title: Changes in GABA and GABA(B)  receptor expressions are involved in neuropathy in the rat cuneate nucleus following median nerve transection.
abstract: This study examined the relationship between changes in GABA transmission and behavioral abnormalities after median nerve transection. Following unilateral median nerve transection, the percentage of GABA-like immunoreactive neurons in the cuneate nucleus and that of GABA(B) receptor-like immunoreactive neurons in the dorsal root ganglion in the injured side decreased and reached a nadir at 4 weeks after median nerve transection. Four weeks after bilateral median nerve transection and intraperitoneal application with saline, baclofen (2 mg kg⁻¹), or phaclofen (2 mg kg⁻¹) before unilateral electrical stimulation of the injured median nerve, we investigated the level of neuropeptide Y release and c-Fos expression in the stimulated side of the cuneate nucleus. The neuropeptide Y release level and the number of c-Fos-like immunoreactive neurons in the baclofen group were significantly attenuated, whereas those in the phaclofen group had increased compared to the saline group. These findings indicate that median nerve transection reduces GABA transmission, promoting injury-induced neuropeptide Y release and consequently evoking c-Fos expression in cuneate nucleus neurons. Furthermore, this study used the CatWalk method to assess behavioral abnormalities in rats following median nerve transection. These abnormalities were reversed by baclofen treatment. Overall, the results suggest that baclofen treatment block neuropeptide Y release, subsequently lessening c-Fos expression in cuneate neurons and consequently attenuating neuropathic signal transmission to the thalamus.
authors.affiliation: Department of Anatomy and Cell Biology, College of Medicine, National Taiwan University, Taipei 10018, Taiwan, Republic of China.
authors.forename: Seu-Hwa
authors.initials: SH
authors.lastname: Chen
authors.forename: Yi-Ju
authors.initials: YJ
authors.lastname: Tsai
authors.forename: Chi-Te
authors.initials: CT
authors.lastname: Lin
authors.forename: Hsin-Ying
authors.initials: HY
authors.lastname: Wang
authors.forename: Shin-Fang
authors.initials: SF
authors.lastname: Li
authors.forename: June-Horng
authors.initials: JH
authors.lastname: Lue
mesh_terms: D000818:Animals; D001418:Baclofen / Q000031:analogs & derivatives / Q000494:pharmacology; D004558:Electric Stimulation; D018756:GABA Antagonists / Q000494:pharmacology; D005684:Gait / Q000187:drug effects; D005727:Ganglia, Spinal / Q000378:metabolism / Q000473:pathology; D008297:Male; D008475:Median Nerve / Q000293:injuries; D020423:Median Neuropathy / Q000378:metabolism*; D008526:Medulla Oblongata / Q000378:metabolism / Q000473:pathology; D009478:Neuropeptide Y / Q000378:metabolism; D016760:Proto-Oncogene Proteins c-fos / Q000378:metabolism; D051381:Rats; D017207:Rats, Sprague-Dawley; D018080:Receptors, GABA-B / Q000378:metabolism*; D005680:gamma-Aminobutyric Acid / Q000378:metabolism*
chemical_list: D018756:GABA Antagonists; D009478:Neuropeptide Y; D016760:Proto-Oncogene Proteins c-fos; D018080:Receptors, GABA-B; C052329:phaclofen; D005680:gamma-Aminobutyric Acid; D001418:Baclofen