Melatonin reverses the decreases in hippocampal protein serine/threonine kinases observed in an animal model of autism

Yun Tian, Yasushi Yabuki, Shigeki Moriguchi, Kohji Fukunaga, Pei Jiang Mao, Ling Juan Hong, Ying Mei Lu, Rui Wang, Muhammad Masood Ahmed, Mei Hua Liao, Ji Yun Huang, Rui Ting Zhang, Tian Yi Zhou, Sen Long, Feng Han

研究成果: Article査読

32 被引用数 (Scopus)

抄録

Lower global cognitive function scores are a common symptom of autism spectrum disorders (ASDs). This study investigates the effects of melatonin on hippocampal serine/threonine kinase signaling in an experimental ASD model. We found that chronic melatonin (1.0 or 5.0 mg/kg/day, 28 days) treatment significantly rescued valproic acid (VPA, 600 mg/kg)-induced decreases in CaMKII (Thr286), NMDAR1 (Ser896), and PKA (Thr197) phosphorylation in the hippocampus without affecting total protein levels. Compared with control rats, the immunostaining of pyramidal neurons in the hippocampus revealed a decrease in immunolabeling intensity for phospho-CaMKII (Thr286) in the hippocampus of VPA-treated rats, which was ameliorated by chronic melatonin treatment. Consistent with the elevation of CaMKII/PKA/PKC phosphorylation observed in melatonin-treated rat, long-term potentiation (LTP) was enhanced after chronic melatonin (5.0 mg/kg) treatment, as reflected by extracellular field potential slopes that increased from 56 to 60 min (133.4 ± 3.9% of the baseline, P < 0.01 versus VPA-treated rats) following high-frequency stimulation (HFS) in hippocampal slices. Accordingly, melatonin treatment also significantly improved social behavioral deficits at postnatal day 50 in VPA-treated rats. Taken together, the increased phosphorylation of CaMKII/PKA/PKC signaling might contribute to the beneficial effects of melatonin on autism symptoms.

本文言語English
ページ(範囲)1-11
ページ数11
ジャーナルJournal of Pineal Research
56
1
DOI
出版ステータスPublished - 2014 1

ASJC Scopus subject areas

  • 内分泌学

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