The role of glial cells in synaptic function. (33/5057)

Glial cells represent the most abundant cell population in the central nervous system and for years they have been thought to provide just structural and trophic support to neurons. Recently, several studies were performed, leading to the identification of an active interaction between glia and neurons. This paper focuses on the role played by glial cells at the level of the synapse, reviewing recent data defining how glia is determinant in synaptogenesis, in the modulation of fully working synaptic contacts and in synaptic plasticity.  (+info)

Development of the chick olfactory nerve. (34/5057)

Gonadotropin releasing hormone (GnRH) is produced and secreted by neurons dispersed throughout the septal-preoptic and anterior hypothalamic areas in adult birds and mammals. These neurons, essential for a functional brain-pituitary-gonadal axis, differentiate in the olfactory placode, the superior aspect of which forms the olfactory epithelium. To reach their final placement within the brain, GnRH neurons migrate out of the epithelium and along the olfactory nerve to the CNS. This nerve is essential for the entrance of GnRH neurons into the CNS. Due to the importance of the nerve for the proper migration of these neurons, we have used immunocytochemistry, DiI labeling and 1 microm serial plastic-embedded sections to characterize the nerve's earliest development in the embryonic chick (stages 17-21). Initially (stage 17) the zone between the placode and prosencephalon is a cellular mass contiguous with the placode. This cluster, known as epithelioid cells, is positive for some but not all neuronal markers studied. The epithelium itself is negative for all neuronal and glial markers at this early stage. By stage 18, the first neurites emerge from the epithelium; this was confirmed at stage 19 by examination of serial 1 microm plastic sections. There is sequential acquisition of immunoreactivity to neuronal markers from stage 18 to 21. The glial component of the nerve appears at stage 21. Axons originating from epithelium, extend to the border of the CNS as confirmed by DiI labeling at stage 21. Small fascicles have entered the CNS at this stage. As previously reported, GnRH neurons begin their migration between stages 20-21 and have also arrived at the border of the brain at stage 21. Despite the penetration of neurites from the olfactory nerve into the CNS, GnRH neurons pause at the nerve-brain junction until stage 29 (2 1/2 days later) before entering the brain. Subsequent studies will examine the nature of the impediment to continued GnRH neuronal migration.  (+info)

Neuronal and glial localization of NR1 and NR2A/B subunits of the NMDA receptor in the human cerebral cortex. (35/5057)

N-Methyl-D-aspartate (NMDA) receptors play a critical role in many cortical functions and are implicated in several neuropsychiatric diseases. In this study, the cellular expression of the NMDAR1 (NR1) and NMDAR2A and B (NR2A and B) subunits was investigated in the human cerebral cortex by immunocytochemistry with antibodies that recognize the NR1 or the NR2A and B subunits of the NMDA receptor. In frontal (areas 10 and 46) and temporal (area 21) association cortices and the cingulofrontal transition cortex (area 32), NR1 and NR2A/B immunoreactivity (ir) were similar and were localized to numerous neurons in all cortical layers. NR1- and NR2A/B-positive neurons were mostly pyramidal cells, but some nonpyramidal neurons were also labeled. Electron-microscopic observations showed that NR1 and NR2A/B ir were similar. In all cases, labeling of dendrites and dendritic spines was intense. In addition, both NR1 and NR2A/B were consistently found in the axoplasm of some axon terminals and in distal astrocytic processes. This investigation revealed that numerous NMDA receptors are localized to dendritic spines, and that they are also localized to axon terminals and astrocytic processes. These findings suggest that the effects of cortical NMDA activation in the human cortex do not depend exclusively on the opening of NMDA channels located at postsynaptic sites, and that the localization of NMDA receptors is similar in a variety of mammalian species.  (+info)

Interference with the development of early generated neocortex results in disruption of radial glia and abnormal formation of neocortical layers. (36/5057)

Early generated layers of neocortex are important factors in forming the subsequent architecture of the cerebral cortex. To further explore the role of early generated cortex, we disrupted formation of an early generated cohort of cells by intraperitoneal injections of the mitotic inhibitor methylazoxymethanol (MAM) into pregnant ferrets timed to coincide with generation of subplate neurons in the ventricular zone. Our studies demonstrate that if early development of the neocortex is interrupted by injection of MAM during embryogenesis (on embryonic day 24 or 28; E24 or E28), a distinct laminar pattern fails to form properly in the parietal cortex. A reduced number of MAP2-positive cells were observed in the region of the subplate when compared with the number of MAP2-positive cells found in normal animals. Interference with the superficial neocortical layers that form later during development (on embryonic day 33) by appropriately timed MAM injections does not result in a severely disrupted laminar pattern. The interrupted laminar pattern that arises after early MAM injections coincides with distorted radial glial cells (identified by immunoreactivity to the intermediate filament protein, vimentin), which occur after early, but not late, MAM injections. Further analysis suggests that interference with early development of neocortex leads to premature differentiation of radial glial cells into astrocytes, as demonstrated by the presence of glial fibrillary acidic protein (GFAP). Experiments involving injections of the thymidine analog, bromodeoxyuridine (BRDU), demonstrated that 4 days after E24 MAM injection cells are generated and migrate into the thin cortical plate. By E38, however, cells continue to be generated in animals treated with MAM on E24 but do not reach their normal positions in the cortical plate. In addition, immunoreactivity using the CR50 antibody, which identifies presumptive Cajal-Retzius cells present in layer 1, demonstrates that the CR50-positive cells, normally precisely located in the outer portion of layer 1, are distributed in disarray throughout the thickness of the neocortex and intermediate zone in early MAM-treated animals, but not in those treated with MAM injections later during gestation. These findings are consistent with the idea that early generated layers are important in providing factors that maintain the environment necessary for subsequent neuronal migration and formation of neocortical layers.  (+info)

Pathogenesis and classification of massive periretinal proliferation. (37/5057)

Massive periretinal proliferation (MPP), a serious complication of retinal detachment, is caused by proliferation and fibrous metaplasia of cells mostly deriving from retinal pigment epithelium and retinal glial cells. Contracting fibrous membranes in the vitreous, and on and also under the retina, cause the intraocular changes of MPP. Early signs such as increased 'tobacco dust', pigmented and unpigmented clumps in the vitreous, and subtle preretinal and even retroretinal membranes are usually overlooked. The late signs such as starfolds, irregular retinal folds, circumferential folds, and funnel-shaped detachments are well known. The pathogenesis of the clinically visible signs is described, and a 4-stage classification of the disease is given.  (+info)

Membrane specializations of dentritic spines and glia in the weaver mouse cerebellum: a freeze-fracture study. (38/5057)

Electron microscopy of thin-sectioned and freeze-fractured preparations of the cerebellum of the weaver mouse indicates that the dendritic spines are morphologically identical to those of their normal littermates. The weaver dendritic spines have been characterized as "unattached" since the synaptic input from the parallel fibers is absent (8-10). The entire region around the dendritic spines is taken up by astrocytic processes in the weaver. The outer fracture face of a normal dendritic spine contains aggregations of 10-nm wide particles in the immediate postsynaptic region. Similar particle aggregations occur in the unattached spines of the weaver. Freeze-fracture preparations reveal rectilinear arrays of particles, having a 7-nm center-to-center distance in the glial membranes. Rectilinear arrays are apparently distributed throughout the astrocyte membrane.  (+info)

Extraventricular neurocytoma with ganglionic differentiation associated with complex partial seizures. (39/5057)

We report an unusual case of extraventricular ("cerebral") neurocytoma with ganglion cells located in the right temporal lobe in a 9-year-old girl with complex partial seizures and precocious puberty. CT showed a calcified mass with central cystic zones. MR imaging showed a markedly hyperintense predominately solid tumor on both T1- and T2-weighted images, without appreciable contrast enhancement. Cerebral neurocytomas are histologically benign and radical surgery is curative; they should be included in the differential diagnosis of temporal lobe tumors in children.  (+info)

Control of hippocampal morphogenesis and neuronal differentiation by the LIM homeobox gene Lhx5. (40/5057)

The mammalian hippocampus contains the neural circuitry that is crucial for cognitive functions such as learning and memory. The development of such circuitry is dependent on the generation and correct placement of the appropriate number and types of neurons. Mice lacking function of the LIM homeobox gene Lhx5 showed a defect in hippocampus development. Hippocampal neural precursor cells were specified and proliferated, but many of them failed to either exit the cell cycle or to differentiate and migrate properly. Lhx5 is therefore essential for the regulation of precursor cell proliferation and the control of neuronal differentiation and migration during hippocampal development.  (+info)