The plasticity of the hippocampus is the reason for its vulnerability |
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| Institution: | 1. Republican Research and Practice Center for Mental Health, Laboratory of Clinical and Epidemiological Research, Dolginovsky Tract, 152, 220053 Minsk, Belarus;2. Belarusian State Medical University, Department of Psychiatry and Medical Psychology, Dolginovsky Tract, 152, 220053 Minsk, Belarus;3. Institute of Genetics and Cytology of the National Academy of Sciences of the Republic of Belarus, Laboratory of Cytoplasmic Inheritance, F. Skoryni, 34, 220141 Minsk, Belarus;4. Department of Psychiatry, Medical University of Białystok, Białystok, Plac Brodowicza 1, 16-070 Choroszcz, Poland;1. NICU and Animal Lab, Dept of Paediatrics, University Hospital of Salamanca, Paseo de San Vicente182, 37007 Salamanca, Spain;2. Division of Paediatrics and Neonatal Critical Care, FAME Dept, South Paris University Hospitals, Medical Center “A.Béclère”-APHP, 157 rue de la Porte de Trivaux, 92140 Clamart, Paris, France;3. Lab of Clinical Molecular Biology, Dept of Laboratory Medicine, University Hospital “A.Gemelli”, Catholic University of the Sacred Heart, L.go A. Gemelli 8, 00168 Roma, Italy;4. Molecular Genetics and Pharmacogenetics Unit, Dept of Clinical Biochemistry, University Hospital of Salamanca, Pase de San Vicente182, 37007 Salamanca, Spain;5. Research Unit on BioActive Molecules, Dept. of Biomedicinal Chemistry, Institute for Advanced Chemistry, Jordi Girona 18, 08034 Barcelona, Spain;1. Center for Radiological Research, College of Physicians and Surgeons, Columbia University, NY, United States;2. Brookhaven National Laboratory, Biosciences Department, Upton, NY, United States;1. Department of Neurosurgery, Leeds Teaching Hospitals NHS Trust, Leeds, England;2. Department of Histopathology, Leeds Teaching Hospitals NHS Trust, Leeds, England;1. Department of Physiology, Faculty of Medicine, Osaka Medical College, 2-7, Daigaku-machi, Takatsuki, Osaka 569-8686, Japan;2. Faculty of Nutrition, Koshien University, 10-1 Momijimachi, Takarazuka, Hyogo 665-0006, Japan;3. RIKEN Center for Life Science Technologies, 2-2-3, Minatojima-minamimachi, Chuo-ku, Kobe 650-0047, Japan |
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| Abstract: | The hippocampal formation is at the same time a very plastic brain region and a very vulnerable one to insults such as head trauma, ischemia, seizures and severe stress. Circulating glucocorticoids and endogenous excitatory amino acids acting as neurotransmitters play important roles in both aspects. Adrenal steroids acting through Type I receptors that are concentrated in the hippocampus produce rapid effects to enhance long-term potentiation (LTP) and slower effects to contain the turnover of dentate gyrus granule neurons, which die and are replaced during adult life in the rat. Type II adrenal steroid receptors mediate acute suppression of LTP and they also participate in glucocorticoid 'endangerment' of pyramidal neurons, which may die as a result of excitatory amino acid stimulation in the presence of high levels of adrenal steroids. Repeated stress, acting through excitatory amino acids released from mossy fiber terminals and elevated adrenal steroid blood levels causes atrophy of dendrites of hippocampal CA3 pyramidal neurons. These changes precede the permanent loss of pyramidal neurons and may be indicative either of the beginning of damage or, alternatively, represent a short-term protective mechanism to avoid greater damage. Imaging studies of the human hippocampus have suggested a negative relationship between cortisol levels and hippocampal volume. |
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