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PubMed1995

Ependymal reactions to injury. A review.

The ependyma reacts to injury with a few stereotypical responses and does not regenerate at any age. Non-neoplastic ependymal cells do not undergo mitotic proliferation and do not re-express fetal cytoskeletal or secretory proteins. Atrophy of ependymal cells accompanies generalized cerebral atrophy. The ependyma may be damaged by stretching during ventricular dilatation, by infarcts of the ventricular wall or by infection and inflammation. Tearing of the epithelium leaves discontinuities that become filled with processes of subventricular astrocytes. In some cases reactive gliosis is minimal, but in most it is extensive and gliotic nodules form beneath intact ependyma and within gaps between ependymal islands. Ependymal rosettes may form in several ways: sequestration of diverticuli from the surface; curling of a torn edge or penetration of an edge into the parenchyma; reactive gliosis overgrowing an ependymal edge; in situ differentiation of ependymal cells from deep neuroepithelial cells. Migration and metaplasia are unlikely mechanisms. Bacterial and fungal ependymitis are highly destructive. Several viruses, especially mumps, selectively infect ependymal cells and are an important cause of acquired aqueductal stenosis without inflammation. Damaged ependyma may not be able to perform its function in the regulation of transport of fluid, ions and small molecules between cerebral parenchyma and ventricular fluid and thus may contribute to hydrocephalus. Damage to the fetal ependyma may result in secondary focal dysplasias of the developing brain.

Animals↗

PubMed2005

Ependymal denudation and alterations of the subventricular zone occur in human fetuses with a moderate communicating hydrocephalus.

In mutant rodents, ependymal denudation occurs early in fetal life, preceding the onset of a communicating hydrocephalus, and is a key event in the etiology of this disease. The present investigation was designed to obtain evidence whether or not ependymal denudation occurs in 16- to 40-week-old human fetuses developing a communicating hydrocephalus (n = 8) as compared to fetuses of similar ages with no neuropathologic alterations (n = 15). Sections through the walls of the cerebral aqueduct and lateral ventricles were processed for lectin binding and immunocytochemistry using antibodies against ependyma, astroglia, neuroblasts, and macrophages markers. Anticaveolin was used as a functional marker of the fetal ependyma. The structural and functional molecular markers are differentially expressed throughout the differentiation of the human fetal ependyma. Denudation of the ependyma of the aqueduct and lateral ventricles occurred in all fetuses developing a communicating hydrocephalus, including the youngest ones studied. The denuded surface area increased in parallel with the fetus age. The possibility is advanced that in many or most cases of human fetal hydrocephalus there is a common defect at the ependymal cell lineage leading to ependymal detachment. Evidence was obtained that in hydrocephalic human fetuses a process to repair the denuded areas takes place during the fetal life. In hydrocephalic fetuses, detachment of the ependyma of the lateral ventricles resulted in the (i) loss of the germinal ependymal zone, (ii) disorganization of the subventricular zone and, (iii) abnormal migration of neuroblasts into the ventricular cavity. Thus, detachment of the ependymal layer in hydrocephalic fetuses would not only be associated with the pathogenesis of hydrocephalus but also to abnormal neurogenesis.

Cerebral Aqueduct↗

PubMed2004

Cell proliferation in the lamprey central nervous system.

After spinal cord transection, axons regenerate both in larval and adult lampreys. It is not known to what degree cells proliferate, even in the uninjured animal. Therefore, we have determined the prevalence of mitosis in the lamprey central nervous system (CNS). Bromodeoxyuridine (BrdU) was injected and incorporated for 4 hours into 2- to 5-year-old larvae, animals undergoing metamorphosis, and young adults. Labeled cells were counted in the rhombencephalon (where most supraspinal projecting neurons are located) and spinal cord. A mitotic index (MI) was calculated as the percentage of nuclei that were labeled. There was a seasonal variation in mitotic activity, with higher MIs occurring in summer. Within the summer, there was an additional transient spike in mitosis, especially in the rhombencephalon. There was no correlation between age and MI within the range of developmental stages examined. Baseline MIs in the rhombencephalon and spinal cord were approximately 0.15% and 0.20%, respectively. In most animals, the highest mitotic rates in both the rhombencephalon and spinal cord were seen in the ependyma, but many labeled cells were found in nonependymal regions as well. During the summer spike, almost all of the additional mitosis in the rhombencephalon was in the ependyma, but this finding was not true in the spinal cord. Many BrdU-labeled cells in the spinal cord and rhombencephalon were also stained by monoclonal antibodies specific for lamprey glial keratin but were never labeled by anti-neurofilament antibodies. These results suggest that (1) neurogenesis is uncommon in the lamprey CNS; (2) during most of the year, baseline gliogenesis occurs mainly in the ependyma with substantial contribution by nonependymal areas. During the summer, a spike of mitotic activity occurs in the ependyma of the rhombencephalon and throughout the spinal cord.

Animals↗

PubMed1978

Development of the diencephalon in the rat. III. Ontogeny of the specialized ventricular linings of the hypothalamic third ventricle.

The development of the specialized linings of the hypothalamic third ventricle was examined autoradiographically in mature rats that were labelled with 3H-thymidine during the developmental period, and in a closely spaced series of embryonic and infant rats. We distinguished in mature rats, apart from the typical ependymal wall, three specialized linings: the convoluted ependyma, the laminated epithelium, and the tanycytic epithelium. The ventricular wall of most of the anterior hypothalamus, and of the dorsal portion of the posterior hypothalamus, is composed of ciliated ependymal cells and most of them are generated several days before birth, soon after the cessation of neurogenesis in the adjacent hypothalamic nuclei. The cells of the rostral convoluted ependyma adjacent to the paraventricular nucleus are produced at about the same time as the neighboring cells of the smooth ependyma. Its cells come from the same germinal region that we have assumed to generate the neurons of the magnocellular neurohypophysial secretory system. The structural differentiation of the convoluted ependyma starts after birth and is completed by the beginning of the second week. Many of the ependymal cells of the laminated epithelium are produced postnatally, and the production of the specialized cells that form a parallel subependymal row extends into the third week. These cells appear to arise from the same matrix that generates earlier the neurons of the dorsomedial and ventromedial hypothalamic nuclei; their structural differentiation begins during the second week. Also the cells of the tanycytic epithelium are produced mostly postnatally, predominantly during the first week. They appear to arise from the same matrix that generated earlier the neurons of the hypophysiotropic tuberomammillary and arcuate nuclei. It is postulated that these three specialized ventricular linings are specifically related to the three cpmponents of the endocrine hypothalamus with which they have shared neuroepithelial sites of origin.

Animals↗

PubMed1976

Morphological aspects of the hypothalamic-hypophyseal system. VI. The tanycytes: their relation to the sexual differentiation of the hypothalamus. An enzyme-histochemical study.

Enzyme-histochemical methods were used to study the metabolic activity of specialized ependyma of the ventrolateral walls and floor of the third ventricle in young male and female rats during the "critical period" of sexual differentiation of the hypothalamus (one week after birth). Histochemical tests were conducted for glutamic dehydrogenase, lactic dehydrogenase, glucose-6-phosphate dehydrogenase, glycerophosphate dehydrogenase and NADH2-dehydrogenase. Enzyme activity was judged by cytospectrophotometry. All the data were treated statistically. It was found that the specialized ependyma of the ventrolateral wall and floor of the third ventricle (median eminence) in rats differed in their enzyme behaviour in males and females during the "critical period" of sexual differentiation of the hypothalamus. At the level of the arcuate nucleus (alpha2-tanycytes) and the medial part of the median eminence (beta2-tanycytes) the ependyma was characterized by similar indices of metabolic activity in males and females in the decisive terms of the "critical period" (days 3, 5, and 7). On day 5 metabolic activity of these cells was reduced both in the males and in the females. Prominent sexual differences in the intensity of the enzyme reactions studied were noted in the ependyma of the lateral parts of the median eminence (beta1-tanycytes) in the "critical period". On day 5 metabolic activity of beta1-tanycytes was reduced in males and increased in females. It is suggested that these differences are caused by the receptor nature of beta1 tanycytes and suggest their implication in the mechanisms of sexual differentiation of hypothalamus.

Animals↗

PubMed1976

Immuno-histochemical localization of LH-RH during different phases of estrus cycle of rat, with reference to the preoptic and arcuate neurons, and the ependymal cells.

Immunohistochemical localization of luteinizing hormone-releasing hormone (LH-RH), during different phases of the estrus cycle, in the preoptic, suprachiasmatic and arcuate nuclei, and in the OVLT of rats, with special emphasis on the ependymal cells, was studied by light, fluorescent and electron microscopy, by using rabbit anti serum to synthetic LH-RH. The LH-RH neurons in the above mentioned areas, were very active during late diestrus and early proestrus phases. Specialized ependymal cells bordering the 3rd ventricle also showed varied LH-RH positive reaction during different phases of the estrus cycle. Immunofluorescent studies showed cyclic variations in the LH-RH material in the CSF of the preoptic and infundibular recesses, as well as in the 3rd ventricle near OVLT, in that, it was maximum during late diestrus and early proestrus phases. Immediately after this, the LH-RH late proestrus was reached. We have also observed that during the proestrus phase, as the LH-RH material started declining in the CSF, it had started building up in the specialized ependyma. Estrus, metaestrus and early diestrus phases showed very weak immunofluorescent LH-RH material in the lumen of the infundibular recess and in the specialized ependyma. Our immuno-electron microscopic observations showed pleomorphic LH-RH granules in the specialized ependyma during late kiestrus and proestrus phases. All these observations lead us to believe that LH-RH is not synthesized in the ependymal cells,but is phagocytosed from the CSF of the 3rd ventricle by the specialized ependyma, which transports it to the ME portal system. In males, the fluorescent LH-RH material did not show any noticeable changes. With the present and previous work,it is concluded that the neurons in differentnuclei synthesize LH-RH and transport it to the ME portal system,primarily through the nerve fibers and secondarily by the ventricular route. It is also suggested that the ependymal transport of LH-RH to the ME portal system is cyclic and thus controls the gonadotropin secretion.

Animals↗

PubMed1995

Antibody-mediated lysis of the bovine subcommissural organ maintained in culture.

The subcommissural organ (SCO) is a brain gland that secretes glycoproteins into the cerebrospinal fluid (CSF). It is an ancient and conserved secretory structure of the brain, developing very early in ontogeny. However, the function of the SCO is unknown. The secretory cells of the SCO are arranged into a single or double, irregularly shaped layer located at the interface of the CSF and nervous tissue. This has prevented its selective surgical destruction. The present investigation was designed to destroy the secretory cells of 30-day-old explants of bovine SCO by use of an immunological approach. A membrane preparation enriched with plasma membrane of the secretory cells of the bovine SCO was obtained. This preparation was further processed to separate the structural proteins. A similar procedure was applied to obtain a fraction of integral proteins of the plasma membrane of a nonsecretory ciliated ependyma. Antisera were prepared against both preparations of integral proteins. The antiserum against the fraction obtained from the SCO cells immunostained the plasma membrane of the bovine SCO cells and in immunoblot it reacted with several proteins of the membrane preparation from SCO cells. When added to the culture medium this antibody bound to the apical plasma membrane of the secretory ependyma of the bovine SCO kept in culture; it caused the lysis of these cells when used together with complement. None of these properties were displayed by the antiserum raised against the integral proteins of the plasma membrane of the ciliated ependyma. This antiserum, however, immunostained the bovine ciliated ependyma neighboring the SCO. These results indicate that immunological surgery of the SCO in living animals may be possible to achieve.

Animals↗

PubMed1979

Axonal-ependymal associations during early regeneration of the transected spinal cord in Xenopus laevis tadpoles.

The nature and organization of the cellular substrate supporting axonal outgrowth during early regeneration of the spinal cord following transection and/or segment removal were examined in Xenopus tadpoles. Longitudinal axonal compartments, formed by radial ependymal processes in unoperated spinal cords, were maintained within the rostral and caudal stumps throughout the early post-operative period. The first neuritic sprouts to appear near the cut ends of the cord were frequently associated with these processes. Between 5 and 7 days after transection either single or multiple cellular aggregates, which consisted primarily of ependyma, began occupying the lesion zone and were encompassed by numerous small fibres. Ependymal processes subsequently extended among the neurites within the lesion gap and re-established longitudinal axonal channels and a surrounding glia limitans. A concurrent outgrowth of fibres and ependyma from the rostral and caudal stumps was also initiated by 5-7 days following resection of the cord. Axons were seen further within the ablation gap at 10 and 12 days either coursing along the surfaces of the emerging ependyma or organized into small fascicles by the radial processes of these cells. Intermediate stages of axonal fasciculation by the underlying ependyma were also seen. In contrast with previous reports, axonal elongation beyond the cut ends of the cord did not consistently entail the formation of pre-existing ependymal channels. These observations provide additional evidence emphasizing the importance of the ependymal cell surface during axonal outgrowth in the regenerating spinal cord. Guided neuritic elongation, however, does not appear to be dependent upon the prior establishment of a specific type of cytoarchitecture.

Animals↗

PubMedDate not supplied

Regional ependymal upregulation of vimentin in Chiari II malformation, aqueductal stenosis, and hydromyelia.

Vimentin, glial fibrillary acidic protein (GFAP) and S-100beta protein were studied by immunocytochemistry in the ependyma of patients with Chiari II malformations, congenital aqueductal stenosis, and hydromyelia. Paraffin sections of brains and spinal cords of 16 patients were examined, 14 with Chiari II malformations, most with aqueductal stenosis and/or hydromyelia as associated features, and 2 patients with congenital aqueductal stenosis without Chiari malformation. Patients ranged in age from 20-wk gestation to 48 years. The results demonstrated: 1) in the fetus and young infant with Chiari II malformations, congenital aqueductal stenosis, and hydromyelia, vimentin is focally upregulated in the ependyma only in areas of dysgenesis and not in the ependyma throughout the ventricular system; 2) GFAP and S-100beta protein are not coexpressed, indicating that the selective upregulation of vimentin is not simple maturational delay; 3) vimentin upregulation also is seen in the ependymal remnants of the congenital atretic cerebral aqueduct, not associated with Chiari malformation; 4) in the older child and adult with Chiari II malformation, vimentin overexpression in the ependyma becomes more generalized in the lateral ventricles as well, hence evolves into a nonspecific upregulation. The interpretation from these findings leads to speculation that it is unlikely that ependymal vimentin is directly involved in the pathogenesis of Chiari II malformation, but may reflect a secondary upregulation due to defective expression of another gene. This gene may be one of rhombomeric segmentation that also plays a role in defective programming of the paraxial mesoderm for the basioccipital and supraoccipital bones resulting in a small posterior fossa. This interpretation supports the hypothesis of a molecular genetic defect, rather than a mechanical cause, as the etiology of the Chiari II malformation.

Acridine Orange↗

PubMed1975

On the pathology of experimental hydrocephalus.

Acute hydrocephalus was produced in newborn rabbits by injection of kaolin into the cisterna magna. The light microscopic changes which occurred in the ependyma and periventricular brain tissue were studied. Some animals also received intraventricular injection of Evans blue albumin (EBA) at various times after the kaolin injection to study the permeability of the ependyma. There was a progressive dilatation of the lateral ventricles from the second day after the kaolin injection. Marked hydrocephalus was seen after 2 weeks. The white matter of the cerebral hemispheres showed increasing reduction in volume with the degree of hydrocephalus. Neither destruction of brain tissue nor macrophage response or inflammation were seen. The ependyma adapted remarkably well to the increased intraventricular pressure by extensive flattening and stretching. No convincing breaks or ruptures were seen. There was a patchy spongy zone beneath the ependyma, probably indicating oedema of the periventricular white matter due to transventricular absorption of the cerebrospinal fluid (CSF). Denudement of the ependymal lining is not necessary for the concept of transventricular flow of CSF. No difference was seen in the penetration of EBA into the periventricular tissue between hydrocephalic and control animals. The reduction of the cerebral mantle thickness was probably caused by simple pressure atrophy. This indicates that the morphological changes may to a large extent be reversible if the hydrocephalus is properly treated within reasonable time. The role of morphological changes in the pathophysiology of hydrocephalus if briefly commented upon in relation to certain aspects of human hydrocephalus.

Animals↗

PubMed2005

Proliferation, migration, and differentiation of endogenous ependymal region stem/progenitor cells following minimal spinal cord injury in the adult rat.

Ependymal cells of the adult mammalian spinal cord exhibit stem/progenitor cell properties following injury. In the present study, we utilized intraventricular injection of 1,1'-dioctadecyl-6,6'-di(4-sulfophenyl)-3,3,3',3'-tetramethylindocarbocyanine (DiI) to label the ependyma lining the central canal to allow tracking of the migration of endogenous ependymal cells and their progeny after spinal cord injury (SCI). We developed a minimal injury model that preserved the integrity of the central canal and did not interfere with ependymal cell labeling. Three days following SCI, there was an 8.6-fold increase in the proliferative labeling index of the ependymal cells at the level of the needle track based on bromodeoxyuridine labeling, compared with 1 day post-injury. Terminal deoxynucleotidyl transferase-mediated dUTP nick end labeling (TUNEL) positive cells were not detected in the ependyma or surrounding gray matter, indicating that ependymal cells do not undergo apoptosis in response to minimal injury. Nestin was rapidly induced in the ependyma by 1 day and expression peaked by 7 days post-injury. We quantitated the number and distance of ependymal cell migration following minimal injury. The number of ependymal cells migrating from the region of the central canal increased by 3 days following minimal injury and DiI-labeled glial fibrillary acidic protein expressing cells were detected 14 days post-SCI, most of which migrated within 70 microm of the region of the central canal. These results show that a minimal SCI adjacent to the ependyma is sufficient to induce an endogenous ependymal cell response where ependymal stem/progenitor cells proliferate and migrate from the region of the central canal, differentiating primarily into astrocytes.

Animals↗

PubMed2003

Cellular mechanisms involved in the stenosis and obliteration of the cerebral aqueduct of hyh mutant mice developing congenital hydrocephalus.

Two phases may be recognized in the development of congenital hydrocephalus in the hyh mutant mouse. During embryonic life the detachment of the ventral ependyma is followed by a moderate hydrocephalus. During the first postnatal week the cerebral aqueduct becomes obliterated and a severe hydrocephalus develops. The aim of the present investigation was to elucidate the cellular phenomena occurring at the site of aqueduct obliteration and the probable participation of the subcommissural organ in this process. Electron microscopy, immunocytochemistry, and lectin histochemistry were used to investigate the aqueduct of normal and hydrocephalic hyh mice from embryonic day 14 (E-14) to postnatal day 7 (PN-7). In the normal hyh mouse, the aqueduct is an irregularly shaped cavity with 3 distinct regions (rostral, middle, and caudal) lined by various types of ependyma. In the hydrocephalic mouse, these 3 regions behave differently; the rostral end becomes stenosed, the middle third dilates, and the caudal end obliterates. The findings indicate that the following sequence of events lead to hydrocephalus: 1) denudation of the ventral ependyma (embryonic life); 2) denudation of dorsal ependyma and failure of the subcommissural organ to form Reissner fiber (first postnatal week); 3) obliteration of distal end of aqueduct; and 4) severe hydrocephalus. No evidence was obtained that NCAM is involved in the detachment of ependymal cells. The process of ependymal denudation would involve alterations of the surface sialoglycoproteins of the ependymal cells and the interaction of the latter with macrophages.

Aging↗

PubMed1977

[Morphological studies of the matrix in human hypothalamus].

The variations of matrix and ependyma in the hypothalamus was histologicaly investigated in 120 human brains of both sexes from the 13 week old fetuses up to the end of the first year of postnatal life. The plane of cuts were in the region of the anterior hypothalamic nucleus, of the ventromedial nucleus, and the arcuate nucleus. We have found that the exhaustion of the matrix begins in the 14 week old embryo in the anterior and medial hypothalamus. A subependymale zone is present in these areas in the 17 week old embryo and exists up to 23 week. The one-cell-layer ependyma appears in the anterior are of the ventromedial nucleus at first in the 24 week week old embryo. After this the ependyma appears from the 25 to the 28 week old embryo in the regions of the anterior hypothalamic nucleus and the other areas of the ventromedial nucleus. In the immediate surrounding of the arcuate nucleus we observed the first alterations in the 15 week old embryo. The exhaustion of matrix is a continuous process up to the 23rd week. The boundary of the third ventricle remained to be a multilayer and in all stages of development cells were found, which reach into the lumen. Only after birth the multilayer boundary was reduced. At the end of the first year of postnatal life the one-layer ependyma was developed at a few sites. We could not find any significant variations of matrix exhaustion in the different sexes.

Ependyma↗

PubMed1994

The ventricular system of the pigeon brain: a scanning electron microscope study.

The fine structural features and regional differences of the ependyma in adult pigeons have been investigated by scanning electron microscopy. Pigeons of either sex were fixed with buffered glutaraldehyde (3%) and formaldehyde (0.5%) by intravascular perfusion. The brain was dissected using section planes adequate to expose each part of the ventricular system. The specimens were then dehydrated, critical point dried and sputtered with gold. Depending upon the distribution of cilia, microvilli and single cilia, different areas were recognised in the 4 ventricles. The topographic locations of these areas were determined using the atlas of Karten & Hodos (1967). The medial surfaces of the 1st and 2nd lateral ventricles are more densely ciliated than the lateral surfaces. In the floor of the 4th ventricle the medial part is less ciliated than the lateral parts. The circumventricular organs (subseptal organ, organum vasculosum of the lamina terminalis, infundibulum, choroid plexus, subcommissural organ, area postrema) show very characteristic surfaces and are surrounded by a transitional zone with the nonspecialized ependyma. In contrast, in the paraventricular organ the transition to the nonspecialized ependyma is rather abrupt. The ependyma covering the trochlear nucleus appears densely ciliated, differing from that of the classic circumventricular organs. Finally, the existence of openings in the caudal medullary velum, which represent direct communications between the ventricles and the subarachnoid space, was demonstrated.

Animals↗

PubMed1976

[Cytophotometric correlation of changes in the RNA and protein concentrations of perineuronal oligodendrogliocytes and ependymal cells of the spinal cord under different experimental conditions].

By means of ultraviolet and visible cytospectrophotometry, RNA and total protein content per cell was determined in perineuronal oligodendrogliocytes of spinal cord anterior horns and in ependyma cells of spinal cord central canal in Wistar rats under various experimental conditions. It was only in one experimental series that the cell kinds compared were characterized by a similar metabolic response: daily adrenaline injections for two weeks resulted in RNA accumulation both in the oligodendroglia and in the ependyma: besides, in both the kinds of spinal cord cells, no changes in RNA amount was found due to acute hypoxic hypoxia and to 6-mercaptopurine administration. In all the other experimental series (aurantin adminstraion: adrenalectomy and hydrocortison treatment; posthypoxic reparation), changes in RNA content markedly differed in the oligodendroglia and in the ependyma. The data are presented concerning the changes in protein content in the cytoplasm of spinal cord ependyma cells under the experimental conditions applied. Importance of topochemical analysis of nervous tissue structures by means of quantitative cytochemical methods is outlined.

Adrenalectomy↗

PubMed1995

A concept of the development of the mammalian rhombencephalon based on physical rotational forces.

The premammalian forms do not show the metencephalic and myelencephalic divisions of the rhombencephalon. The seven longitudinal grey columns, in relation to the seven nerve components are direct cranial uninterrupted continuations from the spinal cord. The isthmus rhombencephali is a tubular structure. The phylogenetically ancient ependyma rich in tanycytes lines the fourth ventricle. The neural canal does not open into the subarachnoid space and the ependyma never becomes directly continuous with the pia mater. On the other hand, in mammals, the rhombencephalon is divided into the metencephalon and myelencephalon. The seven longitudinal grey columns get fragmented and their cell masses undergo migrations. The isthmus loses its tubular nature and undergoes modifications. The fourth ventricle opens into the subarachnoid space through three openings. The phylogenetically ancient ependyma is retained as a continuous structure only along the inferolateral angle of the fourth ventricle. At the openings of the lateral recesses, the ependyma becomes directly continuous with the pia, a neural crest derivative. The oval bundle, the corpus trapezoideum and the myelencephalic component of the nuclei pontis show extensive migrations. The above phenomena can be explained by physical rotation forces and not merely by migrations.

Animals↗

PubMed1974

Physiological and morphological identification of hypothalamic magnocellular neuroendocrine cells in goldfish preoptic nucleus.

1. Intracellular recordings were made from antidromically identified neurones in the goldfish preoptic nucleus and Procion Yellow was ejected from the recording pipette, marking these magnocellular neuroendocrine cells diffusely, for histological identification.2. In confirmation of earlier studies these preoptic neuroendocrine cells showed resting membrane potentials of 47 mV, action potentials up to 85 mV, action potentials of long duration (3.9 msec) occurring in two steps, long-lasting hyperpolarizing after-potentials and orthodromic driving from olfactory input.3. Magnocellular neuroendocrine cells exhibited all-or-none jumps to shorter antidromic latencies as pituitary stimulus strength increased, suggesting multiple branching of the ;axones' either near the preoptic nucleus or within the neural lobe.4. I find three morphological types of neuroendocrine cells throughout the magnocellular part of the preoptic nucleus. Cell Type I is a large (37 mum), multipolar neurone, 48 mum from the ependyma, with fine ;dendrites' projecting into the lateral hypothalamus and within the preoptic nucleus, with multiple branched ;axones'. Cell Type II is a large (31 mum), multipolar neurone, 24 mum from the ependyma, with a coarse ;dendrite' to the ependyma and fine ;dendrites' within the preoptic nucleus, with limited ;axonal' branching. Cell Type III is a small (18 mum), multipolar neurone, 46 mum from the ependyma, with fine ;dendritic' processes distributed within the preoptic nucleus, with limited ;axonal' branching.5. I conclude that magnocellular neuroendocrine cells show electrical membrane properties of other central neurones with both physiological and morphological evidence for multiple ;axonal' branching. The three identifiable neuroendocrine cell types (I, II, III) are distributed widely within the anatomical limits of the preoptic nucleus, pars magnocellularis, with each type receiving ;specific' input connexions and with unique output pathways. I suggest that these three types of neuroendocrine cells may be related to the ;cellular' secretion of ;specific' neurohypophysial hormones and neurophysins.

Action Potentials↗

PubMed1979

Autoradiographic studies on the incorporation of tritiated uridine, leucine and methionine into Gomori-positive glia of rat hypothalamus.

The relative level of metabolic activity in Gomori-positive (Gp) glia was estimated by comparing the incorporation rates of 3H-uridine, 3H-leucine and 3H-methionine into the nuclear macromolecules of the glia, neurons, ependyma and subcommissural organ (SCO). The uptake of 3H-uridine by Gp glia was somewhat lower than that by neurons and SCO but higher than that by ependyma. The incorporation of 3H-leucine was about the same in all studied types of cells, except for a lower uptake by ependyma. The rate of 3H-methionine incorporation into Gp glia and SCO was higher than that into neurons and ependyma. The neuron: Gp glia ratios obtained in the present study (0.9--1.4) are more or less within the range of the neuron: cerebral glia ratios reported by others for newly synthesized molecules of RNA and proteins. The results suggest that Gp glia have a relatively high metabolic activity as compared to that in neurons and perhaps SCO.

Animals↗