ArticleJournal of molecular neuroscience : MN2020
Stathmin Regulates Spatiotemporal Variation in the Memory Loop in Single-Prolonged Stress Rats.
Article in Journal of molecular neuroscience : MN, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
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4 citing papers in PubMed, 6 citations in OpenAlex.
- Association ofAlpha psychiatry · 2025Article
- No Association ofAlpha psychiatry · 2024Article
- Stress-related cellular pathophysiology as a crosstalk risk factor for neurocognitive and psychiatric disorders.BMC neuroscience · 2023Review
- Molecular Mechanism of the ATF6α/S1P/S2P Signaling Pathway in Hippocampal Neuronal Apoptosis in SPS Rats.Journal of molecular neuroscience : MN · 2021Article
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4 authors at 2 institutions in 1 country.
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Abstract
Posttraumatic stress disorder (PTSD) is closely related to brain structures of the memory loop such as the hippocampus, amygdala, and medial prefrontal cortex (mPFC). The fear gene stathmin plays an important role in regulating fear memory. However, whether the fear gene stathmin is related to fear memory loop anomalies caused by PTSD is unclear. A single-prolonged stress (SPS) rat model of PTSD was constructed. Wistar rats were randomly divided into 5 groups: the control group, SPS 1-day group, SPS 4-day group, SPS 7-day group, and SPS 14-day group. Then, we measured the protein and mRNA expression of stathmin, p-stathmin (Ser16, Ser25, Ser38, and Ser63), β-tubulin, and MAP-1B in the hippocampus, amygdala, and mPFC in the 5 groups by immunohistochemistry, Western blotting, and qRT-PCR. The expression of the stathmin protein in the hippocampus, mPFC, and amygdala of the rat memory loop decreased gradually in the SPS 1-day group, the SPS 4-day group, and the SPS 7-day group, in which it was the lowest, and then increased. The trend of the expression of stathmin mRNA in the three areas of the memory loop was consistent with the trend of the expression of the stathmin protein. The trend of the protein expression of p-stathmin (Ser25 and Ser38) was opposite of that of stathmin; it reached a peak on the 7th day, and then decreased in the hippocampus. The protein expression of p-stathmin (Ser63) showed the same trend in the mPFC. The protein and mRNA expression of β-tubulin and MAP-1B was consistent with that of p-stathmin; it reached a peak on the 7th day, and then decreased in the rat hippocampus, mPFC, and amygdala. Stathmin in the memory loop, especially in the hippocampus, regulates microtubule structure through its phosphorylation at Ser25 and Ser38 and thereby participates in the mediation of fear memory abnormalities in PTSD.
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