Thalamic calcification in vitamin D receptor knockout mice

Kalueff, Allan V.; Loseva, E. V.; Haapasalo, Hannu; Rantala, Immo; Keranen, Jaakko; Lou, Yan-Ru; Minasyan, Anna; Keisala, Tiina; Miettinen, Susanna; Kuuslahti, Marianne; Tuchimaa, Pentii

doi:10.1097/01.wnr.0000215770.79281.e4

Cited by 31 publications

(35 citation statements)

References 25 publications

(55 reference statements)

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“…Our previous study also showed that a severe calcification developed in VDR KO mice in the thalamus [Kalueff et al, 2006a] -the brain structure that projects to the inferior colliculus of the auditory pathway and connects with the auditory cortex, as has recently been extensively investigated in both animals and humans [de la Mothe et al, 2006;Devlin et al, 2006;Pearson et al, 2007;Sigalovsky and Melcher, 2006;Takayanagi and Ojima, 2006]. Upon sustaining damage, neuronal retrograde degeneration was observed in the auditory system, and auditory brain stem response (ABR) amplitude decreased after inferior colliculus ablation [Kaga et al, 1999;Yamada et al, 2000].…”

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confidence: 76%

Progressive Hearing Loss in Mice with a Mutated Vitamin D Receptor Gene

Zou¹,

Minasyan

Keisala

et al. 2008

Audiol Neurotol

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Background: Both hypo- and hypervitaminosis D can cause sensorineural hearing loss, and aural symptoms due to vitamin D insufficiency are especially common during gravidity. Hormonal forms of vitamin D regulate transcription by binding with the high-affinity vitamin D receptor (VDR). Objective: To assess the effects of impaired vitamin D action in VDR knockout (KO) mice on hearing, cochlear morphology, and cochlear gene expression. Materials and Methods: Eighteen young male and female mice (10 VDR KO and 8 wild type, WT, ≤6 months old), 33 adult male and female mice (16 VDR KO and 17 WT, between 7 and 14 months old), and 11 aged male and female mice (5 VDR KO and 6 WT, ≧15 months old) on 129S1 genetic background were studied. Auditory thresholds were evaluated by auditory brain stem response. Morphological changes were analyzed using plastic embedding and light microscopy. The expression of key genes (known to play a role in the regulation of cochlear function), and caspase 3 activity, were assessed using immunofluorescent confocal microscopy. Results: There was a statistically significant difference between the young and the adult groups, and between the adult and aged groups of WT mice. There was also a statistically significant difference between the adult and aged groups in VDR KO mice, and between the young WT group and the young VDR KO group. Spiral ganglion cell loss was observed in the basal turn of adult VDR KO mice, a phenomenon infrequently found in WT mice. Expression of connexin 26, KCNJ10, and transient receptor potential channel vanilloid subfamily 4/6 was not affected by VDR KO-mediated hearing loss. Caspase 3 activation was detected in the spiral ganglion cell and its satellite cells, stria vascularis, spiral ligament fibrocytes, and the organ of Corti in both genotypes. However, the percentage of positive cells and the staining intensity were lower in the VDR KO (compared to the WT) mice. Conclusion: These data suggest that sensorineural hearing loss progressively developed at an earlier age in VDR KO mice. While the fundamental gene expressions in the cochlea were not influenced by VDR mutation, it resulted in decrease of caspase 3 activation, which may be one of the factors underlying accelerating age-related hearing loss observed in VDR KO mice.

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confidence: 76%

Progressive Hearing Loss in Mice with a Mutated Vitamin D Receptor Gene

Zou¹,

Minasyan

Keisala

et al. 2008

Audiol Neurotol

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“…Additionally, Garcion et al [11] demonstrated that vitamin D inhibited the synthesis of inducible nitric oxide synthase, an enzyme produced in CNS cells in response to stress and which in high doses results in neuronal cell death. Finally, the protective properties of vitamin D against mineralization in the human brain should be highlighted [1,21] . Calcium deposits have been described in the basal ganglia of subjects with normal calcemia and phosphoremia alongside hypovitaminosis D.…”

Section: Vitamin D and Brain: The Bases Of A Physiological Relationshipmentioning

confidence: 99%

“…deprived of functional VDR) presented with neuromuscular disorders, hypoacousia, and phosphocalcic homeostasis dysregulation associated with thalamic calcifications [21,24] . Moreover, the absence of VDR in the brain is responsible for behavioral disorders related to anxiety and motor disorders [25][26][27][28][29][30][31] ( table 1 ).…”

Section: Non-senile Hypovitaminosis D and Neuropsychopathological Dismentioning

confidence: 99%

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Vitamin D and Ageing: Neurological Issues

et al. 2010

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nervous system as a whole, and in particular on the CNS. During cerebral development, vitamin D may act like a neurosteroid hormone in the areas of neurotrans mission, neuroprotection, and neuroimmunomodulation. Moreover, vitamin D deficiency has been associated with neurological and psychiatric disorders. In older adults, hypovitaminosis D has been associated with neuromuscular disorders, dementia, and Parkinson's disease. Thus, vitamin D supplementation might have a protective effect against these neurological disorders. Conclusions: Vitamin D has been associated with many neurological functions and its deficiency with dysfunction. Low serum 25-hydroxyvitamin D concentrations can potentially be reversed. This simple and low-cost correction might contribute to the primo-secondary prevention of various neuropsychiatric disorders.

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“…55,56 As a possible example of vitamin D deficiency leading to symptoms within the central nervous system, hypoacusis has been documented in rodents deprived of functional vitamin D receptors. 57 Although the mechanism is unclear, vitamin D appears to have a neuroprotective effect on the nervous system 58 promoting an increase in the synthesis of neurotropic agents, 59 an acceleration of neuronal growth, 59 and a protection of neurons against the direct effects of superoxide ions and hydrogen peroxide. 60 Vitamin D also seems to be associated with conduction speeds in the peripheral nervous system.…”

Section: Discussionmentioning

confidence: 99%

A possible correlation between vitamin D deficiency and loss of smell: 2 case reports

Kruse¹,

Cambron

2011

Journal of Chiropractic Medicine

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Objective: The purpose of this report is to present 2 cases of diminished olfaction that improved with increasing serum levels of vitamin D3. Clinical Features: Both patients were under the care of medical and chiropractic physicians for various complaints. A 47-year-old hyposmic woman was diagnosed with vitamin D deficiency who incidentally noticed a progressive return of her sense of smell while taking vitamin D supplements as prescribed by her medical doctor. A 34-year-old anosmic woman noticed a direct relationship with her ability to smell and vitamin D3 supplementation. Intervention and Outcome: Treatment for the first patient consisted of vitamin D supplementation of 10 000 IU a day. Her serum D3 levels increased substantially over a period of 8 months, at which time she reported a marked improvement in her sense of smell. The second patient was prescribed 50 000 IU of vitamin D a week; and she reported an increased ability to smell, although only the strongest of odors. Conclusion: A link between hypovitaminosis D and a diminished sense of smell was noted in these 2 individuals.

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Thalamic calcification in vitamin D receptor knockout mice

Cited by 31 publications

References 25 publications

Progressive Hearing Loss in Mice with a Mutated Vitamin D Receptor Gene

Progressive Hearing Loss in Mice with a Mutated Vitamin D Receptor Gene

Vitamin D and Ageing: Neurological Issues

A possible correlation between vitamin D deficiency and loss of smell: 2 case reports

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