Ascending general visceral pathways within the brainstems of two teleost fishes: Ictalurus punctatus and Carassius auratus.

The primary general visceral nucleus in goldfish (Carassius auratus) and catfish (Ictalurus punctatus) is located at the ventroposterior boundary of the vagal gustatory lobe and receives coelomic visceral, but not gustatory inputs. The neuronal tracer horseradish peroxidase (HRP) was employed to visualize sources of input to and ascending projections from the primary general visceral nucleus in these species. In addition, immunocytochemical techniques were utilized to define the cytological divisions within the pontine gustatory-visceral complex. The pontine secondary visceral nuclei in both catfish and goldfish contains numerous somata and fibers immunoreactive for calcitonin gene-related peptide (CGRP). In contrast, the secondary gustatory nuclei are devoid of fibers and cells immunoreactive for CGRP. In both the goldfish and the channel catfish, the primary general visceral nucleus receives input from the vagal gustatory lobe, as well as the medullary reticular formation. In the channel catfish, the primary general visceral nucleus projects bilaterally to the secondary visceral nucleus, which lies rostrolateral to the secondary gustatory nucleus in the dorsal pons. Fibers cross the midline via the rostral part of the isthmic commissure. Injection of HRP into the primary general visceral nucleus of a goldfish labels ascending fibers that project to a secondary visceral nucleus situated ventral, lateral, and rostral to the secondary gustatory complex. In general, the results indicate that general visceral systems ascend in parallel to gustatory systems within the brainstem, and that general visceral but not gustatory nuclei are immunoreactive for the peptide CGRP.     

Immunocytochemical demonstration of neural cell adhesion molecule (NCAM) along the migration route of luteinizing hormone-releasing hormone (LHRH) neurons in mice.

Contact between the developing forebrain and the ingrowing central processes of the olfactory, vomeronasal and terminal nerves is preceded by a migration of neural cell adhesion molecule (NCAM)-immunoreactive cells from the epithelium of the olfactory pit and the formation of an NCAM-immunoreactive cellular aggregate in the mesenchyme between the olfactory pit and the forebrain. The axons of the olfactory, vomeronasal, and terminal nerves, also NCAM-immunoreactive, grow into the cellular aggregate, which as development proceeds, becomes continuous with the rostral tip of the forebrain. The lateral and more rostral part of the cellular aggregate receives the ingrowing axons of the olfactory nerves and becomes the olfactory nerve layer of the olfactory bulb. The medial, more caudal part receives the central processes of the vomeronasal and terminal nerves. The vomeronasal nerve ends in the accessory olfactory bulb. The central processes of the terminal nerve end in the medial forebrain. Luteinizing hormone-releasing hormone (LHRH)-immunoreactive neurons, like the vomeronasal and terminal nerves, originate from the medial part of the olfactory pit. These LHRH cells migrate into the brain along and within a scaffolding formed by the NCAM-immunoreactive axons of the vomeronasal and terminal nerves, and they are never seen independent of this NCAM scaffold as they cross the nasal lamina propria. The results suggest that: (1) NCAM is likely to be necessary for scaffold formation, and (2) the scaffold may be essential for the subsequent migration of LHRH neurons into the brain. Because they aggregate, migrating LHRH-immunoreactive neurons, on which we did not detect NCAM immunoreactivity, may interact via other cell adhesion molecules (CAM). Inasmuch as the interaction between the LHRH-immunoreactive neurons and the NCAM-immunoreactive scaffold is heterotypic, the possibility of a heterophilic (NCAM to other CAM) interaction is not ruled out. These findings focus our attention on the functional role of NCAM in this migratory system.     

正常人眼筛板的结缔组织纤维结构

采用组化特染，透射电镜和图象分析仪观察了３５只正常人眼筛板结缔组织的纤维成分和结构形态，根据生物力学原理分析了筛束的力学性质和筛板的结构特征，探讨了筛板的损害形式和在眼压与视神经损害间的中介作用及其影响因素。结果显示，筛束含有细胞间质所有三种纤维，具有弹性、塑性和刚性三重复合性质，筛板纵向椭圆、筛束行径和密度象限性差异及筛板厚度个体性差异等与筛板抗损害性能有关。眼压对筛板作用有两种途径，筛板损害是     

Axonal swellings in human intramuscular nerves.

The presence, morphology, distribution, and abundance of axonal swellings in intramuscular nerves were evaluated. Axonal swellings were present in intramuscular nerves in 42% of 127 muscle biopsies from patients with a variety of conditions. The incidence was highest in muscle from patients with peripheral neuropathy, but swellings were present in muscle from patients with motor neuron disease, primary muscle diseases, and some individuals without clinical or histological evidence of neuromuscular disease. The greatest number of swellings in intramuscular nerves was in muscle from patients with chronic inflammatory demyelinating neuropathy. Swellings were spherical or elliptical, 4-20 microns in diameter, 5-30 microns in length, and composed of neurofilaments. Swellings were present only in myelinated axons of intramuscular nerves, proximal to nodes of Ranvier or in internodal regions. Swellings were not associated with axonal degeneration. They were probably not transported. The formation or accumulation of swellings may reflect altered axonal dynamics common to a number of disease processes.     

Activity and distribution of phosphoinositidase C in rat sciatic nerve.

The hydrolysis of phosphatidylinositol-4,5-bisphosphate (PIP2) by rat sciatic nerve cytosolic phosphoinositidase C [phosphoinositide-specific phospholipase C (PIC)] was studied at neutral pH and at ionic concentrations that approximate intracellular conditions. The principal water-soluble product formed was shown to be inositol trisphosphate by anion exchange chromatography. The maximum hydrolysis rate (2.5 nmol/min/mg protein) was achieved at less than 100 nM Ca2+. Hydrolysis was markedly increased to 15 nmol/min/mg protein by inclusion of K+ in the reaction mixture. In the presence of 200 mM K+, the optimum Ca2+ was increased to approximately 600 nM. Higher Ca2+ concentrations progressively inhibited PIP2 hydrolysis. Mg2+ also inhibited the reaction, but the presence of equimolar amounts of ATP and Mg2+ had no effect. Appreciable degradation of phosphatidylinositol-4-phosphate (PIP) also occurred in the nanomolar Ca2+ range, whereas breakdown of phosphatidylinositol (PI) required millimolar Ca2+. The presence of PIP but not PI inhibited PIP2 hydrolysis. Upon subcellular fractionation of nerve, more than 50% of recovered PIC activity was in the cytosol and about 20% was located in a myelin-enriched fraction. Using PIP2 as substrate, PIC activities in nerves from normal and streptozotocin-induced diabetic animals were not different. However, the myelin-associated enzyme from diabetic animals was more labile to freezing and thawing.     

Macrophage-like cells from explant cultures of rat sciatic nerve produce apolipoprotein E

Apolipoprotein E is synthesized and secreted by degenerating peripheral nerve, but the role of resident endoneurial cells in this process is not clear. To exclude the involvement of nonresident cells, we examined the cellular source of endoneurial apolipoprotein E in explant cultures of rat sciatic nerve. The cellular outgrowth from these explant cultures released apolipoprotein E into the culture medium. The cellular outgrowth contained fibroblasts, Schwann cells, and a population of cells with many phenotypic characteristics of macrophages, including the production of apolipoprotein E. No other cell type in the cultures appeared to contribute to this production. These data suggest that apolipoprotein E is produced by resident endoneurial cells in explant cultures and that these cells are macrophages.     

The trajectory of the sympathetic nerve fibers to the rat cochlea as revealed by anterograde and retrograde WGA-HRP tracing

Wheat germ agglutinin-horseradish peroxidase conjugate was injected in the unilateral superior cervical ganglion (SCG), and the projection pathways of postganglionic sympathetic nerve fibers innervating the cochlea were traced in the rat. The labeled axons advanced along the internal carotid artery (ICA), and a few advanced caudally in the major petrosal nerve (MPN) and entered the facial nerve, while the majority ran rostral to the pterygopalatine ganglion at the point where they crossed the MPN in the carotid canal. The rest of the labeled fibers remained on the surface of the ICA and advanced to the cranial cavity. Most of the labeled fibers along the facial nerve joined the cochlear nerve and finally reached the osseous spiral lamina through the spiral ganglion. Some of the labeled fibers ran along the anterior inferior cerebellar artery from the basilar artery which was previously thought to have been the only pathway. We could not find any labeled fiber on the modiolar artery from anterior inferior cerebellar artery in the cochlea. These observations are consistent with our hypothesis that the sympathetic fibers innervating the neural tissues or related structures follow nerve fibers and meninges as matrices of projection pathways rather than arteries.     

MEDIAN NERVE INJURY AND THE TRANSVERSE WRIST CREASE INCISION IN OPEN CARPAL TUNNEL RELEASE

The author has recently had referred to him three patients with median nerve injuries who have had open carpal tunnel decompression via a small transverse wrist incision. Despite previous adverse reports, some surgeons persist with this technique.     

Sodium channels accumulate at the tips of injured axons

The axolemmal distribution of voltage-gated sodium channels largely determines the regions of axonal electrical excitability. Using a wellcharacterized anti–sodium channel antibody, we examined peripheral nerve fibers focally injured by exposure to the neurotoxic agent, potassium tellurite (K₂TeO₃). Immunocytochemical and radioimmunoassay data showed a focal accumulation of sodium channels within the tips of injured axons. The major increase in sodium channel concentration occurred between 7 and 11 days after toxin exposure; however, immunocytochemically, excess sodium channels persisted in several axonal endings for a much longer time. The accumulation of sodium channels at injured axonal tips may be responsible, in part, for ectopic axonal excitability and the resulting abnormal sensory phenomena (especially pain and paresthesias) which frequently complicate peripheral nerve injury in humans. © 1994 John Wiley & Sons, Inc.     

A ring electrode to record extraocular muscle activities during skull base surgery

Summary A ring-shaped electrode was developed and used in 20 patients to record evoked electromyographic responses directly from the extraocular muscles during skull base surgery. Intra-operative monitoring with this electrode helps the surgeon to localize the nerves that innervate the extraocular muscles precisely and to refrain from disturbing important neural structures during operations. Such monitoring also provides some insight into the pathophysiology of the dysfunction of these nerves resulting from skull base lesions.