The mechanism of cytolysis by complement attack of nucleated cells(NC) is of special interest in comparison to that of red blood cells. It is known that NC death by membrane attack comples, C5b-9, is caused by many factors, i.e., efficiency of complex assembly, activation of intrinsic metabolic pathway by signal transduction, cytotoxic effect of the channel itself and natural repair ability. These factors suggest that colloid osmotic lysis, known in red blood cells, does not fully explain the complement-mediated cell death of NC. In this study, the authors investigated correlation between biochemical and morphological changes to prove "Ca2+-mediated metabolic death"8~13) representing a mechanism of NC death caused by C5b-9 attack. The L1210 cells, mouse leukemic cell line carrying small complement channel(TAC5b-91) were used in the experiments. The amounts of intracellular adenine nucleotides to extracellular Ca2+, ouabain, KC1 and dextran were analyzed by bioluminescence method using luminometer. Cell viability was checked by 0.4% trypan blue dye and LDH release. Morphological observation of TAC5b-91 was done by immunocytochemical staining and electron microscope. The results were as follows: 1) The release of ATP, ADP and AMP followed by cell death was rapid and progressive along the incubation time at 37 degrees C and it was accelerated in 1.5 mM of [Ca2+]0. 2) There was no evidence of ATP repairment in the TAC5b-91. 3) Extracellular KC1(150 mM), dextran(0.66 mM) and ATP supplement(0.2 microM) could not effectively inhibit ATP depletion and cell death. Ouabain(27 and 100 microM) enhanced cell death and could not completely prevent ATP loss. 4) Most of the mitochondria showed swelling, loss of cristae and Ca2+ deposit in matrix in the electron microscopic observation. Rapid, sustained and irreversible depletion of adenine nucleotides was due to Ca2+ deposit with destruction of mitochondria and also the leakage through transmembrane channels. Moreover this energy depletion was accelerated by high extracellular Ca2+ concentration. These results indicate that Ca2+-mediated, energy exhaustion is one of the mechanisms of the metabolic cell death by C5b-9 attack of NC.
Mice ; Animals

No abstract available.
Animals ; Immunohistochemistry* ; Neurons* ; Rats* ; Substantia Nigra*

Although the distribution of locus ceruleus terminals has been demonstrated in the fundus striati[nucleus accumbens septi] by light microscopy[Jones & Moore, 1977 ; Mason & Fibiger, 1979 ; Streit or et al., 1979 ; Groenewegen et al., 1980], the synaptic organization of its terminals was not clarified. The purpose of the present investigation was to demonstrate the direct monosynaptic connection of the locus ceruleus terminals to the neuronal elements of the fundus stirati, and to clarify the synaptic structures of its terminals by electron microscopy two days after unilateral electric coagulation of the locus ceruleus. In the ipsilateral fundus striati, many axon terminals undergone dark degeneration were observed. These degenerating terminals containing small clear vesicles have asymmetric synaptic contacts with dendritic spines. Already two days after locus ceruleus lesion, distinct features of terminal degenerations appeared in the fundus striati ; enlarged axon terminals with altered synaptic vesicles, decrease of synaptic vesicles detached from the synaptic site, multiplication of dense bodies and infiltration of floccular material. At the same time, a regressive change occurred in which astrocytic processes encircled totally degenerated synapses spiraled around the synaptic remnants. These observations indicate that monosynaptic noradrenertic afferent connections to the fungus striati are confirmed, and the locus ceruleus terminals characterized by small round vesicles might be formed asymmetrical axo-spinous synapses with spiny neurons in the fundus striati.
Animals ; Cats* ; Dendritic Spines ; Fungi ; Locus Coeruleus* ; Microscopy, Electron ; Neurons ; Presynaptic Terminals ; Synapses ; Synaptic Vesicles

Ulcerative colitis is a chronic, inflammatory disease of colon which is rare in Korea. In the course of ulcerative colitis numerous extraintestinal complication may develop on the joints, skin, liver, kidney, vessel, oral cavity and eyes. The most common ocular lesions complicated in patients with ulcerative colitis are episcleritis and iritis. And the cases of retinal vascular disease in associated with ulcerative colitis are extremely rare. We experienced nonischemic central retinal vein occlusion complicated in a patient with ulcerative colitis, who is 32-year-old male and complained decreased visual acuity and metamorphosis.
Adult ; Colitis, Ulcerative ; Colon ; Humans ; Iritis ; Joints ; Kidney ; Korea ; Liver ; Male ; Mouth ; Retinal Vein* ; Retinaldehyde ; Scleritis ; Skin ; Ulcer* ; Vascular Diseases ; Visual Acuity

Non-metrical morphologic variations of skull foramina were studied with 250 crania of Korean adults. Studied morphologic variationts were presence of supra-orbital foramen(33.3%), frontal foramen(27.7%), accessory infraorbital foramen(13.2%), accessory lesser palatine foramen(41.0%), Vesalius foramen (16.9%), Huschke foramen(18.8%), condylar canal(62.6%) and parietal foramen(49.8%). The ahsence of posterior ethmoidal foramen(0.2%), zygomaticofacial foramen(7.1%) and mastoid foramen(30.2%) was also observed. The variations were presence of the exsutural location of anterior ethmoidal foramen 30.8%), mastoid foramen(35.9%) and incomplete development of oval foramen(4.9%), foramen spinosum(9.6%), hypoglossal foramen(9.6%). And incidence of these variations were compared with 12 different geographical localitics.
Adult ; Humans ; Incidence ; Mastoid ; Rabeprazole ; Skull*

No abstract available.
Dopaminergic Neurons* ; Retina*

No abstract available.
Dopaminergic Neurons* ; Retina* ; Rodentia*

No abstract available.
Mastoid*

The role of glycine as an inhibitory neurotransmitter is well established, and glycinergic neurons appear to play an important role in the mammalian retinae[Ikeda & Sheardown, 1983 ; Bolz et al., 1985]. Though it has been reported that certain conventional and displaced amacrine cells and a few of bipolar cells are consistently labeled with anti-glycine antiserum in the mammalian retinae so far[W ssle et al., 1986 ; Pourcho & Goebel, 1987 ; Davanger et al., 1991 ; Yoo & Chung, 1992], little has been studied on the synaptic circuitry of glycinergic neurons to clarify mechanism of its action in the visual processing of the mammalian retinae. This study was conducted to localize glycinergic neurons and to define their synaptic circuitry in the rat retina by immunocytochemical method using anti -glycine antiserum. The results were as follows : 1. Glycinergic neurons of the rat retina were conventional and displaced amacrine cells, interstitial cells and bipolar cells. 2. Glycinergic amacrine cells could be subdivided into two types, that is, A II amacrine cells and other amacrine cells, according to their ultrastructures. Glycinergic A II amacrine and other amacrine cell processes comprised postsynaptic dyad at the ribbon synapse of rod bipolar axon terminals in the sublamina b of the inner plexiform layer of the retina. Glycinprgic A II amacrine cell processes made gap junctions with axon terminals of unlabeled invaginating cone bipolar cells in the sublamina b, and made chemical synapses onto axon terminals of unlabeled flat cone bipolar cells and onto dendrites of ganglion cells in the sublamina a of the inner plexiform layer. In the sublamina b of the inner plexiform layer, g1ycinergic amacrine cell processes were postsynaptic to axon terminals of unlabeled invaginating cone bipolar cells, and made chemical output synapses onto axon terminals of unlabeled invaginating cone bipolar and rod bipolar cells and onto the dendrites of ganglion cells. Such cases that pre- and post-synaptic processes of glycinergic amacrine cell processes were non- glycinergic amacrine cell processes were frequently observed throughout the inner plexiform layer. In some cases, glycinergic amacrine cell processes receiving synaptic inputs from other glycinergic amacrine cell process made synaptic outputs onto the non-glycinergic or glycinergic amacrine cell processes. 3. Glycinergic bipolar cells could be subdivided into invaginating and flat cone bipolar cells. Postsynaptic dyads of cone bipolar cells at the ribbon synapses were non-glycinergic amacrine and amacrine cell processes, glycinergic amacrine and amacrine cell processes, glycinergic amacrine and non-glycinergic amacrine cell processes, and dendrite and dendrite of ganglion cells. These results demonstrate that [1] glycinergic A II amacrine cell receiving synaptic input from rod bipolar cells inhibit flat cone bipolar cells and OFF ganglion cells via chemical synapse, and excite ON cone bipolar cells via electrical synapse ; thereby visual information in the darkness can be transmitted to ON ganglion cells via ON cone bipolar cells, and [2] glycine released from glycinergic neurons inhibits directly ON and OFF ganglion cells or indirectly ON and OFF ganglion cells via non-glycinergic amacrine or bipolar cells.
Amacrine Cells ; Animals ; Darkness ; Dendrites ; Electrical Synapses ; Ganglion Cysts ; Gap Junctions ; Glycine ; Neurons* ; Neurotransmitter Agents ; Presynaptic Terminals ; Rats* ; Retina* ; Synapses

During development of central nervous system, cell proliferation, cell migration, cell differentiation and cell death are required. It has been reported that a number of cells are dying during development in the mammalian retinae examined so far, but the pattern of cell death has not been clarified yet. In addition. little has been studied on cell proliferation after birth. This study was conducted to identify histogenesis, cell death and cell proliferation in the retinae of the developing rats by light and electron microscopic methods as well as by immunohistochemical method using anti-proliferating cell nuclear antigen [PCNA] antiserum. The results were as follows : 1. In the developing rat, from postnatal 0 through 7 days, retina consisted of ganglion cell layer, inner plexiform layer and neuroblast layer. Neuroblast layer could be subdivided into three sublaminae : sublamina a, sublamina b and sublamina p, from postnatal 3 through 7 days. 2. From postnatal 10 days, retina consisted of ganglion cell layer, inner plexiform layer, inner nuclear layer, outer plexiform layer and outer nuclear layer. 3. Cells undergoing degeneration were observed from postnatal 0 to 13 days, and patterns of cell death were apoptosis, cytoplasmic degeneration and autophagic degeneration. 4. PCNA-immunoreactivity was seen in the cells located in sublaminae b and p of the neuroblast layer at postnatal 0 and 1 days. From postnatal 3 days PCNA immunoreactivity decreased. At 7-day-old rat, PCNA-Immunoreactive cells scattered in the distal part of sublamina p of the neuroblast layer.No immunoreactivity was observed from postnatal 10 days. These results demonstrate that retinal cell proliferation ends at postnatal 7 days, and histogenesis of retina is completed at postnatal 10 days, and superfluous cells during retinal development are eliminated by apoptosis, cytoplasmic degeneration and autophagic degeneration.
Animals ; Apoptosis ; Cell Death* ; Cell Differentiation ; Cell Movement ; Cell Proliferation* ; Central Nervous System ; Cytoplasm ; Ganglion Cysts ; Parturition* ; Proliferating Cell Nuclear Antigen ; Rats* ; Retina* ; Retinaldehyde