کد مقاله | کد نشریه | سال انتشار | مقاله انگلیسی | نسخه تمام متن |
---|---|---|---|---|
9425372 | 1295863 | 2005 | 13 صفحه PDF | دانلود رایگان |
عنوان انگلیسی مقاله ISI
Chemical mediators enhance the excitability of unmyelinated sensory axons in normal and injured peripheral nerve of the rat
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کلمات کلیدی
PBSTNFm-CPBGaCSFPGE25-hydroxytryptamineDRGTRPV15-HTdorsal root ganglion - گانگلیون ریشه پشتیBSA - BSANerve injury - آسیب عصبیbovine serum albumin - آلبومین سرم گاوACh - آهaxon - آکسون Acetylcholine - استیل کولینinterleukin - اینترلوکینexcitability - تحریک پذیریtyrosine hydroxylase - تیروزین هیدروکسیلازPain - دردSympathetic - دلسوزThreshold tracking - ردیابی آستانهtumor necrosis factor - فاکتور نکروز تومورPhosphate buffered saline - فسفات بافر شورartificial cerebrospinal fluid - مایع مغزی نخاعی مصنوعیnorepinephrine - نوراپی نفرینCompound Action Potential - پتانسیل اقدام مشترکProstaglandin E2 - پروستاگلاندین E2CaP - کلاه لبه دارVanilloid receptor - گیرنده وانیلیوئید
موضوعات مرتبط
علوم زیستی و بیوفناوری
علم عصب شناسی
علوم اعصاب (عمومی)
پیش نمایش صفحه اول مقاله
چکیده انگلیسی
Ectopic excitation of nociceptive axons by chemical mediators may contribute to symptoms in neuropathic pain. In this study, we have measured the excitability of unmyelinated rat C-fiber axons in isolated segments of sural nerves under different experimental conditions. (1) We demonstrate in normal rats that several mediators including ATP, serotonin (5-HT), 1-(3-chlorophenyl)biguanide (5-HT3 receptor agonist), norepinephrine, acetylcholine and capsaicin alter electrophysiological parameters of C-fibers which indicate an increase of axonal excitability. Other mediators such as histamine, glutamate, prostaglandin E2 and the cytokines tumor necrosis factor α, interleukin-1β and interleukin-6 did not produce such effects. (2) The effects of several mediators were tested after peripheral nerve injury (partial ligation or spared nerve injury). Sural nerves from such animals did not show significant changes when compared with controls. (3) We tested whether the effects of chemical mediators on axonal excitability are due to actions on the sensory C-fiber afferents or the postganglionic sympathetic efferents. In order to distinguish these effects, we performed surgical sympathectomy of the lumbar sympathetic chain, including the L3, L4 and L5 ganglia. Sympathectomy did not markedly influence the effects of mediators on axonal excitability (except that the norepinephrine effect was significantly diminished). In conclusion, our data suggest a constitutive rather than inducible expression of axonal receptors for some chemical mediators on the axonal membrane of unmyelinated fibers. Most of the changes in axonal excitability take place in sensory C-fiber afferents rather than in postganglionic sympathetic efferents. Thus, it is possible that certain immune and glial cell mediators released in or around the nerve following injury or inflammation influence the excitability of intact nociceptive fibers. This mechanism could contribute to ectopic excitation of axons in neuropathic pain.
ناشر
Database: Elsevier - ScienceDirect (ساینس دایرکت)
Journal: Neuroscience - Volume 134, Issue 4, 2005, Pages 1399-1411
Journal: Neuroscience - Volume 134, Issue 4, 2005, Pages 1399-1411
نویسندگان
G. Moalem, P. Grafe, D.J. Tracey,