Components Of Central Nervous System Research Articles

Loss of central nervous system component of dopaminergic inhibition of prolactin secretion in patients with prolactin-secreting pituitary tumors.

The administration of l-dopa suppresses prolactin (PRL) secretion in normal subjects and in patients with hyperprolactinemia, although it is not known whether this effect, which requires the conversion of dopa to dopamine, is mediated peripherally or through the central nervous system. To distinguish between these effects, 10 normal subjects (6 male, 4 female) and 8 patients with hyperprolactinemia associated with pituitary tumors were given l-dopa, 0.5 g alone, or 0.1 g after a 24-h pretreatment with carbidopa, 50 mg every 6 h, which produces peripheral dopa decarboxylase inhibition. Similar degrees of PRL suppression were observed in normal subjects (basal plasma PRL 13+/-2 ng/ml) after l-dopa alone (48+/-4%) and after l-dopa plus carbidopa (58+/-6%). In patients with pituitary tumors and elevated plasma PRL (73+/-14 ng/ml), l-dopa alone led to PRL suppression comparable with that in normal subjects (47+/-6%). However, l-dopa plus carbidopa resulted in only minimal suppression of plasma PRL (19+/-4%) which was significantly less than after l-dopa alone (P < 0.001). Urinary homovanillic acid excretion, which reflected peripheral dopa decarboxylation was similar in controls and tumor patients after l-dopa both alone and after carbidopa pretreatment. Comparable suppression of PRL levels in response to a dopamine infusion (4 mug/kg per min for 3 h) was observed in controls and tumor patients. The results indicate that although peripheral conversion of exogenous dopa to dopamine can suppress PRL secretion, in normals, the central nervous system conversion of dopa to dopamine in the presence of peripheral dopa decarboxylase inhibition is sufficient to account for its PRL-suppressive effects. In contrast, patients with tumors, while retaining peripheral dopaminergic inhibitory effects on PRL secretion, exhibit a marked reduction of central dopaminergic inhibition of PRL secretion.

Distribution of the Thy-1 Antigen in Cellular and Subcellular Fractions of Adult Mouse Brain

Abstract By using a cytotoxicity inhibition assay employing AKR anti-C3H thymocyte antiserum, we have determined the degree of expression of the thy-1 antigen in fractions of adult mouse brain. As expressed as cytotoxicity inhibitory capacity per mg protein with C3H whole brain arbitrarily assigned a value of 1.0, the following values were found: C3H cerebral cortex, 5.8; C3H cerebral cortex synaptosomes, 2.5: C3H whole brain myelin, 0.65; C3H cerebral cortex neurons, 0.16; and C3H cerebral cortex mitochondria, 0.10. Neither C1300 neuroblastoma cells nor any AKR neural fraction had detectable levels of thy-1. The findings indicate that the thy-1 antigen is found mainly in mouse cerebral cortex and in synaptosomal fractions, whereas myelin fractions contain lower but perhaps significant amounts of thy-1. Cerebral cortex neurons, isolated by a method requiring a 90-min mild trypsinization at 37°C, did not display significant amounts of the thy-1 antigen. These results lend themselves to further study in the area of differentiation and development of central nervous system components and in the area of central nervous system immunopathology.

Protection against Experimental Allergic Encephalomyelitis with Peptides Derived from Myelin Basic Protein: Presence of Intact Encephalitogenic Site Is Essential

Experimental allergic encephalomyelitis (EAE) is a cell-mediated autoimmune response directed toward a component of central nervous system (CNS) tissue, myelin basic protein (BP). Injection of animals with either whole CNS tissue or purified BP in complete Freund's adjuvant (CFA) induces severe and usually fatal disease. Preimmunization of animals with BP in incomplete Freund's adjuvant (IFA) prevents EAE. We have examined the relative abilities of whole guinea pig BP and its fragments to protect guinea pigs from subsequent EAE induction. The data suggest that the presence of the intact encephalitogenic site (residues 113-121) in the molecules used for preimmunization is necessary but may not be sufficient for complete protection against EAE induction.

The origin and distribution of catecholaminergic axon terminals in the cerebral cortex of the turtle ( Chrysemys picta)

Numerous catecholaminergic (CA) axon terminals have been visualized in the dorsal cortex of the rostral half of the turtle ( Chrysemys picta) telencephalic vesicle by means of the Falck-Hillarp fluorescence histochemical method. The highest density of CA axon terminals is found within the outer 100 μm of the molecular layer which contains the superficial segments of the apical dendrites of the cortical cells. The CA terminals gradually become less abundant towards the hippocampal cortex medially and are scarce in the molecular layer of the piriform cortex laterally. The few CA axons ending in the piriform cortex are mainly arborized around the neuronal somata. Unilateral brain stem transections produced either at caudal midbrain or isthmus level result in a marked loss of CA terminals within the cerebral cortex and hypothalamic area of the turtle, on the lesioned side. In contrast, brain stem hemisections placed at various levels caudally to the isthmus produce a severe loss of CA terminals in the hypothalamic area but not in the cerebral cortex. It appears, therefore, that the cortical CA terminals in the turtle arise mainly from CA perikarya located at the isthmus level (nucleus dorsolateralis tegmenti) whereas the hypothalamic CA terminals originate principally from CA neurons located in the medulla. In the present study, both the ‘isthmo-cortical’ and ‘medullo-hypothalamic’ CA pathways of the turtle brain have been tentatively related to the mammalian ‘dorsal and ventral noradrenergic pathways’. As the morphological organization of ascending CA pathways to the cerebral cortex and hypothalamus is very similar in the turtle and mammals, it is postulated that these CA neuronal systems are phylogenetically ancient and thus constitute fundamental components of the vertebrate central nervous system.

Central neural components of the autonomic nervous system.

Central neural components of the autonomic nervous system.

Maturation and water composition of murine cerebrum, cerebellum, brain stem and spinal cord.

AbstractPercentage change in water content and total solids was determined for the developing murine brain for both males and females from birth to 120 days.The central nervous system was divided into four components: (1) cerebrum (2) cerebellum (3) brain stem (4) spinal cord. The percentage of water was determined by dessication for groups of five animals at each day from birth to 20 days and then at five‐day increments to day 60 and at day 90 and day 120.Plots of the per cent solids (water content) against body weight showed a linear relationship for all parts except the cerebellum. No sex differences were noted. The cerebellum showed an early rapid water loss with a changing rate to a linear curve as the animal matured.Growth data were submitted to asymptotic regression using a computer to fit a curve y = α+βρx when y is the per cent solid at time × (in days) and α, β, ρ the constants to be determined. All of the central nervous system components gave constants of the same order of magnitude.

A central nervous system component of epinephrine hyperglycemia.

At least half the hyperglycemic response (in hepatic venous blood) to intravenous epinephrine was found to be dependent on the integrity of the medulla oblongata caudal to the cerebellar peduncles. Transection of the medulla at the level of the fovea inferior unmasked a vagus-mediated hypoglycemic response to epinephrine. Changes in blood glucose concentration after epinephrine administration were independent of blood pressure and the base-line blood glucose levels. Microinjections of epinephrine into the floor of the fourth ventricle initiated an immediate hyperglycemic response without affecting blood pressure. It is concluded that only half the hyperglycemic response to epinephrine is due to direct peripheral action of epinephrine. The balance of the response is initiated by epinephrine-sensitive receptors in a hyperglycemic center in the floor of the fourth ventricle.

Radiographic identification of arthrogryposis multiplex congenita in utero.

Arthrogryposis multiplex congenita (multiple congenital rigid joints; amyoplasia congenita; myodystrophia fetalis deformans) is a condition characterized by varying degrees of joint contractures attributed to the effects of a dystrophic muscular disorder of unknown origin. Disturbances in the spinal cord, notably deficiency of anterior horn cells in the lumbosacral segments, indicate a possible central nervous system component. The interference with joint mobility is due to increased periarticular fibrous tissue. The skin and subcutaneous tissues are sometimes affected, but bone seems to escape except in so far as it is influenced by the muscular, cutaneous, and presumed central nervous system changes. Associated congenital malformations of the skull and spine, polydactyly, and hip dislocation are frequent concomitants. A hereditary factor may exist. The newborn infant with this condition characteristically presents relatively slender extremities with prominent joints fixed in flexion, extension, or both. Muscle weakness with hypotonia is attributed to loss of striated fibers and replacement by endomysial connective tissue. This is seen more often in the extensor groups (1,2). It appears that the abnormal fixation and attitude of the extremities might provide a diagnostic clue on pelvimetric or abdominal roentgenograms. Case Reports Case I. Baby B. was delivered by cesarean section from a mother in whom a polyhydramnios had been present for about two months. Abdominal roentgenograms a week before delivery revealed a single fetus in vertex presentation, with the head hyperextended. The vertebral column appeared intact, but it was noted that the legs were hyperextended on the thighs and that the thighs were flexed on the abdomen. The significance of this observation was not recognized prior to delivery. The maternal pelvic inlet was quite small, and cephalopelvic disproportion was diagnosed both clinically and radiologically. After delivery, it was apparent that the infant had arthrogryposis multiplex congenita and a spina bifida occulta with lumbosacral myelomeningocele. Radiographic examination revealed widening of the lumbosacral neural canal, with normal vertebral bodies. A flat soft-tissue mass about 4 cm. in diameter corresponded with the myelomeningocele. The acetabular rims were elevated, and both hips were dislocated upward and laterally. The legs were fixed in the position noted on the prepartum roentgenograms, but the bones of the lower extremities were not otherwise remarkable; the muscular components appeared reduced in size and were streaked with radiolucent areas believed to represent fatty infiltration. The patient was sent elsewhere for surgical treatment of the myelomeningocele. Case II. Baby S. was the first child of a 29-year-old woman in whom polyhydramnios was recognized about two months before delivery.

SYNDROME OF BILATERAL VESTIBULAR PARALYSIS AND ITS OCCURRENCE FROM STREPTOMYCIN THERAPY

THE DISTURBANCE of equilibrium caused by bilateral loss of vestibular function from streptomycin therapy appears to be basically similar to that of bilateral vestibular paralysis from other causes, whether the site of the lesion is in the peripheral or the central components of the vestibular nervous system. The syndrome of bilateral vestibular paralysis has rarely been noted in the literature, and not before its happening as an untoward effect of streptomycin therapy has there been an opportunity to observe a considerable number of patients with this syndrome from its onset and through the stages of its regression. The practice of prescribing smaller doses of streptomycin than formerly and of substituting other antibiotics with less neurotoxic effects makes the study of the symptomatology of the toxicity of streptomycin, including its pathologic foci, of importance chiefly in obtaining a better understanding of disorders of the function of the acoustic nerve as an

SELECTIVE UTILIZATION OF BARBITURATES

Since the introduction of barbital in 1903, hundreds of barbituric acid derivatives have been synthesized and studied both pharmacologically and clinically. While these derivatives resemble one another in action, their effects on the central nervous system are not identical. Some have more tendency to produce excitement than others. Their depressant actions on various components of the central nervous system differ. Variations are noted in onset, intensity and duration of action and in the fate of these substances in the body. Some act promptly, powerfully and briefly and are destroyed in the body. Others are slower in action and milder, act over longer periods of time and are in large part excreted unchanged. Qualitative differences among the barbiturates enable the clinician to select a specific barbiturate for a specific purpose, i. e., anticonvulsant, hypnotic, sedative or anesthetic. By the same token the physician should also take full advantage of the quantitative