Nestin expressing progenitor cells during establishment of the neural retina and its vasculature / 대한해부학회지

In order to test if nestin is a useful marker for various types of progenitor cells, we explored nestin expression in the retina during development. Nestin expression was co-evaluated with bromodeoxyuridine (BrdU) labeling and Griffonia simplicifolia isolectin B4 (GSIB4) histochemistry. Nestin immunoreactivity appears in cell soma of dividing neural progenitor cells and their leading processes in retinas from embryonic day (E) 13 to E20, in accordance with a BrdU-labeled pattern. At postnatal day (P) 5, it is restricted to the end feet of Muller cells. BrdU-labeled nuclei were mainly in the inner part of the inner nuclear layer in postnatal neonates. The retinal vessels demarcated with GSIB4-positive endothelial cells were first distributed in the nerve fiber layer from P3. Afterward the vascular branches sprouted and penetrated deeply into the retina. The endothelial cells positive for GSIB4 and the pericytes in the microvessels were additionally immunoreactive for nestin. Interestingly, the presumed migrating microglial cells showing only GSIB4 reactivity preceded the microvessels throughout the neuroblast layer during vascular sprouting and extension. These findings may suggest that nestin expression represents the proliferation and movement potential of the neural progenitor cells as well as the progenitor cells of the endothelial cell and the pericyte during retinal development. Thus, Muller glial cells might be potential neural progenitor cells of the retina, and the retinal microvasculature established by both the endothelial and the pericyte progenitor cells via vasculogenesis along microglia migrating routes sustains its angiogenic potential.

Morphological and functional evaluation of an animal model for the retinal degeneration induced by N-methyl-N-nitrosourea / 대한해부학회지

The retinal degeneration (RD) is a general cause of blindness. To study its pathophysiology and evaluate the effects of new therapeutic agents before clinical trials, it is essential to establish reliable and stable animal models. This study evaluated a RD animal model in which blindness was induced by N-methyl-N-nitrosourea (MNU), a potent retinotoxin leading to apoptosis of photoreceptors. MNU was applied to the Sprague-Dawley rats by a single intraperitoneal injection in different doses (40, 50, and 60 mg/kg). The retinal functions were examined at 1 week after MNU injection by electroretinogram (ERG). Afterwards, each retina was examined by hematoxylin and eosin stain and immunohistochemistry with anti-glial fibrillary acidic protein antibody. Upon MNU injection of 40, 50 and 60 mg/kg, the ERG amplitude of a-waves showed significant reductions of 7, 26, and 44%, respectively, when compared to that of normal a-waves. The b-wave amplitudes were about 89, 65, and 58% of normal b-waves in the response to scotopic light stimulus. At 1 week, 2 weeks, and 4 weeks after MNU injection (50 mg/kg), all scotopic ERG components decreased progressively. In addition, degeneration of retinal neurons was observed in a time- and dose-dependent manner after MNU injection. Taken together, functional reduction following RD induced by MNU correlates with morphological changes. Thus, this RD rat model may be a useful model to study its pathophysiology and to evaluate the effects of new therapeutic agents before clinical trials.

Immunochemical changes of calbindin, calretinin and SMI32 in ischemic retinas induced by increase of intraocular pressure and by middle cerebral artery occlusion / 대한해부학회지

The reaction of neuroactive substances to ischemic conditions in the rat retina evoked by different methods was immunochemically evaluated in adult Sprague-Dawley rats. Ocular ischemic conditions were unilaterally produced by elevating intraocular pressure (EIOP) or by middle cerebral artery occlusion (MCAO). Two EF-hand calcium binding proteins, calbindin D28K (CB) and calretinin (CR), in the normal retina showed similar immunolocalization, such as the amacrine and displaced amacrine cells, the ganglion cells, and their processes, particularly CB in horizontal cells. CB immunoreactive neurons in the ganglion cell layer in both types of ischemic retinas were more reduced in number than CR neurons compared to those in a normal retina. The CB protein level in both ischemic retinas was reduced to 60-80% of normal. The CR protein level in MCAO retinas was reduced to about 80% of normal but increased gradually to the normal value, whereas that in the EIOP showed a gradual reduction and a slight recovery. SMI32 immunoreactivity, which detects a dephosphorylated epitope of neurofilaments-M and -H, appeared in the axon bundles of ganglion cells in the innermost nerve fiber layer of normal retinas. The reactivity in the nerve fiber bundles appeared to only increase slightly in EIOP retinas, whereas a moderate increase occurred in MCAO retinas. The SMI32 protein level in MCAO retinas showed a gradual increasing tendency, whereas that in the EIOP showed a slight fluctuation. Interestingly, the MCAO retinas showed additional SMI32 immunoreactivity in the cell soma of presumed ganglion cells, whereas that of EIOP appeared in the Muller proximal radial fibers. Glial fibrillary acidic protein (GFAP) immunoreactivity appeared in the astrocytes located in the nerve fiber layer of normal retinas. Additional GFAP immunoreactivity appeared in the Muller glial fibers deep in EIOP retinas and at the proximal end in MCAO retinas. These findings suggest that the neurons in the ganglion cell layer undergo degenerative changes in response to ischemia, although EIOP retinas represented a remarkable Muller glial reaction, whereas MCAO retinas had only a small-scaled axonal transport disturbance.

Ribbon Synapses Formed at the Axon of the Calbindin-Immunoreactive ON Cone Bipolar Cell in OFF Sublamina of the Inner Plexiform Layer in the Rabbit Retina / 체질인류학회지

Some retinal neurons, including intrinsically photosensitive retinal ganglion cells have their dendrites stratified in sublamina a of the inner plexiform (IPL), the OFF sublayer, but paradoxically show light-driven ON electrophysiological responses. In order to understand the mechanism on this paradoxical response, by using immunoelectron microscopy with a specific antibody against calbindin, we examined the synaptic connections of the calbindin-immunoreactive ON cone bipolar cell of the rabbit retina, which is thought to make the ribbon synapse in sublamina a of the IPL. The ribbon synapses in sublamina a by calbindin-immunoreactive ON cone bipolar cells were mainly found at the border between the inner nuclear layer and the IPL. Interestingly, the output targets at these ribbon synapses turned out as monads, and multiple synaptic ribbons were engaged in each synapse. These findings were different from those at the conventional ribbon synapse formed by calbindin-immunoreactive ON cone bipolar axon terminals. Thus, these findings may be the characteristics of the calbindin-immunoreactive ON cone bipolar ribbon synapse in sublamina a and can be used to classify the synapse in the retinal circuit research.

Changes in transcript and protein levels of calbindin D28k, calretinin and parvalbumin, and numbers of neuronal populations expressing these proteins in an ischemia model of rat retina / 대한해부학회지

Excessive calcium is thought to be a critical step in various neurodegenerative processes including ischemia. Calbindin D28k (CB), calretinin (CR), and parvalbumin (PV), members of the EF-hand calcium-binding protein family, are thought to play a neuroprotective role in various pathologic conditions by serving as a buffer against excessive calcium. The expression of CB, PV and CR in the ischemic rat retina induced by increasing intraocular pressure was investigated at the transcript and protein levels, by means of the quantitative real-time reverse transcription-polymerase chain reaction, western blot and immunohistochemistry. The transcript and protein levels of CB, which is strongly expressed in the horizontal cells in both normal and affected retinas, were not changed significantly and the number of CB-expressing horizontal cells remained unchanged throughout the experimental period 8 weeks after ischemia/reperfusion injury. At both the transcript and protein levels, however, CR, which is strongly expressed in several types of amacrine, ganglion, and displaced amacrine cells in both normal and affected retinas, was decreased. CR-expressing ganglion cell number was particularly decreased in ischemic retinas. Similar to the CR, PV transcript and protein levels, and PV-expressing AII amacrine cell number were decreased. Interestingly, in ischemic retinas PV was transiently expressed in putative cone bipolar cell types possibly those that connect with AII amacrine cells via gap junctions. These results suggest that these three calcium binding proteins may play different neuroprotective roles in ischemic insult by their ability to buffer calcium in the rat retina.

Microvasculature in the Streptozotocin Induced Diabetic Rat Retina / 대한해부학회지

Diabetic retinopathy is characterized by the pericyte loss, microaneurysms and neovascularization eventually leads to blindness. The present study was examined changes of the microvasculature histochemically and immunochemically in the diabetic rat retina previously documented neuronal alterations, in order to verify the usefulness of the animal model of diabetes for the pathophysiology of angiogenesis. Diabetic condition was induced by a single intravenous injection of streptozotocin in Sprague-Dawley rats aged of 8weeks. The animals showing high blood glucose levels (above 300 mg/dL) were cared for 1, 4, 8, and 12 weeks, respectively. The retinas were processed for Griffonia simplicifolia isolection (GSI) B4 histochmistry, and anti-alpha-smooth muscle actin (alpha-SMA) and anti-NG2 immunochemical techniques. The retinal vasculature was well demarcated by endothelial profiles with GSIB4 histochemistry. alpha-SMA immunoreactivity appeared in the arterioles and the primary capillaries, and NG2 in the arterioles and the whole capillary beds. Changes evoked by diabetes were largely occurred in the capillary. Compared to the retina at normal state, the capillary networks were more complicated, enlarged, and dense. NG2 reactivity was reduced especially under the cytoplasmic processes of the pericytes. In the near periphery of the capillary mainly in the ganglion cell layer of the diabetes, GSIB4 reactive microglia were distributed. These results suggest that the retinal microvasculature showed the precedent events of neovascularization due to diabetes and rat model of diabetes is useful for study of neovascularization mechanism of the diabetic retinopathy.

Pre-synaptic Neuronal Changes of AII Amacrine Cells in the Streptozotocin-induced Diabetic Rat Retina / 대한해부학회지

It has been previously reported that parvalbumin expression was downregulated in AII amacrine cells, while upregulated in a subset of cone bipolar cells electrically synapse with AII amacrine cell in the streptozotocin-induced diabetic rat retina. In the present study, we aimed to trace biochemical changes of pre-synaptic neurons to AII amacrine cells in rat retina following diabetic injury. Diabetic condition was induced by streptozotocin injection into Sprague-Dawley rats aged of 8 weeks. The experimental term of induced diabetes was set at 1, 4, 12 and 24 weeks. Changes of pre-synaptic neurons were evaluated by immunohistochemistry and Western blot analysis with anti-protein kinase C (PKC)-alpha and anti-tyrosine hydroxylase (TH) antibodies. Rod bipolar cells immunolocalized with PKC-alpha antibody extended their enlarged axon terminals into stratum 5 of the inner plexiform layer. In later diabetes, the axon was shorten and its terminals of rod bipolar cell are slightly enlarged. The protein levels of PKC-alpha were slightly increased along with the duration of diabetes. TH immunoreactive neurons are morphologically classified into two subtypes of amacrine cells in the inner nuclear layer: one (type 1) has large soma with long and primary dendrites, classified with dopaminergic, and the other (type 2) has small soma with dendritic arborization. In the outermost inner plexiform layer, ring-like structures being composed of type 1 cell processes were densely distributed. In diabetic retina, the intensity of TH immunoreactivity in type 1 neurons was reduced. In accordance with morphological changes, the protein levels of TH were reduced during diabetes. These results demonstrate that TH immunoreactive dopaminergic amacrine cells are more susceptible to diabetic injury than the rod bipolar cells in the rat retina and may suggest that downregulation of parvalbumin expression in AII amacrine cells of diabetic retina is mainly due to dysfunction of pre-synaptic dopaminergic amacrine cells.

Morphometric Analysis of the Korean Thyroid Cartilage for Age-estimation : Radiographic Study / 체질인류학회지

The thyroid cartilage, which is the biggest cartilage in laryngeal cartilages, undergoes the osseous changes with advancing age and the process is ordinary endochondral ossification. With respect to the spread pattern of ossification, there are several reports but study about the Korean is negligible. The purpose of this study is to estimate the age based on radiographic analysis of the Korean thyroid cartilage. Dedicated mammography was carried out on 124 specimens of the thyroid cartilage including 76 males and 48 females. We measured 14 qualitative measurements. The results were as followed ; The Ratio of radio-opacity exhibited increasing value with advancing age on both sexes. The ossification began at the posterior border and involved orderly the inferior border, the anterior angle (anterior border) and notch as advancing age in male subjects. We could propose the pattern of ossification for age-estimation in Korean male subjects. Concerning the female subjects, we could not propose the relation between age and the pattern of ossification. In conclusion, we can estimate the age for male subjects by radiographic quantitative analysis of the Korean thyroid cartilage.

Expression of Substance P in the Experimental Diabetic Rat Retina / 대한해부학회지

Substance P (Sub P) being composed of 11 amino acids sequence is a kind of tachykinin family peptides. It has been known that this substance plays a role of neurotransmitter and/or neuromodulator and is a very potent vascular growth factor in the nervous system. This study has been investigated expression pattern of Sub P in the rat retina at normal and alteration of Sub P expression following diabetic injury using immunohistochemistry. Diabetic condition was induced by a single injection of streptozotocin in Sprague-Dawley rats aged 8 weeks. The animals showing high blood glucose levels (above 300 mg/dL) were cared for 1, 4, 8 and 12 weeks, respectively. The whole-mounted or sectional preparations of the retinas were used for Sub P immunohistochemistry. Sub P immunoreactivity has been localized in subsets of amacrine cells in the inner nuclear layer (INL) and displaced amacrine cells in the ganglion cell layer (GCL) in the normal retina. The dendrites from amacrine cells in the INL were ramified with strata 1 and 3, and those from displaced amacrine cells in the GCL with strata 5 of the inner plexiform layer. Sub P immunoreactive neurons in both the INL and the GCL were more densely populated in the superior half of the retina. During diabetes, the cell number of Sub P immunoreactive neurons was decreased to one third of the normal value at 4 weeks of diabetes and then slightly increased to half of the normal value at 12 weeks of diabetes. In addition, Sub P mRNA levels were reduced at 4 weeks but reincreased at 12 weeks. These results suggest that Sub P in the rat retina at normal state may function differentially in the superior or the inferior halves and Sub P synthetic pathway in the retinal neurons maybe irradiated in earlier stages of diabetic retinopathy.

Altered Expression of Parvalbumin in Neural Retina of the Insulin-dependent Diabetic Rat / 대한해부학회지

Calcium-binding proteins in the nervous system are functioned in Ca2+ buffering and Ca2+ transport and regulation of various enzyme systems. They potentially have a number of different effects on cells includingaltering the duration of action potentials, promoting neuronal bursting activity and protecting cells against the damaging effects of excessive calcium influx. The present study has been designed to clarify the differential responding patterns of parvalbumin immunoreactive neurons in the rat retina following diabetic injury, for better understandings of role of parvalbumin in the retinal circuitry and in calcium homeostasis. Experimental diabetes was induced by a single intravenous injection of streptozotocin in a dose of 60 mg/kg body weight. Diabetic rats showing high blood glucose levels (above 300 mg/dL) were cared for 1, 4, 8, 12 and 24 weeks, respectively. The retinas at each time point were processed for immunohistochemistry and Western blotting using antiparvalbumin antibody. In the rat retina at normal, parvalbumin immunoreactivity appeared in AII amacrine cells, amacrine cells of a widefield type and displaced amacrine cells. A few bipolar cells are also showed the reactivity. During diabetes, the intensity of parvalbumin immunoreactivity is decreased especially in the AII amacrine cells. The cell number of parvalbumin immunoreactive neurons has showed no large changes throughout the diabetes, except that of bipolar cells. That population of parv immunoreactive of bipolar cells has increased remarkably at later diabetic periods. The protein levels of parvalbumin have showed transiently a slight increase at earlier diabetic periods, and then decreased to lower than that of normal. Parvalbumin immunoreactive bipolar cells at diabetes are co-localized not with PKC-alpha or recoverin, but with glutamate transporter Glt-1b. AII amacrine cell processes were joined with each other and with axon terminals of presumed cone bipolar cells by gap junction. These results suggest that the calcium buffering activity of parvalbumin is shifted from AII amacrine cells to a certain type of cone bipolar cells, in response to diabetes. This event may be occurred through electrically coupled gap junction in between these cell processes.

Morphological Changes of the Dopaminergic Network in the Rat Retina after Axotomy / 대한해부학회지

In the retina, dopaminergic cells express the receptor for brain-derived neurotrophic factor (BDNF), which is known to be retrogradely transported from higher center to the retina. This study was conducted to identify the effect of optic nerve transaction on the dopaminergic cells in the rat retina by immunocytochemistry using antityrosine hydroxylase (TH) antiserum. In the control retina, we found two types of TH-immunoreactive amacrine cells, type I and type II, in the inner nuclear layer (INL) adjacent to the inner plexiform layer (IPL). The type I amacrine cell varicosities formed ring-like structures in contact with AII amacrine cell somata in stratum 1 of the IPL. In the axotomized retinas, TH-labeled processes formed loose networks of fibers, unlike the dense networks in the control retina, and the ring-like structures were disrupted. Our data suggest that retrogradely transported neurotrophic factor affects the expression of TH immunoreactivity in the axotomized rat retina and may therefore influence the retinal dopaminergic system.

Effects of Nitric Oxide on Inhibitory Receptors of Rod Bipolar Cells of Rat Retina

The effects of nitric oxide (NO) on inhibitory neurotransmitter receptors and some types of inhibitory receptors in dissociated rod bipolar cell (RBC) were investigated. In the whole cell voltage-clamping mode, the gamma-aminobutyric acid (GABA) activated current showed both sustained and transient components. GABA activated transient current was fully blocked by bicuculine, a GABAA receptor antagonist. The cis-4-aminocrotonic acid (CACA), a GABAC receptor agonist, evoked the sustained current that was not blocked by bicuculline (BIC). Glycine activated the transient current. These results indicate that the RBCs possess GABAA, GABAC, and glycine inhibitory receptors. Sodium nitroprusside (SNP), a NO analogue, reduced the currents activated by GABAA receptor only, however, did not reduce the currents activated by either GABAC or glycine receptors. This study signifies further that only NO depresses the fast inhibitory response activated by GABAA receptor in RBC. We, therefore, postulate that NO might depress the light-on/off transient inhibitory responses in RBCs in the rat retina.

The Study of Cell Killing Mechanism by Membrane Attack Complexes of Complement in the Nucleated Cells

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.

Immunocytochemical Study on the Development of the Rod Pathway in the Rat Retina / 대한해부학회지

Rod bipolar cells constitute the second-order neuron in the rod pathway. Previous investigations of the rat retina have evaluated the development of other components of the rod pathway namely the AII amacrine cell and GABAergic amacrine cell populations. To gain further insights into the maturation of this retinal circuitry, we studied the development of rod bipolar cells, immunocytochemistry with antibodies directed to the protein kinase C (PKC), in the rat retina. PKC immunoreactivity first appeared in postnatal day 9 (P9), faint PKC immunoreactivity was observed in the cell bodies located at the distal inner nuclear layer (INL), dendrites in the outer plexiform layer (OPL) and immunoreactive bands in the proximal inner plexiform layer (IPL). PKC immunoreactive cells and terminal bulbs at P10 show stronger immunostaining. At P15, the time of eye opening, PKC immunoreactive cells display stronger immunostaining than those of P10 and more mature characteristics like in the adult retina. Double fluorescence immunocytochemistry using an antiserum against parvalbumin, a marker for the AII amacrine cells, or GABA revealed that PKC immunoreactive rod bipolar cell terminals make contact with AII amacrine cells and GABAergic neurons in the proximal IPL from P9. Given these results, the different components of the rod pathway follow a similar pattern of maturation, presumably allowing the rod pathway to function at the early developmental stage of retina.

Locus Ceruleus Terminals in the Fundus StriatiNucleus accumbens septi of the Cat : Electron Microscopic Study / 대한해부학회지

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.

Morphology and Synaptic Pattern of Calretinin-immunoreactive Neurons in the Superficial Dorsal Horn of the Rat Spinal Cord / 대한해부학회지

The distribution and the synaptic relationships of calretinin-immunoreactive neurons were studied in the superficial dorsal horn of the rat spinal cord. Calretinin-immunoreactive neurons and fibers were found in all laminae of spinal cord. The densest staining of both cell bodies and fibers occurred in the superficial laminae. In lamina I, marginal cells and other neurons with small round cell bodies showed calretinin-like immunoreactivity. A calretinin-immunoreactive plexus of nerve fibers was also found in this lamina. Lamina II was densely packed with calretinin-immunoreactive neuronal elements. The outer layer of lamina II was primarily composed of calretinin-immunoreactive neurons with a round or oval shape, whereas in the inner layer dorsoventrally orientated labeled neurons with spindle-shaped cell bodies were observed. Densely labeled neuropils with punctate profiles were also seen. By electron microscopy most of the labeled punctate profiles appeared to be dendrites, but axonal profiles were also found in smaller numbers. Labeled dendritic profiles established symmetric or asymmetric synapses with unlabeled axons and labeled axons established primarily symmetric synaptic contacts with unlabeled dendrites. Synaptic contacts between two calretinin-immunoreactive processes were observed infrequently.

Double label immunocytochemistry for dopaminergic and parvalbuminergic neurons using diaminobenzidine and benzidine dihydrochloride in the rat substantia nigra / 대한해부학회지

No abstract available.

Non-Metrical Morphologic Variations of Korean Skull Foramina / 체질인류학회지

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.

Ganglion Cell Death in Rat Retinaby Persistent Intraocular Pressure Elevation

Glaucoma is characterized by loss of retinal ganglion cells (RGCs) and their axons. Retrograde axoplasmic transport blockade and excitotoxicity were proposed to be a major cause of RGC apoptosis. We conducted this study to characterize the episcleral vessel cauterization glaucoma model in the rat with respect to decreased retrograde axoplasmic flow and subsequent apoptotic RGC death. After episcleral vessels were cauterized in Sprague-Dawley rats, Fluorogold was injected into their superior colliculi by stereotactic method. Retrograde axoplasmic flow and TUNEL-stained apoptotic dead cells were observed microscopically. Elevated intraocular pressure was maintained for up to 6 weeks during follow-up. Retrograde axoplasmic flow to the rat retina was significantly decreased. Apoptotic RGC was selectively TUNELstained in the retina, especially at the ganglion cell layers. We concluded that elevated intraocular pressure caused apoptotic RGC death through retrograde axoplasmic flow blockage. Further studies will elucidate the neuroprotection strategies in glaucoma patients.

Differential Expression of GABA Transporters in Developing Rat Retina / 대한해부학회지

To investigate the spatial and temporal distribution of g-aminobutyric acid (GABA) transporters in the developing rat retina, we localized two GABA transporter proteins, GAT-1 and GAT-3 by immunocytochemistry. GAT-1 immunoreactivity appeared from embryonic day 20 (E20) in the punctate-like structures in the inner plexiform layer. At postnatal day 3 (P3), immunolabeling of cell bodies in the inner nuclear and ganglion cell layers and processes in the inner plexiform layer became much stronger, reaching a maximum staining intensity during the second postnatal week, and the expression pattern and intensity became almost identical to those of the adult retina by P14. In addition, Miller cells also began to show weak immunlabeling for GAT-1 from P10 onward. In contrast, develop-mentally transient immunolabeling for GAT-1 was found in horizontal cells located at the scleral border of the inner nuclear layer during the second postnatal week. The initial immunolabeling for GAT-3 immunoreactivity was already noted in scattered cell bodies and processes of the neuroblastic layer at E18, the earliest time point. During the first week of the postnatal life, GAT-3 immunoreactivity increased in the cell bodies in the inner nuclear and ganglion cell layers, and processes in the inner plexiform layer. From P10 onward, this labeling began to decline, and remained faintly in the neuronal somata of the inner nuclear layer by P14. Instead, the labeling was predominantly localized in Mler cells. Astrocytes in the nerve fiber layer showed the transient labeling during the first postnatal week. Our results showed distinct temporal patterns of two GABA transporter proteins in the developing rat retina, and it suggests specialized roles for GABA transporters in the development of the rat retina.