Vitamin D deficiency induces the excitation/inhibition brain imbalance and the proinflammatory shift

Kasatkina, L.A.; Tarasenko, A. S.; Krupko, Olga; Kuchmerovska, Т. М.; Lisakovska, Olha; Тrikash, I. O.

doi:10.1016/j.biocel.2019.105665

Cited by 43 publications

(31 citation statements)

References 47 publications

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“…The general literature information regarding the fact that oxidative stress increase leads to learning disability supports our research results [7]. The 1,25(OH)2D3 which is active form of Vitamin D regulates the expression and functioning of a range of brain-specific proteins, neurotransmitter turnover, neurogenesis and neuroplasticity [37]. For this reason, the lower 25 OH vitamin D levels in the specific learning disorders group in our findings compared to the control group can be explained by the literature.…”

Section: Discussionsupporting

confidence: 82%

Thiol Disulfide Balance Oxidative Stress and Paraoxonase 1 Activities in Children and Adolescents Aged 6-16 Years with Specific Learning Disorders

Savaş¹,

Sayar

Kara³

2021

ELECTRON J GEN MED

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Specific learning disorders (SLD) are some of the most common neurodevelopmental disorders. The aim of this study is to determine the potential relationship between children with SLD and zinc, copper, paraoxonase 1 (PON1), arylesterase (ARY), ischemia-modified albumin, thiol balance, oxidative stress index, total antioxidant status, total oxidant status, and routine biochemical parameters.Methods: All participants were assessed with the Kiddie Schedule for Affective Disorders and Schizophrenia for School-Age Children. Total oxidant status, total antioxidant status, thiol balance, ischemia modified albumin, paraoxonase 1 activity, arylesterase activity, zinc and copper levels were measured by the spectrophotometric methods.Results: Compared to the control, the SLD group had statistically significantly lower values for PON1 antioxidant enzyme activity (p=.045), ARY antioxidant enzyme activity (p<.001), 25 OH Vitamin D (p=.005), reduced thiol ratio (p=.028), thiol oxidation reduction ratio (p=.01), native thiols (p=.024) and significantly higher values for total oxidant status (p=.017), oxidized thiol ratio (p=.028). Conclusion:The relationship between oxidative stress and SLD diagnosis in our results will be very important if it is supported by further new studies. In this case, evaluation of vitamin D, oxidative stress, antioxidant status and thiol balance may come to the agenda in the diagnosis and treatment of SLD.

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Section: Discussionsupporting

confidence: 82%

Thiol Disulfide Balance Oxidative Stress and Paraoxonase 1 Activities in Children and Adolescents Aged 6-16 Years with Specific Learning Disorders

Savaş¹,

Sayar

Kara³

2021

ELECTRON J GEN MED

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“…The size of the smaller peak corresponded to reported SVs size (Mundigl and De Camilli, 1994, https:// www.ncbi.nlm.nih.gov/pubmed/?term=De%20Camilli%20P %5BAuthor%5D&cauthor=true&cauthor_uid=7986534). Cytosolic proteins are known to promote the SVs clustering by bringing them into close proximity, where they become stably bound or docked (Rottman, 1994;Trikash and Kolchinskaya, 2006;Trikash et al, 2008;Kasatkina et al, 2020). When SVs were tested in buffer, the peak of single SVs prevailed (Fig.…”

Section: Resultsmentioning

confidence: 99%

Nicotinic acetylcholine receptors regulate clustering, fusion and acidification of the rat brain synaptic vesicles

Тrikash

Kasatkina

Lykhmus

et al. 2020

Neurochemistry International

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The brain nicotinic acetylcholine receptors (nAChRs) expressed in pre-synaptic nerve terminals regulate neurotransmitter release. However, there is no evidence for the expression of nAChRs in synaptic vesicles, which deliver neurotransmitter to synaptic cleft. The aim of this paper was to investigate the presence of nAChRs in synaptic vesicles purified from the rat brain and to study their possible involvement in vesicles life cycle. According to dynamic light scattering analysis, the antibody against extracellular domain (1-208) of α7 nAChR subunit inhibited synaptic vesicles clustering. Sandwich ELISA with nAChR subunit-specific antibodies demonstrated the presence of α4β2, α7 and α7β2nAChR subtypes in synaptic vesicles and showed that α7 and β2 nAChR subunits are co-localized with synaptic vesicle glycoprotein 2A (SV2A). Pre-incubation with either α7selective agonist PNU282987 or nicotine did not affect synaptic vesicles clustering but delayed their Ca 2+dependent fusion with the plasma membranes. In contrast, nicotine but not PNU282987 stimulated acidification of isolated synaptic vesicles, indicating that α4β2 but not α7-containing nAChRs are involved in regulation of proton influx and neurotransmitter refilling. Treatment of rats with levetiracetam, a specific modulator of SV2A, increased the content of α7 nAChRs in synaptic vesicles accompanied by increased clustering but decreased Ca 2+-dependent fusion. These data for the first time demonstrate the presence of nAChRs in synaptic vesicles and suggest an active involvement of cholinergic regulation in neurotransmitter release. Synaptic vesicles may be an additional target of nicotine inhaled upon smoking and of α7-specific drugs widely discussed as antiinflammatory and pro-cognitive tools.

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“…Importantly, this was reversed in rats in which vitamin D deficiency had been corrected by supplementation. (148) In summary, microglia appear to represent the site for the antioxidant actions of vitamin D in the brain.…”

Section: Vitamin D and Neurotrophic Factorsmentioning

confidence: 99%

“…This occurred along with impairments in GABA and glutamate release. Importantly, all deficits were normalized by reintroducing dietary vitamin D. ( 148 )…”

Section: Vitamin D Regulates Essential Processes In Normal Brain Devementioning

confidence: 99%

“…This occurred along with impairments in GABA and glutamate release. Importantly, all deficits were normalized by reintroducing dietary vitamin D. (148) One long-speculated neuroprotective mechanism of 1,25 (OH) 2 D 3 in the brain has been the potential inhibition of nitric oxide (NO) production. (4) In the brain, microglia are the immunologically responsive cells responsible for the production of inflammatory regulators such as NO.…”

Section: Vitamin D and Neurotrophic Factorsmentioning

confidence: 99%

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Vitamin D: Brain and Behavior

Eyles

2020

JBMR Plus

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It has been 20 years since we first proposed vitamin D as a "possible" neurosteroid. (1) Our work over the last two decades, particularly results from our cellular and animal models, has confirmed the numerous ways in which vitamin D differentiates the developing brain. As a result, vitamin D can now confidently take its place among all other steroids known to regulate brain development. (2) Others have concentrated on the possible neuroprotective functions of vitamin D in adult brains. Here these data are integrated, and possible mechanisms outlined for the various roles vitamin D appears to play in both developing and mature brains and how such actions shape behavior. There is now also good evidence linking gestational and/or neonatal vitamin D deficiency with an increased risk of neurodevelopmental disorders, such as schizophrenia and autism, and adult vitamin D deficiency with certain degenerative conditions. In this mini-review, the focus is on what we have learned over these past 20 years regarding the genomic and nongenomic actions of vitamin D in shaping brain development, neurophysiology, and behavior in animal models.

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Vitamin D deficiency induces the excitation/inhibition brain imbalance and the proinflammatory shift

Cited by 43 publications

References 47 publications

Thiol Disulfide Balance Oxidative Stress and Paraoxonase 1 Activities in Children and Adolescents Aged 6-16 Years with Specific Learning Disorders

Thiol Disulfide Balance Oxidative Stress and Paraoxonase 1 Activities in Children and Adolescents Aged 6-16 Years with Specific Learning Disorders

Nicotinic acetylcholine receptors regulate clustering, fusion and acidification of the rat brain synaptic vesicles

Vitamin D: Brain and Behavior

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