Motor Neurons In Anterior Horn Research Articles

Pulsing electromagnetic field therapy in nerve regeneration: an experimental study in the cat.

A multidisciplinary approach to the study of peripheral nerve regeneration in the cat has been presented. The purpose of this work has been to determine if pulsing electromagnetic field (PEMF) therapy can enhance peripheral nerve regeneration after injury. In equal groups of animals, two types of pulsing electromagnetic field treatment were compared with untreated controls. All animals underwent quantitative electrophysiologic and morphologic assessment at the area of injury. In addition, muscle fiber sizing in the periphery and retrograde labeling of anterior horn motoneurons with horseradish peroxidase were studied. Results have shown no statistical differences between the groups in electrophysiologic or morphologic parameters. However, in animals treated with a pulse-burst electromagnetic field there was a statistically significant improvement in the labeling and localization of anterior horn cells in the central nervous system. These results indicate that pulse-burst electromagnetic radiation can increase the numbers of motor neurons that reestablish appropriate connections to the periphery after nerve injury. It remains to be seen if this improved spinal cord organization can translate to improved peripheral functional return.

A neuropathologic study of Werdnig-Hoffmann disease with special reference to the thalamus and posterior roots.

The brains of five cases of severe infantile form of Werdnig-Hoffmann (W-H) disease were studied to observe the pathologic changes of sensory neurons and the thalamus. The present study disclosed severe cell loss, chromatolytic degeneration, and empty cell beds of the spinal anterior horn and cranial motoneurons (V, VII, X, XII). Glial bundles were also noted in the anterior roots. In the sensory systems, glial bundles in the posterior roots (2/5), ghost cells in Clarke's column (2/5), and degeneration of the thalamus, mainly in the lateral formation (4/4) were noted. It was demonstrated that not only degeneration of lower motor neurons and glial bundles in the anterior roots, but also degeneration of sensory neurons and thalamus were present in W-H disease. These findings suggested the possibility that W-H disease is a multisystemic disease involving both the anterior and posterior root systems. No sensory involvement was found clinically. Characteristic wrist drop was observed in four cases, two of which also having motor nerve conduction velocity (MCV) delay. On the other hand, MCV of another case without wrist drop was normal. The possibility that wrist drop might be one of the clinical features of peripheral nerve dysfunction was discussed, but further pathologic evaluation of peripheral nerves is needed.

The Onuf's nucleus and the external anal sphincter muscles in amyotrophic lateral sclerosis and Shy-Drager syndrome.

The anterior sacral horns and external anal sphincter muscle were examined histologically with special reference to Onuf's nucleus in amyotrophic lateral sclerosis (ALS) and Shy-Drager syndrome. Onuf's nucleus and the external anal sphincter muscles were well preserved in ALS, but in Shy-Drager syndrome both structures showed marked degenerative changes. These findings suggest that Onuf's nucleus does not belong to the autonomic neurons, but to the motoneurons in anterior sacral horn, and it innervates the external sphincter muscles of the anus and urethra.

Effect of artificial gravity in space flight on protein and RNA content in anterior horn motoneurons of the rat spinal cord

Effect of artificial gravity in space flight on protein and RNA content in anterior horn motoneurons of the rat spinal cord

Erratum: Alteration in Connections Between Muscle and Anterior Horn Motoneurons After Peripheral Nerve Repair

In the report "Alteration in connections between muscle and anterior horn motoneurons after peripheral nerve repair" by T. M. Brushart and M.-M. Mesulam (9 May, p. 603), the key to cell types in Fig. 1 was inadvertently omitted. The dashed lines refer to (A) right peroneal, (B to D) postoperative, and (E) peroneal cells. The solid lines refer to (A) left peroneal, (B to D) control, and (E) tibial cells.

Erratum: Controversial Scientist Considers Leaving NCI

In the report "Alteration in connections between muscle and anterior horn motoneurons after peripheral nerve repair" by T. M. Brushart and M.-M. Mesulam (9 May, p. 603), the key to cell types in Fig. 1 was inadvertently omitted. The dashed lines refer to (A) right peroneal, (B to D) postoperative, and (E) peroneal cells. The solid lines refer to (A) left peroneal, (B to D) control, and (E) tibial cells.

Alteration in connections between muscle and anterior horn motoneurons after peripheral nerve repair.

The connections between the spinal cord and lower leg muscles of the rat are significantly altered by repair of the intervening sciatric nerve. Muscles supplied by the peroneal branch of the sciatic are innervated by fewer motoneurons after sciatic repair. Many of these neurons originally innervated the peroneal muscles, and others formerly served the antagonistic tibial muscles. Perikarya in the size range of alpha motoneurons regained peripheral connections with greater frequency than those in the gamma range. There are thus postoperative defects in the extent and specificity of alpha reinnervation as well as in the degree of gamma control.

Pathogenesis of human poliovirus infection in mice. II. Age-dependency of paralysis.

The mechanism of resistance of newborn mice to poliovirus-induced paralysis was studied by comparing regional virus replication in the adult and in the newborn central nervous systems (CNS) after intracerebral (ic) and intraspinal inoculation. Initial virus replication in the brains was similar in both age groups. Paralysis correlated with replication of virus in the spinal cord to a constant threshold, and this replication in newborns was delayed. Intraspinal inoculation of newborns eliminated the delay, indicating that neonatal anterior horn motor neurons were fully susceptible to infection. Cordectomy prevented the spread of virus, despite patent cerebrospinal fluid (CSF) pathways. Thus, poliovirus appeared to spread within the CNS via an axonal transport system. Known maturational changes in the fast transport system may explain the relative resistance of immature mice to poliovirus-induced paralysis.

Pathogenesis of Human Poliovirus Infection in Mice

Human poliovirus infection in mice was studied to determine the similarities to human poliomyelitis, the selective vulnerability of neurons to infection, the role of the immune response in age-dependent susceptibility, and possible viral persistence. Mice inoculated intracerebrally (ic) with the Lansing type 2 poliovirus developed a disease with clinical, pathological, and age-dependent features resembling human poliomyelitis. Adult mice had a shorter incubation period (50% paralysis, Day 8 vs. Day 13) and a higher incidence of paralysis (97% vs. 79%) than newborns. Only paralyzed animals had pathologic changes in the spinal cord, and these corresponded to the degree of paralysis. Fluorescent antibody staining showed that selective infection of neurons was most intense in the anterior horn motor neurons of the spinal cord. There was no extraneural virus replication and no systemic neutralizing antibody response. Cyclophosphamide immunosuppression enhanced rather than diminished disease, indicating that maturation of immune responses did not explain the relative resistance of newborns to paralysis.

Effect of pre- and postnatal protein-calorie undernutrition on RNA-content in rat motor neurons.

Changes in the RNA-content of isolated anterior horn motor neurons from the 7th cervical segment were studied during the postnatal development of pre- and postnatally undernourished, and normally nourished rats. The motor neurons of the anterior horn were isolated by micromanipulation from Carnoy-fixed sections. The neuronal RNA-content was determined by microchemical methods according to Edström (1964). The observation was made that moderate pre- and postnatal undernutrition does not alter the normal RNA-accumulation in anterior horn motor neurons during the preweaning period. After weaning the cellular RNA incorporation decreases but again reaches normal values at the age of 39 days. The present results are compared with those of a previous study (Haltia 1970) in which rats were severely undernourished postnatally.

Quantitative Cytochemical Studies of RNA in Experimental Mercury Poisoning. I. Changes in RNA Content

RNA content in single spinal ganglion neurons and anterior horn motoneurons from mercury intoxicated rats were analyzed by the cytochemical method of Edstrom. The cell volume of these nerve cells was measured by Mickelwright's method. It was found that in the spinal ganglion neurons, there was a continuous decrease in the RNA content after methylmercury poisoning. After inorganic mercury (HgCl2) intoxication, there was in initial decrease in RNA content followed by a partial regaining of RNA after prolonged intoxication. These changes in RNA content were believed to be independent of the morphological changes produced by mercury in these neurons. Except for the cell swelling detected after the first week of methylmercury intoxication, there was a general decrease in cell volume after intoxication by either mercury compound. In the anterior horn motoneurons, there was a moderate increase in RNA after mercury poisoning (organic or inorganic). Since morphological lesions were only observed in the nerve fibers but not in the nerve cell bodies of these neurons, this increase in RNA level was thought to be a reparative response to the axonal injuries produced by the mercury compounds. Only a slight decrease in cell volume was observed at late stages of the intoxication.

Protein Abnormalities in Neuromuscular Diseases—Part 1

<h3>Dr. W. King Engel (Moderator):</h3> We will begin the discussion of protein abnormalities in various neuromuscular diseases by first explaining our use of the term "neuromuscular diseases." Figure 1 is a diagram of what is called the "motor unit." The anterior-horn motor neuron (or lower motor neuron) lies in the anterior horn of the spinal cord, and the peripheral extension of that neuron goes out through the anterior root, through the peripheral nerve, to the terminal branches of that nerve cell. At the end of the terminal branches are the neuromuscular junctions, the connections between the nerve cell and the numerous muscle fibers, generally several hundred, that one neuron innervates. A motor neuron and the muscle fibers innervated by it comprise a "motor unit." Diseases that affect any part of the motor unit—that is, the anterior horn cell, peripheral nerve, neuromuscular junction, or muscle—are termed "neuromuscular diseases." In various conditions,