Biomedical subjects

Ki-Yeon Yoo

Publications and source records attributed to Ki-Yeon Yoo.

48 records · Page 3Linked to original sources

PubMed2004

Elevated substance P (NK-1) receptor immunoreactivity in the cerebellum of seizure prone gerbil.

In the present study, we performed a comparative analysis of the distribution of substance P (SP) receptor (NK-1) immunoreactivity in order to determine the characteristics of the SP system in the cerebelli of rat and gerbils. In the rat cerebellar cortex, only a few Purkinje cells exhibited weak NK-1 receptor immunoreactivity. Similar to the case of rat, NK-1 receptor immunoreactivity in the cerebellar cortex of seizure resistant (SR) gerbils was rarely detected. In contrast, in the cerebellar cortex of seizure sensitive (SS) gerbils, dendrites and cell bodies of Purkinje cell showed strong NK-1 receptor immunoreactivity. Similar to the cerebellar cortex, little NK-1 receptor immunoreactivity in deep cerebellar nuclei was observed in the rat. In SR gerbils, however, deep cerebellar nuclei showed weak NK-1 receptor immunoreactivity. NK-1 receptor immunoreactivity in the deep cerebellar nuclei of SS gerbils was markedly increased, as compared with SR gerbils. Based on the present data, we suggest that the SP system of cerebellar circuit in gerbil are different from rat, and over-expression of NK-1 receptor immunoreactivity in Purkinje cells of SS gerbils may be relevant to Purkinje cell loss induced by seizure activity.

Animals↗

PubMed2004

In vivo protein transduction: biologically active intact pep-1-superoxide dismutase fusion protein efficiently protects against ischemic insult.

Reactive oxygen species (ROS) are implicated in reperfusion injury after transient focal cerebral ischemia. The antioxidant enzyme Cu,Zn-superoxide dismutase (SOD) is one of the major means by which cells counteract the deleterious effects of ROS after ischemia. Recently, we reported that denatured Tat-SOD fusion protein is transduced into cells and skin tissue. Moreover, PEP-1 peptide, which has 21 amino acid residues, is a known carrier peptide that delivers full-length native proteins in vitro and in vivo. In the present study, we investigated the protective effects of PEP-1-SOD fusion protein after ischemic insult. A human SOD gene was fused with PEP-1 peptide in a bacterial expression vector to produce a genetic in-frame PEP-1-SOD fusion protein. The expressed and purified fusion proteins were efficiently transduced both in vitro and in vivo with a native protein structure. Immunohistochemical analysis revealed that PEP-1-SOD injected intraperitoneally (i.p.) into mice can have access into brain neurons. When i.p.-injected into gerbils, PEP-1-SOD fusion proteins prevented neuronal cell death in the hippocampus caused by transient forebrain ischemia. These results suggest that the biologically active intact forms of PEP-1-SOD provide a more efficient strategy for therapeutic delivery in various human diseases related to this antioxidant enzyme or to ROS, including stroke.

Animals↗

PubMed2004

Expression and changes of galanin in neurons and microglia in the hippocampus after transient forebrain ischemia in gerbils.

In the present study, we investigated chronological changes of galanin (GAL), well known as the potassium channel opener, immunoreactivity and GAL protein level in the hippocampus of the gerbil at the various times after 5 min transient forebrain ischemia. In the sham-operated group, weak GAL immunoreactivity was found in non-pyramidal cells. At 12 h after ischemia-reperfusion, the number of GAL-immunoreactive neurons and GAL immunoreactivity were significantly increased in the hippocampus compared to 3 h after ischemic insult, especially in the hippocampal CA1 region. Thereafter the number of GAL-immunoreactive neurons and GAL immunoreactivity decrease time-dependently in the hippocampus. Four days after transient ischemia, GAL immunoreactivity was low as compared with the sham-operated group. At this time point after ischemic insult, GAL immunoreactivity was shown in microglia in the CA1 region because delayed neuronal death happened in the CA1 pyramidal cells. The result of Western blot showed the pattern of GAL expression similar to that of immunohistochemical data. These results suggest that the early increase of GAL in the CA1 pyramidal cells may be associated with the reduction of the excitotoxic damage, that long-lasting enhanced expression of endogenous GAL at 12 h-2 days after ischemia may be associated with efflux of potassium ion into the extracellular space, and that GAL expression in microglia 4 days after ischemia may be associated with reduction of ischemic damage.

Analysis of Variance↗

PubMed2004

Neuroprotective effects of grape seed extract on neuronal injury by inhibiting DNA damage in the gerbil hippocampus after transient forebrain ischemia.

Grape seed extract (GSE) possess cardioprotective abilities by functioning as in vivo antioxidants and by virtue of their ability to directly scavenge ROS including hydroxyl and peroxyl radicals. In the present study, we investigated the neuroprotective effects of grape seed extract (GSE) in the gerbil hippocampus after 5 min transient forebrain ischemia. Neuronal cell density in GSE-treated ischemic animals was significantly increased as compared with vehicle-treated ischemic animals 4 days after ischemic insult. In the GSE-treated groups, about 60% of pyramidal cells of the sham-operated group were stained with cresyl violet 4 days after ischemic insult. In this study, we found that GSE had neuroprotective effects on neuronal injury by inhibiting DNA damage in the CA1 region after ischemia. In vehicle-treated groups, 8-hydroxy-2'-deoxyguanosine (8-OHdG) immunoreactivity was significantly changed time-dependently, whereas the immunoreactivity in the GSE-treated group was similar to the sham-operated group. In addition, we confirmed that astrocytes and microglia did not show significant activation in the CA1 region 4 days after ischemia-reperfusion, because many CA1 pyramidal cells were not damaged. Therefore, these results suggest that GSE can protect ischemic neuronal damage by inhibiting DNA damage after transient forebrain ischemia.

8-Hydroxy-2'-Deoxyguanosine↗

PubMed2004

Very delayed neuronal loss occurs in the glomerular layer of the main olfactory bulb following transient ischemia in gerbils.

Olfactory dysfunction could happen following various insults such as ischemic-hypoxic state. Neurons of the main olfactory bulb (MOB) are resistant to ischemic damage. In the present study, we investigated the ischemia-related changes of neurons and glial cells in the glomerular layer (GL) of the gerbil MOB after transient ischemia. The number of NeuN-immunoreactive neurons became to decrease from 10 days after ischemic insult. Fifteen days after ischemic insult, astrocytes and microglia were increased in number. By 60 days after ischemia, NeuN-immunoreactive neurons were significantly decreased by 42% per glomerulus. At this time period, astrocytes and microglia were pronouncedly increased. This result indicates that neuronal loss must be much delayed in the GL following transient ischemia.

Animals↗

PubMed2004

Age-related changes of gamma-aminobutyric acid transaminase immunoreactivity in the hippocampus and dentate gyrus of the Mongolian gerbil.

We investigated the age-related changes of gamma-aminobutyric acid transaminase (GABA-T, a GABA degradation enzyme) in the hippocampus and dentate gyrus of the gerbil at postnatal month 1 (PM 1), PM 3, PM 6, PM 12, and PM 24. Age-related changes of GABA-T immunoreactivity were distinct in the hippocampal CA1 region and in the dentate gyrus. GABA-T immunoreactivity was weak at PM 1, but at PM 3, it had increased significantly, and then increased further. Between PM 6 and PM 12, strong GABA-T immunoreactivity was found in nonpyramidal cells (GABAergic) in the stratum pyramidale of the CA1 region, and at PM 6, strong GABA-T immunoreactivity was found in neurons of the dentate gyrus subgranular zone. At PM 24, CA1 pyramidal cells showed strong GABA-T immunoreactivity. Western blot analysis showed a pattern of GABA-T expression similar to that shown by immunohistochemistry at various ages. In conclusion, our results suggest that the age-related changes of GABA-T provide important information about the aged brain with GABA dysfunction.

4-Aminobutyrate Transaminase↗

PubMed2004

Chronological alterations of neurofilament 150 immunoreactivity in the gerbil hippocampus and dentate gyrus after transient forebrain ischemia.

In this study, we observed the chronological alterations of neurofilament 150 (NF-150) immunoreactivity in the gerbil hippocampus and dentate gyrus after 5 min transient forebrain ischemia. NF-150 immunoreactivity in the sham-operated group was mainly detected in mossy fibers and in the hilar region of the dentate gyrus. NF-150 immunoreactivity and protein contents of NF-150 and RT 97 (polyphosphorylation epitopes of neurofilament) were significantly decreased at 15 min after ischemic insult. Between 30 min and 12 h after ischemic insult, NF-150 immunoreactivity and protein content were significantly increased as compared with the sham-operated group. Thereafter, NF-150 immunoreactivity and protein content started to decrease. At 12 h after ischemic insult, unlike dentate gyrus, NF-150 immunoreactivity increased in pyramidal cells of the CA1 region. Thereafter, NF-150 immunoreactivity in the CA1 region started to decrease, and 4 days after ischemic insult, NF-150 immunoreactivity nearly was similar to that of the sham-operated group. These biphasic patterns of NF-150 immunoreactivity in the hippocampus and dentate gyrus are reverse correlated with that of the intracellular calcium influx. For calcium detection in the CA1 region, we also conducted alizarin red staining. Alizarin red positive neurons were detected in some neurons at 15-30 min after ischemic insult. At 12 h after ischemia, alizarin red positive neurons were decreased. Thereafter, alizarin red positive neurons started to decrease, but alizarin positive neurons were significantly increased in dying neurons 4 days after ischemia. These results suggest that ischemia-related changes of NF-150 expression may be caused by the calcium following transient forebrain ischemia.

Animals↗

PubMed2004

Changes in parvalbumin immunoreactivity in the parietofrontal cortex after transient forebrain ischemia in the Mongolian gerbil.

We investigated the changes in parvalbumin (PV)-immunoreactive (IR) neurons in the parietofrontal cortex after transient forebrain ischemia. In the sham-operated group, PV-IR neurons were present in all layers of the parietofrontal cortex except layer I. Shortly after ischemia the number of PV-IR neurons in layer II/III first increased, and then declined dramatically 12 h after ischemic insult, followed by a second increase after 2 days. At this time the PV immunoreactivity was very weak and only present in the peripheral neuronal cytoplasm. The reversible increase in the number of PV-IR neurons and in the level of their immunoreactivity could result from a transient ischemia-induced increase in intracellular calcium. This pattern of expression was particularly pronounced in layer II/III of the parietofrontal cortex, suggesting that these neurons are especially\susceptible to ischemic insult.

Animals↗

PubMed2004

GABAA, not GABAB, receptor shows subunit- and spatial-specific alterations in the hippocampus of seizure prone gerbils.

In the present study, we investigated site-specific expressions of GABA(A) and GABA(B) receptor subunits in the seizure-sensitive (SS) and seizure-resistant (SR) gerbil hippocampus to elucidate the function of the gamma-aminobutyric acid (GABA) receptor in seizure activity in this animal. There were no differences of the immunoreactivities of GABA(B) receptor and some GABA(A) receptor subunits (alpha3, alpha4, pan beta and delta) in the hippocampus between SR and SS gerbils. The alpha1 subunit expression was mainly detected in interneurons of stratum radiatum and hilar region of dentate gyrus in the SR gerbil. However, in SS gerbil, interneurons were nearly devoid of alpha1 subunit immunoreactivity and mainly detected in the molecular layer of dentate gyrus. In SR gerbil, alpha2 subunit immunoreactivity was detected in Ammon's horn, particularly in the CA2 region. In SS gerbil, granule cell layer of the dentate gyrus in SS gerbil showed strong alpha2 subunit immunoreactivity. The distribution of alpha5 and gamma2 subunit immunoreactivity in the hippocampus was similarly detected in SR and SS gerbil. However, alpha5 immunodensity of SR gerbil was slightly lower than that of SS gerbil in CA1 region and was slightly strong than that of SS gerbil in subiculum. These differences in distribution of GABA(A) receptor, not GABA(B) receptor, in the SR and SS gerbil hippocampus may indicate that abnormal hyperactive neuronal discharges are occurred in SS gerbil, which presumably result in spontaneous and repetitive seizure activity in this animal.

Animals↗

PubMed2004

Ischemia-related change of ceruloplasmin immunoreactivity in neurons and astrocytes in the gerbil hippocampus and dentate gyrus.

In the present study, we investigated the temporal and spatial alterations of ceruloplasmin immunoreactivity in the gerbil hippocampus and dentate gyrus after 5 min transient forebrain ischemia. In sham-operated animals, ceruloplasmin immunoreactivity in the hippocampal CA2/3 areas was higher than that of other areas. Ceruloplasmin immunoreactivity and its protein content significantly increased and were highest in the CA1 area 1 day after ischemia-reperfusion. At this time point, the immunoreactivity was shown in pyramidal cells of the CA1 area. Four days after ischemia-reperfusion, ceruloplasmin immunoreactivity was shown in astrocytes in the hippocamapal CA1 area. These results suggest that reactive oxygen species (ROS) do not immediately damage neuronal cytosol, unlike DNA. An interval of time is required for the full expression of the cytoplasmic protein injury by ROS. This delayed neuronal injury 1 day after ischemic insult might provide a window of opportunity for therapeutic interventions using antioxidants.

Animals↗

PubMed2004

Expression and changes of endogenous insulin-like growth factor-1 in neurons and glia in the gerbil hippocampus and dentate gyrus after ischemic insult.

In the present study, we focused upon expression and changes of endogenous insulin-like growth factor-1 (IGF-1) in the hippocampus of the Mongolian gerbil after ischemic insult. In sham-operated animals, IGF-1 immunoreactivity was absent from the hippocampus. IGF-1-immunoreactive (IR) neurons were detected at 12 h and 1 day after ischemic insult. In the hippocampal CA1 area, the IGF-IR neurons were non-pyramidal cells (GABAergic neurons). In the hippocampal CA2/3 areas, the IGF-1-IR neurons were pyramidal and non-pyramidal cells, and in the dentate gyrus the IGF-1-IR neurons were hilar neurons. Four days after ischemia-reperfusion, IGF-1 immunoreactivity disappeared from neurons, and significantly increased in astrocytes and microglia. These results suggest that the induction of IGF-1 in the CA1 area during the early stage (12-24 h after ischemic insult) is associated with the relative vulnerabilities of pyramidal glutamatergic neurons and non-pyramidal GABAergic neurons. The later increase (4 days after ischemic insult) of IGF-1 expression and protein content was found to promote the activities of astrocytes and microglia. These increases of IGF-1 in astrocytes and in microglia are associated with mechanisms that compensate for the effects of delayed neuronal death.

Animals↗

PubMed2004

Changes in the expression of calbindin D-28k in the gerbil hippocampus following seizure.

Previous studies have reported that calbindin D-28k (CB), a calcium-binding protein, containing neurons in the hippocampus play an important role in hippocampal excitability in epilepsy, because CB modulates the free calcium ion during seizure. Hence, in the present study, we investigated changes of CB expression in the hippocampus and its association in the Mongolian gerbil to identify roles of CB in epileptogenesis. CB immunoreactivity in the hippocampus was significantly lower in the pre-seizure group of seizure sensitive (SS) gerbils as compared with those seen in the seizure resistant (SR) gerbils. The distribution of CB immunoreactivity in the hippocampus showed significant difference after seizure on-set in SS gerbils. CB immunoreactivity in the hippocampal CA1, CA2 areas, and subiculum was lowest at 3h after seizure on-set; thereafter, the immunoreactivity became to increase to 12h after seizure on-set. Mossy fibers, Schaffer collaterals and dentate granule cells showed the highest CB immunoreactivity at 3h after seizure on-set; thereafter, the immunoreactivity became to decrease. In the case of the intrinsic and output connections of the hippocampus, a rapid decrease of CB serves an inhibitory function, which regulates the seizure activity and output signals from the hippocampus.

Animals↗