The influence of muscle-conditioned media on chick embryo brainstem neurons in culture

Brainstem pieces from the trigeminal region of the metencephalic basal plate of 10-day chick embryos were dissociated and cultured in control conditions or in the presence of muscle-conditioned medium (MCM). The MCM was derived from age-matched target tissue relevant to this neuronal region (jaw musculature), from relevant target tissue of an age at which innervation would initially be taking place (4 days), and from nonrelevant target tissue also of an early stage (4-day limb bud). Neuronal survival and differentiation was assessed daily, for 7 days. Survival and differentiation were significantly enhanced by the 4-day jaw MCM compared to both the controls and the cultures grown with 10-day jaw MCM and 4-day limb MCM. These measures in the presence of 10-day jaw MCM and 4-day limb MCM did not differ, but surpassed that seen in control cultures. The results are compared to the more specific responsiveness seen in earlier (2-day) neural tube cultures, and their relationship to in vivo regenerative nerve fiber outgrowth is considered.     

Pathological forms of brain electrical activity and localization of its sources in patients with trigeminal neuralgia

No significant differences from the typical electroencephalogram were observed in patients with trigeminal neuropathy. In patients with typical trigeminal neuralgia, the electroencephalogram variations were detected both in the changes of dominant activity and in the appearance of individual pathological phenomena. The three-dimensional localization of pathological activity generators points to the involvement of the median nonspecific brainstem structures into pathological process evoked by trigeminal neuralgia. Translated fromByulleten' Eksperimental'noi Biologii i Meditsiny, Vol. 124, No. 9, pp. 275–279, September, 1997     

A microiontophoretic study of the action of kainic acid and putative neurotransmitters in the rat mesencephalic trigeminal nucleus

The ‘excitotoxic’ hypothesis proposes that neurotoxic amino acids exert their effect through neuronal excitation (Olney, Ho &;Rhee, 1971).Colonnier, Steriade &;Landry (1979) have found that trigeminal mesencephalic neurons in the cat are resistant to the neurotoxic effect of kainic acid. In the present study it was found that the same neurons in the rat also resist the cytotoxic action of this amino acid. In addition, kainic acid, applied iontophoretically onto these neurons failed to alter their firing frequency. The resistance of these neurons to both neurotoxic and excitatory actions of kainic acid is consistent with the ‘excitotoxic’ hypothesis.Other putative neurotransmitters were applied by microiontophoresis on these neurons and none were found to alter their rate of discharge. Procaine however applied with relatively low ejecting currents consistently reduced their firing rates. The failure of the putative neurotransmitters tested to influence the rate of discharge of the trigeminal mesencephalic neurons suggests that the chemical synapses present on these neurons in the rat (Hinrichsen &;Larramendi, 1970) utilize another neurotransmitter from those tested. Alternatively the synapses might have a role other than the direct regulation of the firing frequency of these primary afferent neurons.     

Apoptotic cascade of neurons in the subcortical sensory relay nuclei following the neonatal infraorbital nerve transection

A terminal transferase-mediated dUTP nick end labeling (TUNEL) method was utilized for detection of neuronal death in the subcortical relay nuclei of the trigeminosensory system following the infraorbital nerve transection in newborn rats. At 18-24 h after injury, numerous TUNEL-positive profiles were found within the ventroposteromedial thalamic nucleus (VPM) contralateral to the injury, whereas the VPM on the ipsilateral side and of the age-matched normal control contained only a few profiles per section. Electron microscopy revealed that the TUNEL-positive profiles were apoptotic neurons. The ventral part of the ipsilateral brainstem sensory trigeminal nuclear complex (the nucleus principalis, and the subnuclei oralis and interpolaris) exhibited statistically significant 65-70% increase in number of apoptotic neurons compared to the contralateral side. Taken together with our previous study [T. Sugimoto, C. Xiao, H. Ichikawa, Neonatal primary neuronal death induced by capsaicin and axotomy involves an apoptotic mechanism, Brain Res. 807 (1998) 147-154], the present results demonstrated a cascade of apoptosis in the primary, secondary and tertiary order sensory neurons along the neuroaxis.     

c-Jun expression after axotomy of corneal trigeminal ganglion neurons is dependent on the site of injury

The proto-oncogene c-Jun has been implicated in the control of neuronal responses to injury and in axonal growth during regenerative processes. We have investigated the expression of c-Jun during normal terminal remodelling in trigeminal ganglion neurons innervating the cornea and after acute injury of epithelial nerve terminals or parent axons. Remodelling and rearrangement, or damage limited to corneal epithelium endings, was not a trigger for activation of c-Jun expression. However, injury of parent axons in the stroma or in the orbital ciliary nerves induced c-Jun expression in 50% of the population of corneal neurons, which included all of the large myelinated and 20% of the small neuropeptide-containing corneal neurons. This suggests that c-Jun expression in trigeminal ganglion neurons is not associated with normal remodelling or regeneration of peripheral nerve terminals, and that it takes place only when parent axons are injured. A substantial number of damaged neurons do not express c-Jun, indicating that in primary sensory neurons, injury and regeneration may not always be coupled to the expression of this proto-oncogene.     

Spatiotemporal distribution of dying neurons during early mouse development

Apoptosis is a critical cellular event during several stages of neuronal development. Recently, we have shown that biotinylated annexin V detects apoptosis in vivo in various cell lineages of a wide range of species by binding to phosphatidylserines that are exposed at the outer leaflet of the plasma membrane. In the present study, we tested the specificity by which annexin V binds apoptotic neurons, and subsequently investigated developmental cell death in the central and peripheral nervous system of early mouse embryos at both the cellular and histological level, and compared the phagocytic clearance of apoptotic neurons with that of apoptotic mesodermal cells. Our data indicate: (i) that biotinylated annexin V can be used as a sensitive marker that detects apoptotic neurons, including their extensions at an early stage during development; (ii) that apoptosis plays an important part during early morphogenesis of the central nervous system, and during early quantitative matching of brain-derived neurotrophic factor and neurotrophic factor 3 responsive postmitotic large clear neurons in the peripheral ganglia with their projection areas; and (iii) that apoptotic neurons are removed by a process that differs from classical phagocytosis of non-neuronal tissues.     

A dynamic regulation of GDNF-family receptors correlates with a specific trophic dependency of cranial motor neuron subpopulations during development

Glial cell line-derived neurotrophic factor (GDNF) family ligands promote the survival of developing motor neurons in vivo and in vitro. However, not all neurons survive with any single ligand in culture and GDNF null mutant mice display only a partial motor neuron loss. An interesting possibility is that subpopulations of motor neurons based on their function and/or their myotopic organization require distinct members of GDNF family ligands. Because responsiveness to the different ligands depends on the expression of their cognate ligand-binding receptor we have herein addressed this issue by examining the expression of GDNF-family receptors (gfr) during development and in the adult in cranial motor nuclei subpopulations. We have furthermore examined the in vivo role of GDNF for cranial motor neuron subpopulations. The shared ret receptor was expressed in all somatic, branchial and visceral cranial embryonic motor nuclei examined, showing that they are all competent to respond to GDNF family ligands during development. At early stages of development both the GDNF receptor, gfralpha1, and the neurturin (NTN) receptor, gfralpha2, were expressed in the oculomotor, facial and spinal accessory, and only gfralpha1 in the trochlear, superior salivatory, trigeminal, hypoglossal and weakly in the dorsal motor nucleus of the vagus and the ambiguous nucleus. The abducens nucleus was negative for both gfralpha1 and gfralpha2. The artemin (ART) receptor, gfralpha3, was expressed only in the superior salivatory nucleus. A motor neuron subnuclei-specific expression of gfralpha1 and gfralpha2 was seen in the facial and trigeminal nuclei which corresponded to their dependence on GDNF in null mutant mice. We found that the expression was dynamic in these nuclei, which may reflect developmental changes in their trophic factor dependency. Analysis of GDNF null mutant mice revealed that the dynamic receptor expression is regulated by the ligand in vivo, indicating that the attainment of changes in dependency could be ligand induced. Our results indicate that specific GDNF family ligands support selective muscle-motor neuron circuits during development.     

调神止痛法针刺治疗枕神经痛疗效观察

目的观察调神止痛法针刺治疗枕神经痛的疗效。方法以调神止痛法针刺治疗枕神经痛30例,并与常规针刺法治疗30例进行对照,观察两组疗效及对疼痛指数的影响。结果与结论观察组总有效率为93.3%,对照组为76.7%,观察组疗效明显高于对照组(P<0.05);观察组止痛效果优于对照组(P<0.05)。     

复方甘草酸苷联合局部浸润治疗带状疱疹后神经痛及其对免疫功能的影响

目的探讨复方甘草酸苷注射液联合局部浸润治疗老年带状疱疹后神经痛(PHN)的临床效果及其对免疫功能的影响。方法老年PHN20例,静脉滴注复方甘草酸苷40mg(5%葡萄糖注射液250ml),1次/d,连续3周为1个疗程,同时口服复方甘草酸苷片50mg,3次/d;以0·2%布比卡因20ml(含加入醋酸泼尼松龙30mg、利巴韦林0·4g,弥可保1mg)在皮损疼痛区皮下浸润,2次/d。以VAS评分法评价治疗前后的临床效果;检测治疗前和治疗后7、14、21d外周血淋巴细胞亚群变化。结果治疗后VAS评分显著降低(P<0·01);治疗后CD3 、CD4 、CD4 /CD8显著回升(P<0·01),并接近正常水平。结论老年PHN免疫功能可受到不同程度抑制,采用复方甘草酸苷联合皮损区局部浸润对缓解PHN患者的神经病理性疼痛有显著效果,并有提高及调节免疫功能的作用。     

骨折治疗仪联合药物治疗老年带状疱疹后遗神经痛的疗效观察

目的寻找治疗老年带状疱疹后遗神经痛有效而安全的治疗方法。方法将80例老年带状疱疹后遗神经痛患者随机分为试验组和对照组,对照组应用消炎痛、VitB1、VitB12。试验组在对照组治疗的基础上加全电脑骨折治疗仪的治疗及心理治疗。结果治疗期间及治疗后3m内试验组的治愈率和有效率明显优于对照组,秩和检验有显著性差异（P〈0.01或P〈0.05）。结论骨析治疗仪联合药物和心理学治疗带状疱疹后遗神经痛,疗效显著而安全。