title: Kindling-induced learning deficiency and possible cellular and molecular involved mechanisms.
abstract: Hippocampus learning disturbance is a major symptom of patients with seizure, hence hippocampal dysfunction has essential role in worsening the disease. Hippocampal formation includes neurons and myelinated fibers that are necessary for acquisition and consolidation of memory, long-term potentiation and learning activity. The exact mechanism by which seizure can decrease memory and learning activity of hippocampus remains unknown. In the present study, electrical kindling-induced learning deficit in rats was evaluated by Morris water maze (MWM) test. The hippocampus was removed and changes in neurons and myelin sheaths around hippocampal fibers were investigated using histological and immunohistochemical methods. Demyelination was assessed by luxol fast blue staining, and immunohistological staining of myelin-binding protein (MBP). The TUNEL assay was used for evaluation of neuronal apoptosis and the glial fibriliary acetic protein (GFAP) was used for assessment of inflammatory reaction. The results indicated that electrical kindling of hippocampus could induce deficiency in spatial learning and memory as compared to control group. In addition, electrical kindling caused damage to the myelin sheath around hippocampal fibers and produced vast demyelination. Furthermore, an increase in the number of apoptotic cells in hippocampal slices was observed. In addition, inflammatory response was higher in kindled animals as compared to the control group. The results suggested that the decrease in learning and memory in kindled animals is likely due to demyelination and augmentation in apoptosis rate accompanied by inflammatory reaction in hippocampal neurons of kindled rats.
authors: Neuroscience Research Center, Shahid Beheshti University of Medical Sciences, Tehran, Iran.
authors: Mohammad Amin
authors: MA
authors: Sherafat
authors: Abdolaziz
authors: A
authors: Ronaghi
authors: Leila
authors: L
authors: Ahmad-Molaei
authors: Mohammad
authors: M
authors: Nejadhoseynian
authors: Rasoul
authors: R
authors: Ghasemi
authors: Arman
authors: A
authors: Hosseini
authors: Nima
authors: N
authors: Naderi
authors: Fereshteh
authors: F
authors: Motamedi
mesh_terms: D000818:Animals; D017209:Apoptosis / Q000187:drug effects / Q000502:physiology; D001362:Avoidance Learning / Q000502:physiology; D003711:Demyelinating Diseases / Q000209:etiology / Q000473:pathology; D004195:Disease Models, Animal; D003576:Electron Transport Complex IV / Q000378:metabolism; D018691:Excitatory Amino Acid Antagonists / Q000633:toxicity; D005786:Gene Expression Regulation / Q000187:drug effects / Q000502:physiology; D005904:Glial Fibrillary Acidic Protein / Q000378:metabolism; D006624:Hippocampus / Q000473:pathology; D007211:Indoles; D007649:Ketamine / Q000633:toxicity; D007696:Kindling, Neurologic / Q000187:drug effects; D007859:Learning Disabilities / Q000209:etiology* / Q000473:pathology*; D008124:Locomotion / Q000502:physiology; D008297:Male; D018782:Maze Learning; D004676:Myelin Basic Protein / Q000378:metabolism; D051381:Rats; D017208:Rats, Wistar; D011930:Reaction Time / Q000502:physiology; D012640:Seizures / Q000139:chemically induced / Q000150:complications*
chemical_list: D018691:Excitatory Amino Acid Antagonists; D005904:Glial Fibrillary Acidic Protein; D007211:Indoles; D004676:Myelin Basic Protein; C018588:Luxol Fast Blue MBS; D007649:Ketamine; D003576:Electron Transport Complex IV