Changes in metabotropic glutamate receptor expression following spinal cord injury

Spinal cord injury (SCI) initiates biochemical events that lead to an increase in extracellular excitatory amino acid concentrations, resulting in glutamate receptor-mediated excitotoxic events. These receptors include the three groups of metabotropic glutamate receptors (mGluRs). Group I mGluR activation can initiate a number of intracellular pathways that increase neuronal excitability. Group II and III mGluRs may function as autoreceptors to modulate neurotransmission. Thus, all three groups may contribute to the mechanisms of central sensitization and chronic central pain. To begin evaluating mGluRs in SCI, we quantified the changes in mGluR expression after SCI in control (naive), sham, and impact injured adult male Sprague-Dawley rats (200-250 g). SCI was produced at spinal segment T10 with a New York University impactor (12.5-mm drop, 10-g rod of 2-mm diameter). Expression levels were determined by Western blot and immunohistochemistry analyses at the epicenter of injury, as well as segments rostral and caudal. The group I subtype mGluR1 was increased over control levels in segments rostral and caudal by postsurgical day (PSD) 7 and remained elevated through PSD 60. The group I subtype mGluR5 was unchanged in all segments rostral and caudal to the injury at every time point measured. Group II mGluRs were decreased compared to control levels from PSD 7 through PSD 60 in all segments. These results suggest that different subtypes of mGluRs have different spatial and temporal expression patterns following SCI. The expression changes in mGluRs parallel the development of mechanical allodynia and thermal hyperalgesia following SCI; therefore, understanding the expression of mGluRs after SCI may give insight into mechanisms underlying the development of chronic central pain.     

Changes in the somatotopic organization of the cat lumbar spinal cord following peripheral nerve transection and regeneration

Glass microelectrodes were used to record the activity of neurones in the left dorsal horn of the L6 segment of the spinal cord of normal cats and cats in which the left sciatic and saphenous nerves had been cut 1 or 9 months previously. In the normal animals the receptive fields of L6 dorsal horn neurones excited by tactile stimulation of the leg were somatotopically organized, with neurones in the medial and central dorsal horn having receptive fields on the distal parts of the leg, particularly the toes, and neurones in the lateral dorsal horn having receptive fields on the proximal parts of the leg, buttock and lower back. This somatotopy has been shown before. One month after nerve section no cells responded to tactile stimulation of the distal leg and cells in the medial and central parts of the dorsal horn now had receptive fields on the proximal leg, buttock and back. There did not appear to be any somatotopic organization of these new receptive fields. Lateral dorsal horn neurones had normal receptive fields. Nine months after nerve section neurones in the medial and central parts of the lumbar dorsal horn had receptive fields on the distal leg but they showed several abnormal features and there was no evidence of a return of the somatotopic organization seen in normal animals. Lateral dorsal horn cells still had normal receptive fields.     

Changes in truncated trkB and p75 receptor expression in the rat spinal cord following spinal cord hemisection and spinal cord hemisection plus neurotrophin treatment

Although numerous studies have examined the effects of neurotrophin treatment following spinal cord injury, few have examined the changes that occur in the neurotrophin receptors following either such damage or neurotrophin treatment. To determine what changes occur in neurotrophin receptor expression following spinal cord damage, adult rats received a midthoracic spinal cord hemisection alone or in combination with intrathecal application of brain-derived neurotrophic factor (BDNF) or neurotrophin-3 (NT-3). Using immunohistochemical and in situ hybridization techniques, p75, trkA, trkB, and trkC receptor expression was examined throughout the spinal cord. Results showed that trkA, full-length trkB, and trkC receptors were not present in the lesion site but had a normal expression pattern in uninjured parts of the spinal cord. In contrast, p75 receptor expression occurred on Schwann cells throughout the lesion site. BDNF and NT-3 (but not saline) applied to the lesion site increased this expression. In addition, the truncated trkB receptor was expressed in the border between the lesion and intact spinal cord. Truncated trkB receptor expression was also increased throughout the white matter ipsilateral to the lesion and BDNF (but not NT-3 or saline) prevented this increase. The study is the first to show changes in truncated trkB receptor expression that extend beyond the site of a spinal cord lesion and is one of the first to show that BDNF and NT-3 affect Schwann cells and/or p75 expression following spinal cord damage. These results indicate that changes in neurotrophin receptor expression following spinal cord injury could influence the availability of neurotrophins at the lesion site. In addition, neurotrophins may affect their own availability to damaged neurons by altering the expression of the p75 and truncated trkB receptor.     

Interfacing peripheral nerve with macro-sieve electrodes following spinal cord injury

Macro-sieve electrodes were implanted in the sciatic nerve of five adult male Lewis rats following spinal cord injury to assess the ability of the macro-sieve electrode to interface regenerated peripheral nerve fibers post-spinal cord injury. Each spinal cord injury was performed via right lateral hemisection of the cord at the T_(9–10) site. Five months post-implantation, the ability of the macro-sieve electrode to interface the regenerated nerve was assessed by stimulating through the macro-sieve electrode and recording both electromyography signals and evoked muscle force from distal musculature. Electromyography measurements were recorded from the tibialis anterior and gastrocnemius muscles, while evoked muscle force measurements were recorded from the tibialis anterior, extensor digitorum longus, and gastrocnemius muscles. The macro-sieve electrode and regenerated sciatic nerve were then explanted for histological evaluation. Successful sciatic nerve regeneration across the macro-sieve electrode interface following spinal cord injury was seen in all five animals. Recorded electromyography signals and muscle force recordings obtained through macro-sieve electrode stimulation confirm the ability of the macro-sieve electrode to successfully recruit distal musculature in this injury model. Taken together, these results demonstrate the macro-sieve electrode as a viable interface for peripheral nerve stimulation in the context of spinal cord injury.     

BDA皮质脊髓束神经顺行示踪在大鼠脊髓损伤模型中的应用

目的本研究采用生物素标记葡聚糖(Biotin Dextran Amine,BDA)顺行示踪技术来观察大鼠皮质脊髓束(CST)在中枢神经系统中的走行及脊髓损伤后的表现特征。方法20只雌性成年Sprague-Dawley大鼠,分为脊髓损伤组(n=10)和损伤对照组(n=10)。在相当于T7椎板水平用做好标记的显微剪刀剪断脊髓的后2/3。对照组动物术中仅咬除棘突、椎板,不切断脊髓。术后第15 d,所有动物通过立体定向开颅,将10％BDA溶液注入右侧的感觉运动区皮质内。BDA注射2周后,取出大脑和脊髓组织,采用自由漂浮法行BDA染色显影。实验动物于脊髓损伤术前、术后3d、1周、2周、4周采用Basso、Beatlie、Bresnahan(BBB)评分法测量运动功能,所得数据采用两组均数比较t检验进行统计学处理。结果1.脊髓损伤组动物双后肢瘫痪,BBB运动功能评分明显低于损伤对照组,统计学比较差异十分显著(P<0.01);2.BDA顺行示踪显示大脑皮层BDA注射区内见大脑皮层的锥体细胞及其发出的轴突呈阳性染色,BDA阳性染色的皮质脊髓束神经纤维在中脑、桥脑及延髓的腹侧面行走,但在锥体交叉后皮质脊髓束主要(约99％)在对侧脊髓白质的后索中行走。在致伤组动物中,位于脊髓白质后索中的皮质脊髓束纤维在脊髓损伤处终止;在对照组皮质脊髓束纤维染色可一直延伸至L1水平。结论BDA顺行神经     

丹参酮对大鼠脊髓缺血再灌注损伤NMDAR1蛋白表达的影响

BACKGROUND： Tanshinone has been previously shown to be involved in the prevention and treatment of cerebral ischemia/reperfusion injury. In addition, excitatory amino acid-mediated neu- rotoxicity may induce neuronal damage following spinal cord ischemia/reperfusion injury.
OBJECTIVE： To explore the interventional effect of tanshinone on N-methyl-D-aspartate receptor 1 （NMDAR1） protein expression in a rat model of spinal cord ischemia/reperfusion injury.
DESIGN, TIME AND SETTING： A randomized molecular biology experiment was conducted at the Traumatology ＆ Orthopedics Laboratory of Fujian Hospital of Traditional Chinese Medicine （Key Laboratory of State Administration of Traditional Chinese Medicine） between September 2007 and May 2008. MATERIALS： A total of 88 Sprague Dawley rats were randomly divided into a sham operation （n = 8）, model （n = 40）, and tanshinone （n = 40） groups. Thirty minutes after ischemia, rats in the model and tanshinone groups were observed at hour 0.5, 1, 4, 8, and 12 following perfusion, with eight rats for each time point. METHODS： Abdominal aorta occlusion was performed along the right renal arterial root using a Scoville-Lewis clamp to induce spinal cord ischemia. Blood flow was recovered 30 minutes following occlusion to establish models of spinal cord ischemia/reperfusion injury. Abdominal aorta occlusion was not performed in the sham operation group. An intraperitoneal injection of tanshinone ⅡA sulfonic sodium solution （0.2 L/g） was administered to rats in the tanshinone group, preoperatively. In addition, rats in the sham operation and model groups were treated with an intraperitoneal injection of the same concentration of saline, preoperatively.
MAIN OUTCOME MEASURES： NMDAR1 protein expression in the anterior horn of the spinal cord, accumulative absorbance, average absorbance, and area of positive cells were detected in the three groups through immunohistochemistry.
RESULTS： All 88 rats were included in the final analysis. （1） NMDAR1 protein expression increased following 30-minute ischemia/1-hour reperfusion injury to the spinal cord, and reached a peak 4 hours after reperfusion. （2） Accumulative absorbance and average absorbance of NMDAR1, as well as area of positive cells in the model group, were significantly greater than the sham operation group at each time point （P 〈 0.05）. However, values in the tanshinone group were significantly less than the model group （P 〈 0.05）.
CONCLUSION： NMDAR1 protein expression was rapidly increased following spinal cord ischemia/reperfusion injury and reached a peak 4 hours following reperfusion. In addition, tanshinone downregulated NMDAR1 protein expression in the anterior horn of the spinal cord.     

Changes in the expression of parvalbumin immunoreactivity in the lumbar spinal cord of the rat following neonatal nerve injury

Nerve injury in newborn animals results in the loss of motoneurons and dorsal root ganglion neurons and long-term changes in reflex activation of surviving motoneurons. Parvalbumin has been previously shown to be found in large-diameter primary afferent axons and interneurons in the spinal cord, and was used here to study the changes in parvalbumin-immunoreactive appositions onto identified tibialis anterior/extensor digitorum longus (TA/EDL) motoneurons, during both normal development and following neonatal nerve injury in the rat spinal cord. During normal development, there was a decrease in the number of parvalbumin-immunoreactive appositions onto TA/EDL motoneurons. Thus, at postnatal day 7 (P7), there were 72.8 +/- 17.5 (mean +/- SD) appositions per motoneuron and by P14, it had decreased to 38.8 +/- 13.2 (mean +/- SD; p > 0.05). Following neonatal nerve injury at P2, there were fewer parvalbumin-positive afferent appositions close to the TA/EDL motoneurons than normal, so that at P7, there were 53.5 +/- 17.1 (mean +/- SD), and at P14, it further decreased to 25.8 +/- 8.6 (mean +/- SD; p > 0.05). This injury-induced reduction in the number of parvalbumin-immunoreactive boutons apposing TA/EDL motoneurons may result, at least in part, from the death of dorsal root ganglion cells with the consequent loss of their central projections. The alterations in the number of parvalbumin-positive appositions close to motoneurons observed in this study may contribute to the changes in the pattern of reflex activity observed in the developing spinal cord both during normal development and following neonatal injury.     

Nerve grafting from spinal cord to spinal nerve: a microsurgical technique in cats

A ventral surgical approach is described for the grafting of autologous saphenous nerves between the spinal cord and the avulsed C7 ventral root in the cat. To overcome serious blood loss from the epidural venous plexus, the cats were hyperventilated (end tidal

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to about 23 mmHg) and controlled hypotension was induced (mean arterial pressure to about 60 mmHg). After selective avulsion of the ventral rootlets C7 the saphenous grafts were implanted into the spinal cord and coaptated to the avulsed spinal nerve. The combination of advanced anesthetic methods and microsurgical techniques appeared to be mandatory to achieve a low surgical mortality. Regenerated axons were retrogradely traced using retrograde horseradish peroxidase (HRP), and their functional recovery was evaluated by means of electrophysiological methods.     

Effect of 17 beta-estradiol on gene expression in lumbar spinal cord following sciatic nerve crush injury in ovariectomized mice

Previously, we observed that estrogen treatment enhances regeneration of the sciatic nerve after crush injury [Brain Res. 943 (2002) 283]. In this research, we studied expression of estrogen receptors and effects of estrogen on gene expression in the lumbar spinal cord, following sciatic nerve crush injury. Using the Atlas Mouse 1.2 Array, changes in the expression of 267 of 1176 genes were registered 4 days after nerve injury. Those genes that exhibited a change in signal intensity ratios of 2-fold or greater were selected as up-regulated (42) or down-regulated (21). In estrogen treated mice, we have observed up-regulation of the genes known to control apoptosis, cell proliferation, and growth, which might account for the positive effects of estrogen on the regeneration of motor neurons. Immunohistochemical staining revealed estrogen receptor-alpha and estrogen receptor-beta localized in the nucleus and cytoplasm of lumbar motor neurons, and in the regenerating neurites of the sciatic nerve. Expression of estrogen receptor-alpha and estrogen receptor-beta mRNA in lumbar spinal cord was shown by traditional RT-PCR. Using real-time quantitative RT-PCR, we demonstrated increased expression of estrogen receptors-alpha and -beta mRNA on the injured side of the lumbar spinal cord. Western blot analysis showed the accumulation of ERs in regenerating sciatic nerve, and revealed a 40% increase of activated ERK1/2 in estrogen treated mice, compared to placebo. Our findings indicate that: (i). axotomized motor neurons increase expression of estrogen receptors-alpha and -beta mRNA, (ii). estrogen mediates the expression of genes which accelerate the growth and maturation of axons, and (iii). estrogen receptors are transported from the perikaryon into regenerating neurites, and estrogen promotes regeneration locally through the non-genomic ERK-activated signaling pathway.     

陈旧性脊髓损伤的修复与神经功能重建

背景：脊髓损伤尤其是陈旧性脊髓损伤所致的瘫痪是一种较为严重的伤残,如何对脊髓损伤患者采取有效的修复治疗方法进行功能重建一直是临床上的难点。目的：探讨陈旧性脊髓损伤的修复与神经功能重建的有效方法,总结陈旧性脊髓损伤修复治疗与神经功能重建的临床经验。方法：应用计算机检索CNKI 期刊全文数据库(1996-10/2009-12)和PubMed数据库(1999-10/2009-10)与陈旧性脊髓损伤的治疗和神经功能重建有关的文章,检索词分别为“陈旧性脊髓损伤;神经功能重建;细胞移植;手术治疗;痉挛疼痛”和“obsolete spinal cord injury;surgery;transplants;spasm pain;nerve functional reconstruction”。纳入所述内容与陈旧性脊髓损伤、细胞移植或神经功能重建等方式修复脊髓损伤相关的文章。排除重复研究或Meta分析类文章。结果与结论：收集到107篇相关文献,排除61篇不符合标准的文献,共纳入46篇符合标准的文献。经分析得出以下结论：对于陈旧性非完全性损伤患者,采取细胞移植治疗和显微外科手术治疗可刺激神经细胞再生和解除脊髓、神经根压迫,从而促进神经功能的恢复或再生;对完全性脊髓损伤患者采用截瘫平面以上的正常周围神经旁路转位于平面以下的神经相嫁接,可重建膈肌呼吸功能、部分上肢和手功能、迈步、尿便和足底感觉等关键神经功能,是一种可行的治疗策略。     

Role of group II and group III metabotropic glutamate receptors in spinal cord injury.

Spinal cord injury (SCI) produces an increase in extracellular excitatory amino acid (EAA) concentrations that results in glutamate receptor-mediated excitotoxic events. An important class of these receptors is the metabotropic glutamate receptors (mGluRs). mGluRs can activate a number of intracellular pathways that increase neuronal excitability and modulate neurotransmission. Group I mGluRs are known to modulate EAA release and the development of chronic central pain (CCP) following SCI; however, the role of group II and III mGluRs remains unclear. To begin evaluating group II and III mGluRs in SCI, we administered the specific agonists for group II, APDC, or group III, L-AP4, by interspinal injection immediately following SCI. Contusion injury was produced at spinal segment T10 with a New York University impactor (12.5-mm drop, 10-g rod 2 mm in diameter) in 30 adult male Sprague-Dawley rats (175-200 g). Evoked and spontaneous behavioral measures of CCP, locomotor recovery, changes in mGluR expression, and amount of spared tissue were examined. Neither APDC nor L-AP4 affected locomotor recovery or the development of thermal hyperalgesia; however, L-AP4 and APDC attenuated changes in mechanical thresholds and changes in exploratory behavior indicative of CCP. APDC- and L-AP4-treated groups had higher expression levels of mGluR2/3 at the epicenter of injury on post contusion day 28; however, there was no difference in the amount of spared tissue between treatment groups. These results demonstrate that treatment with agonists to group II and III mGluRs following SCI affects mechanical responses, exploratory behavior, and mGluR2/3 expression without affecting the amount of tissue spared, suggesting that the level of mGluR expression after SCI may modulate nociceptive responses.     

Glial cell reactions in the spinal cord after sensory nerve stimulation are associated with axonal injury

Astroglial and microglial reactions in the dorsal and ventral horns of the adult rat spinal cord were studied after graded electrical stimulation of the rat sciatic nerve and after topical application of mustard oil to the hindlimb foot. Antibodies to glial fibrillary acidic protein and complement receptor 3 (OX-42) were used as markers for astroglia and microglia, respectively. The results showed that electrical nerve stimulation resulted in increased immunoreactivity for GFAP and OX-42 in the spinal cord dorsal and ventral horns only after the use of stimulation strengths which were associated with nerve fiber degeneration in the stimulated nerve. Application of mustard oil to the foot caused no changes in GFAP or OX-42 immunoreactivity. These findings indicate that peripheral nerve stimulation in itself is insufficient to induce astroglial and microglial responses in the spinal cord. The signal(s) mediating these responses, regularly seen after nerve injury, are therefore most probably not related to the afferent barrage of action potentials evoked by the injury.     

Effect of electro-acupuncture on the expression of heat shock protein-70 gene in rat spinal cords following spinal cord injury

BACKGROUND: It is generally believed that the mechanism by which heat shock protein-70 (HSP70) protects cells is related to its effectiveness in maintaining the normal stereochemical structure of intracellular proteins, and in participating in the process of cell apoptosis. Whether electro-acupuncture participates in HSP70 expression and produces neuroprotective effects remain unclear. OBJECTIVE: This study aimed at detecting HSP70 expression after electro-acupuncture in rats with transected spinal cord, in order to further validate the mechanism of electro-acupuncture-induced effects in the treatment of spinal cord injury. DESIGN: A controlled observational experiment. SETTING: Shanghai University of Traditional Chinese Medicine and Toho University, School of Medicine. MATERIALS: Seventy adult male Sprague-Dawley rats of SPF grade, weighing 200±20 g, were provided by the Laboratory Animal Center of Shanghai University of Traditional Chinese Medicine, with permission No. SYXK (hu) 2004–2005. The animals were handled in accordance with the requests from Animal Ethics Committees for guidance. A G6805-2 multiple purpose treatment machine was used (Shanghai Medical Instruments High-Tech Co.,Ltd., Shanghai, China). METHODS: This study was carried out in the state level laboratories of Shanghai University of Traditional Chinese Medicine and Toho University, School of Medicine between January 2005 and July 2007. The rats were randomly divided into the electro-acupuncture treated group, which received electro-acupuncture treatment in addition to spinal cord surgery and the control group, which received only spinal cord surgery, with 35 rats in each group. All the rats underwent the same surgery consisting of spinal cord transection at the T10 level. If the spinal cord was completely transected and the two posterior limbs were completely paralyzed, then the surgery was considered successful and the animal was kept for further analysis and testing. After surgery, rats in the experimental group were electro-acupunctured with a G6805-2 multiple purpose treatment machine. Two needle electrodes were inserted under the T7 and T10 spinal processes, The treatment was administered once a day for 20 minutes. Rats in the control group were not given any treatment after surgery. Five rats were sacrificed separately in each group on days 1, 2, 3, 7, 14, 21 and 28 after surgery. HSP70 gene expression at the site of lesion was located and quantitatively analyzed by immunohistochemistry and real-time PCR methods. Simultaneously, the spinal cord injury region and neurons were observed by HE and Klüver-Barrera stainings. MAIN OUTCOME MEASURES: ①HSP70 gene expression in the spinal cord injury region. ② The number of neurons in the spinal cord injury region. RESULTS: Seventy rats were involved in the final analysis. ①At the end of each pre-determined block of time, HSP70 mRNA level in the spinal cord injury region of rats in the electro-acupuncture treated group was significantly higher than that in the control group (P < 0.05). HSP70 gene expression in the two groups reached peak levels on day 2 after surgery. ② On days 7, 14, 21 and 28 after surgery, the number of neurons in the spinal cord injury region in the electro-acupuncture treated group was significantly higher than that in the control group (P < 0.05). CONCLUSION: Electro-acupuncture can effectively enhance HSP70 expression in the spinal cord injury region. HSP70 may participate in this apparent neuroprotective effect.     

Glutamatergic activities in neonatal rat spinal cord heterogeneously regulate single-fiber splanchnic nerve discharge

Kynurenic acid (KYN) is a metabolite of tryptophan and is involved in various neurological disorders. Using whole-bundle nerve recording techniques, we previously observed that applications of KYN to block endogenous ionotropic glutamate receptor activities in neonatal rat spinal cords in vitro cause a reversible fluctuation of splanchnic sympathetic nerve discharge (SND). We hypothesized that the SND fluctuation was due to a heterogeneous single-fiber response. To detail individual fiber activities, we used the so-called ‘oligofiber recordings’. Spontaneous single-fiber activities were recorded from the collagenase-dissociated splanchnic nerve fascicles. Applications of KYN increased, decreased or did not change firing rates. The heterogeneous responses in spontaneous spiking activities were confirmed by applications of APV or CNQX, suggesting an effect mediated by endogenous NMDA- or non-NMDA receptor activities. In addition to changes in firing rates, apparent drug-induced changes in firing patterns were also observed in some fiber activities. Using the oligofiber recording techniques, we confirmed a differential role of endogenous ionotropic glutamate receptor activities in regulating sympathetic outflows from the spinal cord of neonatal rats. Fine-tuning of ionotropic glutamate receptor activities in the spinal cord may serve as a simple way for heterogeneous regulation of various sympathetic-targeting tissues.     

Substance pin spinal cord dorsal horn decreases following peripheral nerve injury

Substance P was located in the spinal cord of rats by immunocytochemistry.Section and ligation of the sciatic nerve produced a depleted area low in substance P in the medial two-thirds of laminae 1 and 2 of segments L4 and 5.The time of depletion began about 5 days after the nerve had been cut and substance P reached a steady minimum by about 9 days and remained depleted for the entire period examined, 31 days.Crush lesions of the sciatic nerve failed to produce the marked and rapid changes of spinal cord substance P observed after section and ligation.     

乙交酯-丙交酯共聚物/神经生长因子复合支架植入大鼠损伤脊髓后的

背景：前期体外实验已经证明神经生长因子乙交酯-丙交酯共聚物与神经生长因子复合支架具有良好的细胞黏附亲和性;同时观察到其随时间推移可稳定释放神经生长因子。 目的：将生物可降解材料乙交酯-丙交酯共聚物与神经生长因子复合支架移植入大鼠脊髓半横断损伤动物模型中,观察其对脊髓损伤髓鞘再生的影响。 设计、时间及地点：随机对照动物实验,于2006-05/07在首都医科大学附属北京市神经外科研究所损伤修复实验室完成。 材料：乙交酯-丙交酯共聚物与神经生长因子复合支架材料,其中0.02 g乙交酯-丙交酯共聚物中含有1 μg 神经生长因子。 方法：45只成年Wistar大鼠制备T8~9脊髓半横断损伤模型,随机分为单纯支架组20只和复合支架组25只,分别移植乙交酯-丙交酯共聚物支架和掺有神经生长因子的乙交酯-丙交酯共聚物支架。 主要观察指标：于术后1,4,8和12周进行髓鞘碱性蛋白免疫组织化学及超微结构检测观察髓鞘再生的情况。 结果：复合支架组苏木精-伊红染色观察脊髓损伤程度较单纯支架组明显减轻。复合支架组髓鞘碱性蛋白免疫组织化学阳性颗粒明显多于单纯支架组。透射电镜观察复合支架组大鼠新生髓鞘明显多于单纯支架组。 结论：乙交酯-丙交酯共聚物联合神经生长因子促进髓鞘再生的效果优于单纯乙交酯-丙交酯共聚物。