Jin-Woong Chung

Catholic University of Korea, Sŏul, Seoul, South Korea

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Publications (20)58.51 Total impact

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    ABSTRACT: Bis (Bcl-2 interacting death suppressor), identified as a Bcl-2-binding protein, has been suggested to have diverse functions in addition to binding to Bcl-2, thereby regulating cell death. To investigate the potential role of Bis in the developing brain, the spatiotemporal expression of Bis protein was studied in the rat forebrain during prenatal and early postnatal development using immunohistochemistry. Initial expression of Bis was detected in the medial telencephalic wall of the lateral ventricle, the area most likely corresponded to the cortical hem from the earliest age examined (E13). There was an abrupt increase of immunoreactive neurons in the cortex and hippocampus during the first postnatal week, which declined thereafter. Two populations of Bis-immunoreactive neurons can be clearly distinguished in the developing forebrain: a population of differentiating and postmitotic neurons coexpressing Bis and microtubule-associated protein-2 (MAP-2), and a population of neurons with the characteristic morphology of Cajal-Retzius cells located exclusively in the marginal zone/layer I of the cortex and in the hippocampal equivalents of the marginal zone. The latter neurons were colabeled with reelin, a marker for Cajal-Retzius cells. While Bis expression in the cerebral cortex and hippocampus exists only transiently by P14, considerable expression was found to be maintained in the rostral migratory stream and the subventricular zone of the lateral ventricle, where Bis-immunoreactive cells were glutamine synthetase-positive glial cells. Our results suggest that Bis may contribute to the developmental processes, including the differentiation and maturation of specific neuronal populations in relation to Bcl-2 in the developing rat forebrain.
    Brain Research 06/2006; 1092(1):69-78. · 2.88 Impact Factor
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    ABSTRACT: We investigated the distribution and time course of expression of two subtypes of prostaglandin E(2) (PGE(2)) receptors, EP2 and EP4, in a rat model of cerebral ischemia and ischemic tolerance. Adult male Sprague-Dawley rats were subjected to either lethal global ischemia (10 min) with or without sublethal ischemic preconditioning (3 min), or ischemia only (3 min). A short 3-min cerebral ischemia and a 3-min ischemia followed by a second lethal ischemia enhanced the expression of EP2 and EP4 receptors in CA1 pyramidal neurons of the hippocampus. In tolerance-acquired CA1 neurons, the immunoreactivities of EP2 and EP4 were upregulated after 4 h and 12 h, respectively. The immunoreactivities were most prominent at 3 days and were sustained for at least 14 days, consistent with results of immunoblotting experiments. However, immunoreactivities for these PGE(2) receptors increased in reactive glial cells in the vulnerable CA1 and hilar regions of rats subjected to lethal ischemia without ischemic preconditioning. Most of the EP2 immunoreactivity occurred in microglial cells and some astrocytes, whereas increased immunoreactivity for EP4 was found only in astrocytes. These data suggest that ischemia and the induction of ischemia tolerance have different regulatory effects on the expression of EP2 and EP4 receptors. Moreover, PGE(2) may exert its unique pathophysiological functions in relation to delayed neuronal death and ischemic tolerance induction in the rat hippocampus via specific PGE(2) receptors.
    Cell and Tissue Research 06/2006; 324(2):203-11. · 3.68 Impact Factor
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    ABSTRACT: Nitric oxide (NO) can play either a neuroprotective or a neurotoxic role in diverse neurodegenerative conditions. This study investigated the differential expression of neuronal nitric oxide synthase (nNOS) in the streptozotocin-induced diabetic rat retina to clarify the involvement of NO produced from neurons in the early pathogenesis of diabetic retinopathy. A decrease in thickness of the outer retina was evident at 12 and 24 weeks after onset of diabetes. nNOS was immunolocalized in two subtypes of amacrine cells, displaced amacrine cells and in some bipolar cells in the normal retinas. The densities of each type of nNOS-expressing neuron showed no significant differences in the diabetic retinas with the exception of the bipolar cells. The numbers of nNOS bipolar cells at 12 weeks of diabetes increased threefold, showing dendritic polarity of nNOS expression. Protein levels of nNOS increased throughout the diabetic retinas reaching a peak value at 24 weeks of diabetes. Thus, diabetes up-regulates the expression of nNOS in bipolar cells, and NO from these cells may aggravate the degeneration of the outer retina in the diabetic retinas.
    Neurobiology of Disease 02/2006; 21(1):43-9. · 5.62 Impact Factor
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    ABSTRACT: We investigated the temporal changes and cellular localization of cyclooxygenase-2 (COX-2) in the rat hippocampus during the induction of acquired ischemic tolerance by sublethal ischemia, and compared these changes with those occurring following transient forebrain ischemia. Adult male Sprague Dawley rats were subjected to either 10 min of lethal global ischemia with or without 3 min of sublethal ischemic preconditioning, or 3 min of ischemia only. A short (3 min) cerebral ischemia as well as lethal ischemia with preconditioning substantially and significantly upregulated COX-2 expression in dentate granule cells, as confirmed by immunoblot analysis. This became evident by 4 h, peaked at 1-3 days, and returned to the basal level around 7 days. COX-2 expression was also increased in CA2 and CA3 neurons, although with weaker staining intensity, but in CA1 neurons very weak immunoreactivity was transiently observed. In the ischemic hippocampus, however, in agreement with previous reports, COX-2 expression was induced strongly in vulnerable CA1 and hilar neurons as well as in resistant CA3 and dentate granule cells. These data demonstrated that COX-2 expression is upregulated in neuronal subpopulations destined to survive, i.e., in CA3 and dentate granule cells after ischemia and ischemia-tolerance induction, as well as in ischemia-vulnerable neurons, i.e., in CA1 neurons after lethal ischemia, suggesting that hippocampal neuronal subpopulations have differential sensitivity to COX-2 upregulation.
    Neuroscience Letters 02/2006; 393(2-3):231-6. · 2.03 Impact Factor
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    ABSTRACT: To ascertain whether the PTEN (phosphatase and tensin homolog deleted on chromosome 10)/Akt signaling pathway is activated during ischemic brain injury, we investigated the expression and phosphorylation of PTEN and Akt by immunohistochemistry in the rat hippocampus after transient forebrain ischemia. Weak immunoreactivity for PTEN and its phosphorylated form (p-PTEN) was constitutively expressed in hippocampal neurons and astrocytes of the control rats, but their upregulation was detected mainly in reactive astrocytes in the ischemic hippocampus. Increased immunoreactivity for PTEN and p-PTEN occurred specifically in astrocytes by day 1 and was sustained for more than 2 weeks. The spatiotemporal activation of Akt in the ischemic hippocampus mirrored that of p-PTEN expression. Post-ischemic activation of Akt, revealed by phosphorylated Akt (p-Akt) immunoreactivity, was first detected at day 1 and was maintained for at least 2 weeks. Double-labeling experiments revealed that the cells expressing PTEN, p-PTEN, or p-Akt were reactive astrocytes expressing glial fibrillary acidic protein. These results demonstrate the increased phosphorylation of PTEN and Akt in reactive astrocytes of the post-ischemic hippocampus, suggesting that the PTEN/Akt pathway is involved in the astroglial reaction in the rat hippocampus after transient forebrain ischemia.
    Cell and Tissue Research 04/2005; 319(3):359-66. · 3.68 Impact Factor
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    ABSTRACT: To better understand the pathophysiological role of Src protein, a non-receptor protein tyrosine kinase of 60kDa, in the ischemic brain, we investigated the time course and regional distribution of active Src expression by using a specific antibody against Tyr416 phosphorylated Src (phospho-Src) in the rat hippocampus after transient forebrain ischemia. In the hippocampus of the control animals, active Src expression was too low to be detected by immunolabeling. Beginning 4h after reperfusion, active Src expression became evident and, after 1 day, had increased preferentially in the CA field of the hippocampus proper and the dentate gyrus. By day 3, active Src expression markedly increased in the pyramidal cell layer of CA1 and the dentate hilar region in temporal correlation with neuronal cell death occurring in these areas, where cells typical of phagocytic microglia showed phospho-Src immunoreactivity. Double-labeling experiments revealed that cells expressing active Src were microglia that stained for biotinylated lectin derived from Griffonia simplicifolia (GSI-B4). Active Src expression began to decline at day 7 and returned to the basal level by day 14 after reperfusion. These results demonstrate increased phosphorylation of Src in activated microglia of the post-ischemic hippocampus, indicating that Src signaling may be involved in the microglial reaction to an ischemic insult.
    Neuroscience Letters 01/2005; 380(1-2):1-5. · 2.03 Impact Factor
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    ABSTRACT: We analyzed the changes in expression of ciliary neurotrophic factor (CNTF) and its receptor, ligand-binding subunit a (CNTFRa), in the hippocampus following intraperitoneal administration of a convulsant dose of kainic acid (KA). Immunohistochemistry and immunoblotting showed that CNTF levels rose dramatically between day 1 and day 10, and that the CNTF was located in reactive astrocytes. In contrast, upregulation of CNTFRalpha mRNA, occurred in neurons as well as astrocytes. A rapid, and short-lived (3 h-2 d) increase in CNTFRalpha was also observed in the more resistant granule cells and CA2 pyramidal neurons. The increase in astrocytes was detected by day 1 and was sustained for more than 5 d. These results show that CNTF and CNTFRalpha are differentially regulated in hippocampal neurons and reactive astrocytes following KA injection, indicating that these proteins may be involved in the regulation of astrocyte and neuronal degenerative responses.
    Molecules and Cells 05/2004; 17(2):292-6. · 2.21 Impact Factor
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    ABSTRACT: The present study has characterized the cellular and temporal localization of the phospholipase D2 (PLD2) protein in the embryonic rat brain, using immunohistochemistry. PLD2 immunoreactivity was first observed in the choroid plexus and in the most ventricular zone of the lateral and third ventricles at embryonic day 15 (E15), followed by gradual restriction to the limited zone of ventricles at E20. In addition, PLD2 expression was high in the developing cerebral cortex and hippocampus. In the cortex, PLD2 expression was observed in the marginal zone from the earliest stage (E15) and then declined and had completely disappeared by E20. Double-labelling studies demonstrated co-expression of the anti-class III beta-tubulin antibody in most of the PLD2 immunoreactive cells. Therefore, our findings suggest that PLD2 may be involved in early developmental processes of some neuronal progenitors.
    Neuroscience Letters 04/2004; 357(2):147-51. · 2.03 Impact Factor
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    ABSTRACT: Disabled 1 (Dab1) is an adapter molecule in a signaling pathway, stimulated by Reelin, which controls cell positioning in the developing brain. It has been localized to AII amacrine cells in the mouse and guinea pig retinas. This study was conducted to identify whether Dab1 is commonly localized to AII amacrine cells in the retinas of other mammals. We investigated Dab1-labeled cells in human, rat, rabbit, and cat retinas in detail by immunocytochemistry with antisera against Dab1. Dab1 immunoreactivity was found in certain populations of amacrine cells, with lobular appendages in the outer half of the inner plexiform layer (IPL) and a bushy, smooth dendritic tree in the inner half of the IPL. Double-labeling experiments demonstrated that all Dab1-immunoreactive amacrine cells were immunoreactive to antisera against calretinin or parvalbumin (i.e., other markers for AII amacrine cells in the mammalian retina) and that they made contacts with the axon terminals of the rod bipolar cells in the IPL close to the ganglion cell layer. Furthermore, all Dab1-labeled amacrine cells showed glycine transporter-1 immunoreactivity, indicating that they are glycinergic. The peak density was relatively high in the human and rat retinas, moderate in the cat retina, and low in the rabbit retina. Together, these morphological and histochemical observations clearly indicate that Dab1 is commonly localized to AII amacrine cells and that antiserum against Dab1 is a reliable and specific marker for AII amacrine cells of diverse mammals.
    The Journal of Comparative Neurology 04/2004; 470(4):372-81. · 3.66 Impact Factor
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    ABSTRACT: The FVB/N mouse is a model of retinitis pigmentosa which shows a rapid loss of photoreceptors during early postnatal (P) life. We investigated the cellular localization of glycine transporter 1 (GlyT-1) in the developing FVB/N mouse retina. In control retinas, the developmental pattern of GlyT-1-immunoreactive amacrine cells was well in accordance with a previous report. However, in the FVB/N mouse retina, some GlyT-1-labeled amacrine cells sent their processes into the outer plexiform layer (OPL) from P14 onward. From P21 onward, GlyT-1-labeled cells were visible in the OPL. These cells were further characterized by double-label immunofluorescence experiments with an antiserum against disabled 1 (Dab-1), and showed Dab-1 immunoreactivity, indicating that these cells are putative AII amacrine cells. These results clearly demonstrate that AII amacrine cells have the potential capacity to respond to photoreceptor degeneration by migrating or sprouting their processes into the OPL in the developing FVB/N mouse retina.
    Cell and Tissue Research 04/2004; 315(3):407-12. · 3.68 Impact Factor
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    ABSTRACT: To investigate a potential role of osteopontin (OPN) in developing rat brain, the expression of OPN mRNA and protein in the developing rat brain relative to the distribution of brain macrophages was investigated using in situ hybridization and immunohistochemistry, and the phagocytic capability of OPN-expressing cells was accessed using rhodamine isothiocyanate (RhIc) as a tracer. OPN-expressing cells appeared from embryonic day 16. During the first week of postnatal life, OPN-labeled cells increased markedly, and peaked around P7, then declined and had completely disappeared by the end of the second postnatal week. The spatiotemporal distribution pattern of OPN mRNA closely matched that of OPN protein. Their morphology and localization were compared with those of cells expressing the established microglial marker OX-42 in adjacent sections, and double-labeling studies demonstrated that OPN was localized to the amoeboid microglia which stain with the lectin GSI-B4, another marker for microglia. Furthermore, OPN-labeled cells were confirmed to be active phagocytes emitting RhIc fluorescence indicating that the tracer into the brain tissues was engulfed by phagocytosis. Therefore, these results provide the first evidence that OPN is transiently expressed in active brain macrophages in the embryonic and early postnatal brain, and suggest that OPN may contribute to the migration and phagocytic function of brain macrophages in the developing brain.
    Experimental Brain Research 03/2004; 154(3):275-80. · 2.22 Impact Factor
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    ABSTRACT: Connexin 36 (Cx36) is a channel-forming protein found in the membranes of apposed cells, forming the hexameric hemichannels of intercellular gap junction channels. It localizes to certain neurons in various regions of the brain including the retina. We characterized the expression pattern of neuronal Cx36 in the guinea pig retina by immunocytochemistry using specific antisera against Cx36 and green/red cone opsin or recoverin. Strong Cx36 immunoreactivity was visible in the ON sublamina of the inner plexiform layer and in the outer plexiform layer, as punctate labelling patterns. Double-labelling experiments with antibody directed against Cx36 and green/red cone opsin or recoverin showed that strong clustered Cx36 immunoreactivity localized to the axon terminals of cone or close to rod photoreceptors. By electron microscopy, Cx36 immunoreactivity was visible in the gap junctions as well as in the cytoplasmic matrices of both sides of cone photoreceptors. In the gap junctions between cone and rod photoreceptors, Cx36 immunoreactivity was only visible in the cytoplasmic matrices of cone photoreceptors. These results clearly indicate that Cx36 forms homologous gap junctions between neighbouring cone photoreceptors, and forms heterologous gap junctions between cone and rod photoreceptors in guinea pig retina. This focal location of Cx36 at the terminals of the photoreceptor suggests that rod photoreceptors can transmit rod signals to the pedicle of a neighbouring cone photoreceptor via Cx36, and that the cone in turn signals to corresponding ganglion cells via ON and OFF cone bipolar cells.
    European Journal of Neuroscience 01/2004; 18(11):2925-34. · 3.75 Impact Factor
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    ABSTRACT: Hyperpolarization-activated cation currents (I(h)) have been identified in neurons in the central nervous system, including the retina. There is growing evidence that these currents, mediated by the hyperpolarization-activated cyclic nucleotide-gated cation channel (HCN), may play important roles in visual processing in the retina. This study was conducted to identify and characterize HCN1-immunoreactive (IR) bipolar cells by immunocytochemistry, quantitative analysis, and electron microscopy. The HCN1-IR bipolar cells were a subtype of OFF-type cone bipolar cells and comprised 10% of the total number of cone bipolar cells. The axons of the HCN1-IR cone bipolar cells ramified narrowly in the border of strata 1 and 2 of the inner plexiform layer (IPL). These cells formed a regular distribution, with a density of 1,825 cells/mm(2) at a position 1 mm ventral to the visual streak, falling to 650 cells/mm(2) in the ventral periphery. Double-labeling experiments demonstrated that their axons stratified narrowly within and slightly proximal to the OFF-starburst amacrine cell processes. In the IPL, they were presynaptic to amacrine cell processes. The most frequent postsynaptic dyads formed of HCN1-IR bipolar cell axon terminals are pairs composed of both amacrine cell processes. These results suggest that these HCN1-IR cone bipolar cells might be the same as the DAPI-Ba1 bipolar population, and might therefore be involved in a direction-selective mechanism, providing inputs to the OFF-starburst amacrine cells and/or the OFF-plexus of the ON-OFF ganglion cells.
    The Journal of Comparative Neurology 01/2004; 467(3):389-402. · 3.66 Impact Factor
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    ABSTRACT: We studied the distribution of Bis (Bcl-2 interacting death suppressor) protein in the adult rat brain and spinal cord using immunohistochemistry. Immunoreactivity was observed in specific neuronal populations in distinct nuclei. The most intensely labeled cells were associated with the motor system, including most cranial nerve motor nuclei, Purkinje cells of the cerebellum, the red nucleus, and the ventral motor neurons of the spinal cord. Bis protein was also expressed in several structures associated with the ventricular system, including the subventricular zone of the lateral ventricle and its rostral extension, in the subcommissural organ, and in tanycytes, radial glial cells in the hypothalamus. Using double-labeling techniques, Bis-immunoreactive cells in the rostral migratory stream, coexpressing Bcl-2, were confirmed as glial fibrillary acidic protein-positive astrocytes comprising the glial tubes. The widespread distribution of Bis suggests that this protein has broader functions in the adult rat central nervous system than previously thought, and that it could be associated with a particular role in the rostral migratory system.
    Cell and Tissue Research 12/2003; 314(2):207-14. · 3.68 Impact Factor
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    ABSTRACT: We investigated the activation and cellular distribution of two signaling pathways, the signal transducers and activators of transcription (STATs) and mitogen-activated protein kinases (MAPKs) following kainic acid (KA)-induced seizures, in relation to the expression of gp130, a common cytokine signal transducer for the interleukin (IL)-6 family of cytokines. Rapid and short-lasting upregulation of gp130 was observed in the granule cells. This became evident in astrocytes by 3 h, increased progressively to peak at 3 days, and was sustained for 10 days. STATs, including STAT1 and STAT3, and p42/44 MAPK were activated in distinct cellular and spatial distributions within the hippocampus following seizures. A rapid and sustained seizure-induced activation of STAT3 and STAT1, revealed by nuclear STAT3 and STAT1 immunoreactivities, was observed exclusively in reactive astrocytes in the hippocampus, nearly coinciding with the time course of gp130 expression; however, STAT3 activation was greater. In contrast, seizure induced the rapid and transient activation of p42/44 MAPK in a subpopulation of hippocampal neurons and in astrocytes, although with weaker staining intensity. Two signaling pathways involving gp130, STATs and MAPK, were differentially activated in reactive astrocytes after KA injection, indicating that STATs and MAPK may differentially mediate the astroglial reaction in the rat hippocampus after KA-induced seizures.
    Molecular Brain Research 12/2003; 119(1):10-8. · 2.00 Impact Factor
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    ABSTRACT: We analyzed expression of osteopontin (OPN), a cytokine regulating tissue repair and inflammation, in astrocytes and microglia in response to systemic lipopolysaccharide (LPS) administration (250 microg/100 g). OPN mRNA expression appeared in subpial astrocytes as early as 6 h, and then spread over the brain parenchyma. The signal for OPN mRNA reached a peak at 24 h post-injection, and returned to basal levels after 48 h. Changes in OPN immunoreactivity in the LPS-injected rat mirrored OPN mRNA induction patterns. These results provide the first evidence of OPN induction in astrocytes and microglia following peripheral immune challenge, and suggest that OPN may play a key role in the pathogenesis of neuroinflammation.
    Journal of Neuroimmunology 09/2003; 141(1-2):65-73. · 3.03 Impact Factor
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    ABSTRACT: To determine whether the pathophysiological processes after transient forebrain ischemia are mediated via a signal pathway involving gp130 (a signal transducer for the interleukin-6 family), we analyzed changes in the expression of gp130 and its downstream transcription factor, signal transducer and activator of transcription factor 3 (STAT3), in the rat hippocampus of a four-vessel occlusive ischemia model. Expression of gp130 mRNA was restricted to neurons of the pyramidal cell and granule cell layers in control animals. Four hours after ischemic injury, astrocytes expressed gp130 mRNA. Expression of gp130 increased preferentially in the CA1 and dentate hilar regions, and was maintained for at least 2 weeks. Increase in gp130 expression was accompanied by the activation of STAT3 following ischemic injury. Four hours after injury, STAT3 and phosphorylated STAT3 (pSTAT3) were observed in the nuclei of the dentate hilar region, and sequentially in the CA1 region at day 1. By day 3, STAT3 immunoreactivity markedly increased in these areas, where small cells with the morphology of astrocytes showed nuclear and cytoplasmic STAT3 and nuclear pSTAT3 immunoreactivities. These patterns were especially maintained in the CA1 area until 14 days of reperfusion. Double-labeling experiments revealed that the cells expressing STAT3 and pSTAT3 were glial fibrillary acidic protein-expressing reactive astrocytes. These results show a coordinated and long-lasting upregulation of gp130 mRNA and STAT3 activation in reactive astrocytes of the postischemic hippocampus, indicating that they may be involved in the astrocytic response to an ischemic insult.
    Glia 03/2003; 41(3):237-46. · 5.07 Impact Factor
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    ABSTRACT: We investigated the effect of L-glutamate on horizontal cell growth after postnatal photoreceptor degeneration in the developing FVB/N mouse retina, using immunocytochemistry with antisera against calbindin D-28 K (calbindin) or neurofilament 200 NE14. The numbers of horizontal cells and amount of axonal arborization in the outer plexiform layer were unchanged in FVB/N mice injected with L-glutamate. Instead, more numerous processes emerging from horizontal cells descended into the inner plexiform layer (IPL) and formed a loose network in stratum 1. Our results clearly demonstrate that horizontal cells are resistant to excitotoxicity by excessive glutamate, and that sprouting of horizontal cell axons into the IPL is potentiated by excessive glutamate in FVB/N mice as they mature.
    Neuroreport 12/2002; 13(16):2091-5. · 1.40 Impact Factor
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    ABSTRACT: The present study was performed to investigate the spatial and temporal expression of osteopontin (OPN) mRNA in the rat brain after kainic acid-induced seizures, and to determine whether this phenomenon is associated spatiotemporally with the microglial reaction. The expression of OPN mRNA was detected using an in situ hybridization technique and Northern blot analysis. Following intraperitoneal injection of kainic acid (10 mg/kg), OPN mRNA was expressed in selective vulnerable areas, including the hippocampus, thalamus, hypothalamus, amygdala, and entorhinal cortex. Comparison of the morphology and localization with the established microglial marker OX-42 in the adjacent sections positively identified the OPN-expressed cells as microglia. Furthermore, double labeling experiments revealed that OPN mRNA expression was confined to ameboid-like cells among microglia stained with GSI-B4, an another microglial marker. These findings from a rat model of seizure support the notion that OPN can be synthesized in a subpopulation of reactive microglial cells. It can therefore be assumed that in the response of the brain to excitotoxic injury, synthesis of OPN occurs generally in a subset of activated microglia.
    Molecules and Cells 07/2002; 13(3):429-35. · 2.21 Impact Factor
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    ABSTRACT: Urea transport in the kidney is mediated by a family of transporter proteins that includes renal urea transporters (UT-A) and erythrocyte urea transporters (UT-B). The cDNA of five isoforms of rat UT-A, UT- A1, UT-A2, UT-A3, UT-A4, and UT-A5 have been cloned. The purpose of this study was to examine the expression of UT-A (L194), which marked UT-A1, UT-A2 and UT-A4. Male Sprague-Dawley rats, weighing approximately 200 g, were divided into three group: control rats had free access to water, dehydrated rats were deprived of water for 3 d, and water loaded rats had free access to 3% sucrose water for 3 d before being killed. The kidneys were preserved by in vivo perfusion through the abdominal aorta with the 2% paraformaldehyde-lysine- periodate (PLP) or 8% paraformaldehyde solution for 10 min. The sections were processed for immunohistochemical studies using pre-embedding immunoperoxidase method and immuno- gold method. In the normal rat kidney, UT-A1 was expressed intensely in the cytoplasm of the inner medullary collecting duct (IMCD) cell and UT-A2 was expressed on the plasma membrane of the terminal portion of the short- loop descending thin limb (DTL) cells (type I epithelium) and of the long-loop DTL cells (type II epithelium) in the initial part of the inner medulla. Immunoreactivity for UT-A1 in the IMCD cells, was decreased in dehydrated animals whereas strongly increased in water loaded animals compared with control animals. In the short-loop DTL, immunoreactivity for UT-A2 was increased in intensity in both dehydrated and water loaded groups. However, in the long-loop DTL of the outer part of the inner medulla, immunoreactivity for UT-A2 was markedly increase in intensity in dehydrated group, but not in water loaded group. In conclusion, in the rat kidney, UT-A1 is located in the cytoplasm of IMCD cells, whereas UT-A2 is