Disinhibition in pathological pain
¹è¿ëö, °íÇü°ï,
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¹è¿ëö ( Bae Yong-Chul ) - Kyungpook National University School of Dentistry Department of Anatomy and Neurobiology
°íÇü°ï ( Ko Hyoung-Gon ) - Kyungpook National University School of Dentistry Department of Anatomy and Neurobiology
KMID : 0355820200410010065
Abstract
À¯ÇØ ¹× ÃË°¢ ÀÚ±ØÀº ô¼ö ¶Ç´Â »ïÂ÷½Å°æÇÙÀ» °ÅÃļ ³ú·Î Àü´ÞµÈ´Ù. ¾ïÁ¦»çÀ̽Ű漼Æ÷ (inhibitory interneuron)´Â ô¼ö ¶Ç´Â »ïÂ÷½Å°æÇÙ °°Àº Áß°è Áö¿ª¿¡ °í·ç °ÉÃļ ºÐÆ÷Çϸç, °¡¹Ù (¥ã-aminobutyric acid, GABA) ¶Ç´Â ±Û¶óÀ̽Š(glycine)À» ºÐºñÇÏ¿© ÀÏÂ÷ ±¸½É¼º ¸»´Ü°ú ô¼ö »çÀ̽Ű漼Æ÷¸¦ ¾ïÁ¦ÇÔÀ¸·Î½á °¨°¢ ÀÚ±ØÀÇ Àüµµ¸¦ Á¶ÀýÇÑ´Ù. º´¸®Àû ÅëÁõ°ú °ü·ÃÇÏ¿© ¾ïÁ¦»çÀ̽Ű漼Æ÷´Â Åë°¢°ú¹Î, ¹«ÇØÀÚ±ØÅëÁõ, ÀÚ¹ßÅëÁõ, ¿¬°üÅëÁõÀÇ ¹ß»ý¿¡ °ü¿©ÇÑ´Ù. Å»¾ïÁ¦´Â ¾ïÁ¦»çÀ̽Ű漼Æ÷¿¡ ÀÇÇØ ¸Å°³µÇ´Â ¾ïÁ¦·ÂÀÇ ¼Õ½ÇÀ» ÀǹÌÇÏ¿©, ÀÌ·¯ÇÑ Áõ»óµéÀÇ ±âÀú¿¡ °ü¿©ÇÏ°í ÀÖ´Ù. ±×µ¿¾ÈÀÇ ¾ï¼¼»çÀ̽Ű漼Æ÷¿¡ ´ëÇÑ ¿¬±¸¸¦ ÅëÇØ ¼¼Æ÷³» ¿°¼ÒÀÌ¿Â ³óµµ Á¶Àý°ï¶õ, ¾ïÁ¦»çÀ̽Ű漼Æ÷ÀÇ »ç¸ê, ¾ïÁ¦»çÀ̽Ű漼Æ÷ÀÇ Àü±â»ý¸®ÇÐÀû º¯È µîÀÌ Å»¾ïÁ¦ÀÇ ±âÀÛÀ¸·Î ¹àÇôÁ³´Ù. ÃÖ±ÙÀÇ ¿¬±¸µéÀº Àüü ¾ïÁ¦»çÀ̽Ű漼Æ÷¸¦ ´ë»óÀ¸·Î ÇÑ ¿¬±¸º¸´Ù´Â ¾ïÁ¦»çÀ̽Ű漼Æ÷µé¿¡¼ ƯÀÌÀûÀ¸·Î ¹ßÇöµÇ´Â ½Å°æÈÇÐÀû Ç¥Áö¸¦ ÀÌ¿ëÇÏ¿© °³º° Á¾·ùÀÇ ¾ïÁ¦»çÀ̽Ű漼Æ÷µéÀÇ ¿¬°á¼º°ú ±â´É¿¡ ´ëÇØ ¿¬±¸ÇÏ°í ÀÖ´Â Ãß¼¼ÀÌ´Ù. ÀÌ·¯ÇÑ ¿¬±¸ÀÇ È帧Àº º´¸®Àû ÅëÁõ¿¡¼ ³ªÅ¸³ª´Â ¾ïÁ¦»çÀ̽Ű漼Æ÷ÀÇ Å»¾ïÁ¦ Çö»ó¿¡ ´ëÇÑ ÀÌÇظ¦ ³ÐÇôÁÖ°í, Â÷ÈÄ º´¸®Àû ÅëÁõ Ä¡·á¿¡ ±â¹ÝÀ» ¸¶·ÃÇØ ÁÙ °ÍÀÌ´Ù.
Noxious and tactile stimuli are transmitted into the spinal cord or in the trigeminal nucleus before being delivered to the brain. Inhibitory interneurons are distributed throughout these relay regions and modulate sensory stimuli by inhibiting primary afferent terminals (presynaptic inhibition) and spinal interneurons (postsynaptic inhibition) by releasing ¥ã-aminobutyric acid (GABA) and/or glycine. Regarding pathological pain, the spinal inhibitory interneurons are involved in hyperalgesia, allodynia, spontaneous pain, and referred pain. Disinhibition is the loss of inhibitory power mediated by the inhibitory interneurons, underlying these symptoms. Studies on global GABAergic neurons have shown that dysregulation of intracellular Cl? concentration, death of inhibitory interneurons, and change of electrophysiological properties are the mechanisms underlying disinhibition. Recent studies exploring the connectivity and function of each specific class of inhibitory interneurons using neurochemical markers will strengthen the basic knowledge of disinhibition in inhibitory interneuron and help develop novel and effective treatments for pathological pain.
Å°¿öµå
disinhibition; pathological pain; inhibitory interneuron
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