Kyung-ho Shin
Korea University · 神経科学
研究室紹介
Professor Kyung-ho Shin's research lab focuses on the neural and metabolic mechanisms underlying energy balance, stress responses, and neurogenesis in the adult brain. The lab investigates how chronic stress, obesity, and pharmacological agents like nicotine and metformin influence hippocampal neurogenesis, hypothalamic neuropeptide regulation, and energy homeostasis. Key areas of inquiry include the role of brain-derived neurotrophic factor (BDNF), stress hormones, and central signaling pathways such as AMPK and S6K in regulating neuronal plasticity and body weight. The lab employs behavioral, molecular, and neurochemical approaches in rodent models to explore the interplay between stress, metabolism, and brain function.
Research Overview
Research Output Trend
Figures are computed from collected data and may differ slightly.
Selected Papers
15New-born cells continue to proliferate and survive to become mature granule cells in adult rat hippocampus. Although this process, known as neurogenesis, is inhibited by acute stress, it is not clear whether chronic stress affects neurogenesis. To determine whether chronic mild stress (CMS) influences neurogenesis in the adult rat hippocampus, male Sprague-Dawley rats were exposed to CMS and administered bromodeoxyuridine (BrdU) before or after CMS to observe the survival/differentiation or prol
New-born cells continue to proliferate and survive to become mature granule cells in adult rat hippo-campus. Although this process, known as neuro-whether chronic stress affects neurogenesis. To de-termine whether chronic mild stress (CMS) influ-ences neurogenesis in the adult rat hippocampus, male Sprague-Dawley rats were exposed to CMS and administered bromodeoxyuridine (BrdU) before or after CMS to observe the survival/differentiation or proliferation of new-born cells, respectively. In addit
These results suggest depot-specific differences in AT angiogenesis and a potential role in the susceptibility to diet-induced obesity.
Nicotine treatment has known to produce an inverse relationship between body weight and food intake in rodents. Present study determined the effect of repeated treatment with nicotine and withdrawal in control and obese mice,on: (1) body weight, caloric intake and energy expenditure;(2) hypothalamic neuropeptides mRNA expression; and (3)serum leptin. 21-week-old C57BL/6 mice (n = 65) received nicotine (3.0 mg/kg/day; 2 weeks) and saline (1 ml/kg/day;2 weeks) subcutaneously. Animals were given ei
Administration of metformin is known to reduce both body weight and food intake. Although the hypothalamus is recognized as a critical regulator of energy balance and body weight, there is currently no evidence for an effect of metformin in the hypothalamus. Therefore, we sought to determine the central action of metformin on energy balance and body weight, as well as its potential involvement with key hypothalamic energy sensors, including adenosine monophosphate-activated protein kinase (AMPK)
Stress is known to inhibit granule cell proliferation in the hippocampus. However, recent studies suggest that the commonly used dose of bromodeoxyuridine (BrdU) is insufficient to label all fractions of granule cells. Furthermore, stress-induced changes in BrdU availability may influence the labeling of newly born cells. To investigate whether changes in BrdU availability affect measurements of stress-induced granule cell proliferation, granule cell proliferation was assessed using injection of
Stress is known to inhibit granule cell proliferation in the hippocampus. However, recent studies suggest that the commonly used dose of bromodeoxyuridine (BrdU) is insufficient to label all fractions of granule cells. Fur-thermore, stress-induced changes in BrdU availability may influence the labeling of newly born cells. To investi-gate whether changes in BrdU availability affect meas-urements of stress-induced granule cell proliferation, granule cell proliferation was assessed using injection