Bands of Fontana are caused exclusively by the sinusoidal path of axons in peripheral nerves and predict axon path; evidence from rodent nerves and physical models

The precise cause of the bands of Fontana, striations on peripheral nerves visible to the naked eye, has been the subject of debate for hundreds of years. Some researchers have described them as reflecting the sinuous course of nerve fibres passing through nerves, and others have proposed that endoneurial collagen and sheaths surrounding nerves play a role in their appearance. We hypothesised that the bands are caused exclusively by reflection of light from the surfaces of nerve fibres travelling in phase in sinusoidal waveforms through peripheral nerves. We aligned images of obliquely illuminated nerves with confocal images of axons in those nerves, and the numbers and positions of the bands precisely matched the axonal waves. We also developed three‐dimensional models of nerves with representations of the sinusoidal path of axons at their surface. We observed patterns resembling the bands of Fontana when these models were obliquely illuminated. This provides evidence that the bands of Fontana can be caused by light reflected sinusoidal path of axons alone. We subsequently describe a mechanism of band production based on our observations of both nerves and models. We report that smaller diameter nerves such as phrenic nerves and distal branches of sciatic nerves have shorter band intervals than larger nerves, such as proximal trunks of sciatic nerves, and that shorter band intervals correlate with longer axons per unit length of nerve, which suggests a greater tolerance to stretch. Inspection of banding patterns on peripheral nerves may permit prediction of axon length within nerves, and assist in the interpretation of nerve conduction data, especially in diseases where axon path has become altered.     

补阳还五汤对大鼠缺血性脑中风损伤后轴突再生的影响

目的:探索补阳还五汤促进缺血性脑中风大鼠轴突再生和神经康复的作用。方法:SD大鼠共180只,建立大脑中动脉梗死(MCAO)模型,选取造模成功的大鼠随机分成模型组、补阳还五汤组(12 g·kg~(-1))和尼莫地平组(20 mg·kg~(-1)),另设假手术组,每组28只。连续灌胃给药7 d后,断头取脑,通过TTC染色检测脑梗死率,测定脑含水量检测脑水肿程度,改良银染法观察轴突变性,免疫荧光染色观察神经微丝蛋白-200(NF-200)的表达,实时荧光定量PCR(Real-time PCR)检测排斥性导向分子a(RGMa),Ras同源酶(Rho),Rho激酶(ROCK)和脑衰反应调节蛋白2(CRMP2)的mRNA表达,并通过改良神经功能评分观察神经功能恢复情况。结果:与假手术组比较,模型组的脑梗死体积和脑含水量显著上升(P0.01),神经功能显著下降(P0.01),轴突变性和神经纤维损伤严重,轴突生长相关蛋白的mRNA表达异常(P0.01);与模型组比较,补阳还五汤组和尼莫地平组的脑损伤程度明显降低,表现为脑梗死率和脑含水量显著降低(P0.01),轴突变性减少;NF-200阳性染色增多;RGMa,Rho和ROCK的mRNA表达明显降低(P0.05),CRMP2的mRNA表达显著升高(P0.01),神经功能明显提高(P0.05)。结论:补阳还五汤可通过调节轴突生长相关蛋白的mRNA表达促进缺血性脑中风损伤后轴突再生,从而改善神经功能。     

Axonal dysfunction,dysmyelination, and conduction failure in hereditary neuropathy with liability to pressure palsies

Introduction: Patients with hereditary neuropathy with liability to pressure palsies (HNPP) manifest with episodes of focal paresis when exposed to mechanical stress, although the basis for vulnerability to conduction block remains relatively unexplained. Methods: Axonal excitability techniques were utilized to provide insights into pathophysiological mechanisms in 13 HNPP patients, stimulating median motor and sensory axons at the wrist. Results: In HNPP, distal latencies were prolonged, and motor and sensory amplitudes were reduced. Threshold was increased. Depolarizing and hyperpolarizing electrotonus was greater, and resting current–threshold slope was reduced. There were greater threshold changes in superexcitability, and refractoriness was decreased. Conclusions: Taken together, excitability testing in patients with HNPP established axonal hyperpolarization in both motor and sensory axons that may be attributable to changes in nerve architecture. In turn, the hyperpolarized resting membrane potential in HNPP may be a major predisposing factor for development of conduction block with mechanical stresses. Muscle Nerve 49 : 858–865, 2014     

L-carnitine alleviates sciatic nerve crush injury in rats：functional and electron microscopy assessments

Several studies have demonstrated that L-carnitine exhibits neuroprotective effects on injured sciatic nerve of rats with diabetes mellitus. It is hypothesized that L-carnitine exhibits neuro-protective effects on injured sciatic nerve of rats. Rat sciatic nerve was crush injured by a forceps and exhibited degenerative changes. After intragastric administration of 50 and 100 mg/kg L-carnitine for 30 days, axon area, myelin sheath area, axon diameter, myelin sheath diameter, and numerical density of the myelinated axons of injured sciatic nerve were similar to normal, and the function of injured sciatic nerve also improved signiifcantly. These ifndings suggest that L-carnitine exhibits neuroprotective effects on sciatic nerve crush injury in rats.     

Proteoglycans: Road Signs for Neurite Outgrowth

Proteoglycans in the central nervous system play integral roles as ＂traffic signals＂ for the direction of neurite outgrowth. This attribute of proteoglycans is a major factor in regeneration of the injured central nervous system. In this review, the structures of proteoglycans and the evidence suggesting their involvement in the response following spinal cord injury are presented. The review further describes the methods routinely used to determine the effect proteoglycans have on neurite outgrowth. The effects of proteoglycans on neurite outgrowth are not completely understood as there is disagreement on what component of the molecule is interacting with growing neurites and this ambiguity is chronicled in an historical context. Finally, the most recent findings suggesting possible receptors, interactions, and sulfation patterns that may be important in eliciting the effect of proteoglycans on neurite outgrowth are discussed. A greater understanding of the proteoglycan-neurite interaction is necessary for successfully promoting regeneration in the iniured central nervous system.