle

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