Effect of sodium selenite on synaptic plasticity and neurogenesis impaired by hypothyroidism


Babur E., CANÖZ Ö., TAN B., SÜER C., DURSUN N.

International Journal of Neuroscience, cilt.132, sa.7, ss.662-672, 2022 (SCI-Expanded) identifier identifier identifier

  • Yayın Türü: Makale / Tam Makale
  • Cilt numarası: 132 Sayı: 7
  • Basım Tarihi: 2022
  • Doi Numarası: 10.1080/00207454.2020.1835898
  • Dergi Adı: International Journal of Neuroscience
  • Derginin Tarandığı İndeksler: Science Citation Index Expanded (SCI-EXPANDED), Scopus, Academic Search Premier, EMBASE, MEDLINE, Psycinfo
  • Sayfa Sayıları: ss.662-672
  • Anahtar Kelimeler: Selenium, neurogenesis, hippocampus, long-term potentiation, LONG-TERM POTENTIATION, THYROID-HORMONE, DENTATE GYRUS, HIPPOCAMPAL NEUROGENESIS, GENE-EXPRESSION, IN-VITRO, MEMORY, RAT, CA1, PERFORMANCE
  • Kayseri Üniversitesi Adresli: Hayır

Özet

© 2020 Informa UK Limited, trading as Taylor & Francis Group.Aim of the study: We investigated protective effect of sodium selenite (Se) on hypothyroidism-induced impairments in, Morris water maze (MWM), long-term potentiation (LTP) and hippocampal neurogenesis male Wistar rats aged of 2 months. Materials and methods: Hypothyroidism was induced by administration of propylthiouracil (Ptu, 1 mg/kg/d) solution to the rats from postnatal day 60 for 81 days with or without Se (0.5mg/kg/d). Neurogenesis was examined by Ki-67 immunohistochemical staining. Se values on plasma and hippocampus were measured with inductively coupled plasma-mass spectrometry (ICP-MS). Results: Measurement of fT3 and fT4 levels confirmed that the fT3 levels, but not fT4, in Ptu-treated rats (5435.44±816.05 fg/ml, p < 0.05) has returned to control values (8721.66±2567.68 fg/ml) by Se treatment (8661.65±711.43 fg/ml). Analysis of learning performance in water escape learning task showed that Se supplementation disappeared memory deficit in Ptu-treated rats as shown by significantly decreased time spent in the target quadrant (33.7±0.24% in control group; 26.1±0.48% in Ptu-group, p < 0.05; 33.9±0.44 in Ptu+Se group), although there was no significant difference among groups in any measurement of learning performance on the last day. Considering LTP, Se supplementation improved the deficit in synaptic plasticity in Ptu-treated rats, as shown by significant increase in the excitatory postsynaptic potential slope (% 243±31 in control group; 172±49 in Ptu-group, p < 0.05; 222±65 in Ptu+Se group) without affecting of the impairment in somatic plasticity. Se supplementation did not improve the decrease in the number of progenitor cells in the subgranular layer (SGL) of dentate gyrus (DG) of Ptu treated rats. Conclusions: These findings suggest that selenium supplementation in hypothyroid patients may improve learning and memory disorders with different physiological mechanisms.Highlights Se increased serum fT3 levels and hippocampus Se levels in hypothyroid rats. Se attenuated impairment of population spike-LTP in hypothyroid rats Hypothyroidism disrupts neurogenesis process in the dentate gyrus of hippocampus. Se supplementation could not increase new born cells in hypothyroid rats.