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1.
Bing Chun Yan Joon Ha Park Sung Koo Kim Jung Hoon Choi Choong Hyun Lee Ki-Yeon Yoo Young-Geun Kwon Young-Myeong Kim Jong-Dai Kim Moo-Ho Won 《Cellular and molecular neurobiology》2012,32(8):1231-1242
In the present study, we investigated neuronal death/damage in the gerbil hippocampal CA1 region (CA1) and compared changes in some trophic factors, such as brain-derived neurotrophic factor (BDNF), glial cell line-derived neurotrophic factor (GDNF) and vascular endothelial growth factor (VEGF), in the CA1 between the adult and young gerbils after 5?min of transient cerebral ischemia. Most of pyramidal neurons (89?%) were damaged 4?days after ischemia?Creperfusion (I?CR) in the adult; however, in the young, about 59?% of pyramidal neurons were damaged 7?days after I?CR. The immunoreactivity and levels of BDNF and VEGF, not GDNF, in the CA1 of the normal young were lower than those in the normal adult. Four days after I?CR in the adult group, the immunoreactivity and levels of BDNF and VEGF were distinctively decreased, and the immunoreactivity and level of GDNF were increased. However, in the young group, all of their immunoreactivities and levels were much higher than those in the normal young group. From 7?days after I?CR, all the immunoreactivities and levels were apparently decreased compared to those of the normal adult and young. In brief, we confirmed our recent finding: more delayed and less neuronal death occurred in the young following I?CR, and we newly found that the immunoreactivities of trophic factors, such as BDNF, GDNF, and VEGF, in the stratum pyramidale of the CA1 in the young gerbil were much higher than those in the adult gerbil 4?days after transient cerebral ischemia. 相似文献
2.
Lee CH Yoo KY Choi JH Park JH Kim DH Park JH Hwang IK Cho JH Kim YM Won MH 《Cellular and molecular neurobiology》2011,31(3):449-457
In this study, the authors examined the difference of phosphorylated extracellular signal-regulated kinase 1/2 (pERK1/2) in
the hippocampal CA1 region (CA1) between adult and aged gerbils after 5 min of transient cerebral ischemia. Delayed neuronal
death in the CA1 of the aged group was much slower than that in the adult group after ischemia/reperfusion (I/R). pERK1/2
immunoreaction was observed in the CA1 region of the sham-operated adult gerbil. pERK1/2 immunoreactivity and protein levels
in the ischemic CA1 region of the adult group were markedly increased 4 days after I/R, and then reduced up to 10 days after
I/R. In contrast, pERK1/2 immunoreaction was hardly detected in the CA1 region of sham-operated aged gerbils, and the immunoreactivity
increased from 1 day after the ischemic insult, and still observed until 10 days post-ischemia. In addition, pERK1/2-immunoreaction
was expressed in astrocytes in the ischemic CA1 region: The expression in the ischemia-operated aged gerbils was later than
that in the ischemia-operated adult gerbils. These results indicate that different patterns of ERK1/2 immunoreactivity may
be associated with different processes of delayed neuronal death in adult and aged animals. 相似文献
3.
Yan BC Park JH Ahn JH Lee YJ Lee TH Lee CH Cho JH Kim MJ Kim TY Kang IJ Won MH 《Neurochemical research》2012,37(5):1019-1030
In the present study, we compared the immunoreactivities and levels of Trx/prx redox system, thioredoxin 2 (Trx2), thioredoxin reductase 2 (TrxR2) and peroxiredoxin 3 (Prx3), as well as neuronal death in the hippocampal CA1 region between the adult and young gerbil after 5 min of transient cerebral ischemia. At 4 days post-ischemia, pyramidal neurons (about 90%) in the adult stratum pyramidale of the CA1 region showed "delayed neuronal death (DND)"; however, at this time point, few pyramidal neurons showed DND in the young stratum pyramidale. At 7 days post-ischemia, about 56% of pyramidal neurons showed DND in the young stratum pyramidale. The immunoreactivities of all the antioxidants in the young sham-group were similar to those in the adult sham-group. At 4 days post-ischemia, the immunoreactivity of TrxR2, not Trx2 and Prx3 in the adult ischemia-group was dramatically decreased in CA1 pyramidal neurons. At this time point, the immunoreactivities of all the antioxidants in the young ischemia-group were apparently increased compared to the adult ischemia-group. From 7 days pots-ischemia, non-pyramidal cells showed the immunoreactivities of all the antioxidants in the ischemic CA1 region; however, in the young ischemia-groups, the immunoreactivities were much lower than those in the adult ischemia-groups. In brief, our results showed that the immunoreactivities of Trx2, TrxR2 and Prx3 were dramatically increased in CA1 pyramidal neurons of the young ischemia-groups at 4 days post-ischemia compared to those in the adult ischemia-groups induced by transient cerebral ischemia. 相似文献
4.
Takeshi Hashimoto Toshio Kawamata Naoaki Saito Masahiro Sasaki Masamichi Nakai Sanyoung Niu Taizo Taniguchi Akira Terashima Minoru Yasuda Kiyoshi Maeda Chikako Tanaka 《Journal of neurochemistry》1998,70(3):1289-1298
Abstract: To investigate isoform-specific roles of Ca2+ /calmodulin-dependent phosphatase [calcineurin (CaN)] in ischemia-induced cell death, we raised antibodies specific to CaN Aα and CaN Aβ and localized the CaN isoforms in the hippocampal CA1 region of Mongolian gerbils subjected to a 5-min occlusion of carotid arteries. In the nonischemic gerbil, immunoreactions of both isoforms were highly enriched in CA1 regions, especially in the cytoplasm and apical dendrites of CA1 pyramidal neurons. At 4–7 days after the induced ischemia, immunoreactivities of the CaN Aα isoform in CA1 pyramidal cells were markedly reduced, whereas they were enhanced in the CA1 radiatum and oriens layers. In contrast, CaN Aβ immunoreactivities were reduced in all layers of the ischemic CA1 region, whereas they were enhanced in activated astrocytes, colocalizing with glial fibrillary acidic protein. These findings suggest that up-regulation of CaN Aα in afferent fibers in CA1 and up-regulation of CaN Aβ in reactive astrocytes may be involved in neuronal reorganization after ischemic injury. 相似文献
5.
Joon Ha Park Bich Na Shin Ji Hyeon Ahn Jeong-Hwi Cho In Hye Kim Dae Won Kim Moo-Ho Won Seongkweon Hong Jun Hwi Cho Choong-Hyun Lee 《Cellular and molecular neurobiology》2016,36(5):821-828
Proline-rich Akt substrate of 40-kDa (PRAS40) is one of the important interactive linkers between Akt and mTOR signaling pathways. The increase of PRAS40 is related with the reduction of brain damage induced by cerebral ischemia. In the present study, we investigated time-dependent changes in PRAS40 and phospho-PRAS40 (p-PRAS40) immunoreactivities in the hippocampal CA1 region of the gerbil after 5 min of transient cerebral ischemia. PRAS40 immunoreactivity in the CA1 region was decreased in pyramidal neurons from 12 h after ischemic insult in a time-dependent manner, and, at 5 days post-ischemia, PRAS40 immunoreactivity was newly expressed in astrocytes. p-PRAS40 immunoreactivity in the CA1 pyramidal neurons was hardly found 12 h and apparently detected again 1 and 2 days after ischemic insult. At 5 days post-ischemia, p-PRAS40 immunoreactivity in the CA1 pyramidal neurons was not found. These results indicate that ischemia-induced changes in PRAS40 and p-PRAS40 immunoreactivities in CA1 pyramidal neurons and astrocytes may be closely associated with delayed neuronal death in the hippocampal CA1 region following transient cerebral ischemia. 相似文献
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8.
Jae-Chul Lee Joon Ha Park Bing Chun Yan In Hye Kim Geum-Sil Cho Dooil Jeoung Young-Geun Kwon Young-Myeong Kim Yun Lyul Lee Hyung-Cheul Shin Moo-Ho Won 《Neurochemical research》2013,38(1):74-81
DNA methylation is a key epigenetic modification of DNA that is catalyzed by DNA methyltransferases (Dnmt). Increasing evidences suggest that DNA methylation in neurons regulates synaptic plasticity as well as neuronal network activity. In the present study, we investigated the changes in DNA methyltransferases 1 (Dnmt1) immunoreactivity and its protein levels in the gerbil hippocampal CA1 region after 5 min of transient global cerebral ischemia. CA1 pyramidal neurons were well stained with NeuN (a neuron-specific soluble nuclear antigen) antibody in the sham-group, Four days after ischemia–reperfusion (I–R), NeuN-positive (+) cells were significantly decreased in the stratum pyramidale (SP) of the CA1 region, and many Fluro-Jade B (a marker for neuronal degeneration)+ cells were observed in the SP. Dnmt1 immunoreactivity was well detected in all the layers of the sham-group. Dnmt1 immunoreactivity was hardly detected only in the stratum pyramidale of the CA1 region from 4 days post-ischemia; however, at these times, Dnmt1 immunoreactivity was newly expressed in GABAergic interneurons or astrocytes in the ischemic CA1 region. In addition, the level of Dnmt1 was lowest at 4 days post-ischemia. In brief, both the Dnmt1 immunoreactivity and protein levels were distinctively decreased in the ischemic CA1 region 4 days after transient cerebral ischemia. These results indicate that the decrease of Dnmt1 expression at 4 days post-ischemia may be related to ischemia-induced delayed neuronal death. 相似文献
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10.
Yoo DY Kim W Nam SM Chung JY Choi JH Yoon YS Won MH Hwang IK 《Neurochemical research》2012,37(5):1011-1018
In a previous study, we reported that the administration of pyridoxine (vitamin B6) to mice for 3 weeks significantly increased cell proliferation and neuroblast differentiation in the dentate gyrus without
any neuronal damage. In the present study, we investigated the restorative potentials of pyridoxine on ischemic damage in
the hippocampal CA1 region of Mongolian gerbils. Gerbils were subjected to 5 min of transient ischemia, and surgical operation
success was assessed by ophthalmoscope during occlusion of common carotid arteries and spontaneous motor activity at 1 day
after ischemia/reperfusion. Pyridoxine (350 mg/kg) or its vehicle (physiological saline) was intraperineally administered
to ischemic gerbils twice a day starting 4 days after ischemia/reperfusion for 30 or 60 days. The repeated administration
of pyridoxine for 30 and 60 days significantly increased doublecortin-immunoreactive neuroblasts in the dentate gyrus and
increased NeuN-immunoreactive mature neurons and βIII-tubulin-immunoreactive dendrites in the hippocampal CA1 region. Furthermore,
brain-derived neurotrophic factor (BDNF) protein levels were significantly increased in pyridoxine-treated groups compared
to those in the vehicle-treated groups. These results suggest that chronic administration of pyridoxine enhances neuroblast
differentiation in the dentate gyrus and induces new mature neurons in the hippocampal CA1 region by up-regulating BDNF expression
in hippocampal homogenates. 相似文献
11.
Oxidative stress is a major pathogenic event occurring in several brain disorders and is a major cause of brain damage due
to ischemia/reperfusion. Thiol proteins are easily oxidized in cells exposed to reactive oxygen species (ROS). In the present
study, we investigated transient ischemia-induced chronological changes in hyperoxidized peroxiredoxins (Prx-SO3) and glyceraldehyde-3-phosphate dehydrogenase (GAPDH-SO3) immunoreactivity and protein levels in the gerbil hippocampus induced by 5 min of transient forebrain ischemia. Weak Prx-SO3 immunoreactivity is detected in the hippocampal CA1 region of the sham-operated group. Prx-SO3 immunoreactivity was significantly increased 12 h and 1 day after ischemia/reperfusion, and the immunoreactivity was decreased
to the level of the sham-operated group 2 days after ischemia/reperfusion. Prx-SO3 immunoreactivity in the 4 days post-ischemia group was increased again, and the immunoreactivity was expressed in glial components
for 5 days after ischemia/reperfusion. GAPDH-SO3 immunoreactivity was highest in the CA1 region 1 day after ischemia/reperfusion, the immunoreactivity was decreased 2 days
after ischemia/reperfusion. Four days after ischemia/reperfusion, GAPDH-SO3 immunoreactivity increased again, and the immunoreactivity began to be expressed in glial components from 5 days after ischemia/reperfusion.
Prx-SO3 and GAPDH-SO3 protein levels in the ischemic CA1 region were also very high 12 h and 1 day after ischemia/reperfusion and returned to the
level of the sham-operated group 3 days after ischemia/reperfusion. Their protein levels were increased again 5 days after
ischemia/reperfusion. In conclusion, Prx-SO3 and GAPDH-SO3 immunoreactivity and protein levels in the gerbil hippocampal CA1 region are significantly increased 12 h-24 h after ischemia/reperfusion
and their immunoreactivity begins to be expressed in glial components from 4 or 5 days after ischemia/reperfusion. 相似文献
12.
Choi JH Yoo KY Lee CH Park JH Yan BC Kwon SH Seo JY Cho JH Hwang IK Won MH 《Neurochemical research》2012,37(4):802-810
In the present study, we compared differences in cell proliferation, neuroblast differentiation and neuronal maturation in
the hippocampal dentate gyrus (DG) between the adult and aged gerbil induced by 5 min of transient global cerebral ischemia
using Ki-67 and BrdU (markers for cell proliferation), doublecortin (DCX, a marker for neuroblast differentiation) and neuronal
nuclei (NeuN, a marker for mature neuron). The number of Ki-67-immunoreactive (+) cells in the DG of both the groups peaked 7 days after ischemia/reperfusion (I/R). However, the number in the aged DG was
40.6 ± 1.8% of that in the adult DG. Thereafter, the number decreased with time. After ischemic damage, DCX immunoreactivity
and its protein level in the adult and aged DG peaked at 10 and 15 days post-ischemia, respectively. However, DCX immunoreactivity
and its protein levels in the aged DG were much lower than those in the adult. DCX immunoreactivity and its protein level
in the aged DG were 11.1 ± 0.6% and 34.4 ± 2.1% of the adult DG, respectively. In addition, the number of Ki-67+ cells and DCX immunoreactivity in both groups were similar to those in the sham at 60 days postischemia. At 30 days post-ischemia,
the number of BrdU+ cells and BrdU+/NeuN+ cells in the adult-group were much higher (281.2 ± 23.4% and 126.4 ± 7.4%, respectively) than the aged-group (35.6 ± 6.8%
and 79.5 ± 6.1%, respectively). These results suggest that the ability of neurogenesis in the ischemic aged DG is much lower
than that in the ischemic adult DG. 相似文献
13.
Ohk TG Yoo KY Park SM Shin BN Kim IH Park JH Ahn HC Lee YJ Kim MJ Kim TY Won MH Cho JH 《Neurochemical research》2012,37(4):826-834
Ischemic damage occurs well in vulnerable regions of the brain, including the hippocampus and striatum. In the present study, we examined neuronal damage/death and glial changes in the striatum 4?days after 5, 10, 15 and 20?min of transient cerebral ischemia using the gerbil. Spontaneous motor activity was increased with the duration time of ischemia-reperfusion (I-R). To examine neuronal damage, we used Fluoro-Jade B (F-J B, a marker for neuronal degeneration) histofluorescence staining. F-J B positive cells were detected only in the 20?min ischemia-group, not in the other groups. In addition, we examined gliosis of astrocytes and microglia using anti-glial fibrillary acidic protein (GFAP) and anti- ionized calcium-binding adapter molecule 1 (Iba-1), respectively. In the 5?min ischemia-group, GFAP-immunoreactive astrocytes were distinctively increased in number, and the immunoreactivity was stronger than that in the sham-group. In the 10, 15 and 20?min ischemia-groups, GFAP-immunoreactivity was more increased with the duration of I-R. On the other hand, the immunoreactivity and the number of Iba-1-immunoreactive microglia were distinctively increased in the 5 and 10?min ischemia-groups. In the 15?min ischemia-group, cell bodies of microglia were largest, and the immunoreactivity was highest; however, in the 20?min ischemia-group, the immunoreactivity was low compared to the 15?min ischemia-group. The results of western blotting for GFAP and Iba-1 were similar to the immunohistochemical data. In brief, these findings showed that neuronal death could be detected only in the 20?min ischemia-group 4?days after I-R, and the change pattern of astrocytes and microglia were apparently different according to the duration time of I-R. 相似文献
14.
Arachidonic Acid and Leukotriene C4: Role in Transient Cerebral Ischemia of Gerbils 总被引:14,自引:0,他引:14
Rao A. Muralikrishna Hatcher J. F. Kindy M. S. Dempsey R. J. 《Neurochemical research》1999,24(10):1225-1232
Accumulation of arachidonic acid (AA) is greatest in brain regions most sensitive to transient ischemia. Free AA released after ischemia is either: 1) reincorporated into the membrane phospholipids, or 2) oxidized during reperfusion by lipoxygenases and cyclooxygenases, producing leukotrienes (LT), prostaglandins, thromboxanes and oxygen radicals. AA, its metabolite LTC4 and lipid peroxides (generated during AA metabolism) have been implicated in the blood-brain barrier (BBB) dysfunction, edema and neuronal death after ischemia/reperfusion. This report describes the time course of AA release, LTC4 accumulation and association with the physiological outcome during transient cerebral ischemia of gerbils. Significant amount of AA was detected immediately after 10 min ischemia (0 min reperfusion) which returned to sham levels within 30 min reperfusion. A later release of AA occurred after 1 d. LTC4 levels were elevated at 0–6 h and 1 d after ischemia. Increased lipid peroxidation due to AA metabolism was observed between 2–6 h. BBB dysfunction occurred at 6 h. Significant edema developed at 1 and 2 d after ischemia and reached maximum at 3 d. Ischemia resulted in ~80% neuronal death in the CA1 hippocampal region. Pretreatment with a 5-lipoxygenase inhibitor, AA861 resulted in significant attenuation of LTC4 levels (Baskaya et al. 1996. J. Neurosurg. 85:112–116) and CA1 neuronal death. Accumulation of AA and LTC4, together with highly reactive oxygen radicals and lipid peroxides, may alter membrane permeability, resulting in BBB dysfunction, edema and ultimately to neuronal death. 相似文献
15.
Hiroto Uchida Yuki Fujita Misato Matsueda Masahiro Umeda Shunsuke Matsuda Hiroyuki Kato Jiro Kasahara Tsutomu Araki 《Cellular and molecular neurobiology》2010,30(7):1125-1134
Focal brain lesions such as transient focal cerebral ischemia can lead to neuronal damage in remote areas, including the ipsilateral
substantia nigra and hippocampus, as well as in the ischemic core. In this study, we investigated acute changes in the ipsilateral
hippocampus from 1 up to 7 days after 90 min of transient focal cerebral ischemia in rats, using anti-NeuN (neuronal nuclei),
anti-Cu/Zn-superoxide dismutase (Cu/Zn-SOD), anti-Mn-SOD, anti-neuronal nitric oxide synthase (nNOS), anti-inducible NOS (iNOS),
anti-glial fibrillary acidic protein (GFAP), anti-ionized calcium-binding adaptor molecule 1(Iba 1) and anti-2′,3′-cyclic
nucleotide 3′-phosphodiesterase (CNPase) antibodies. In our western blot and histochemical analyses, present results show
that transient focal cerebral ischemia in rats can cause a severe and acute damage of neurons and oligodendrocytes in the
ipsilateral hippocampal CA1 sector. The present findings also demonstrate that the expression of iNOS produced by Iba 1-immunopositive
microglia precedes the damage of neurons and oligodendrocytes in the ipsilateral hippocampal CA1 sector after transient focal
cerebral ischemia. In contrast, our results suggest that increased reactive oxygen species (ROS) production during reperfusion
cannot lead to damage of neurons and oligodendrocytes in the ipsilateral hippocampal CA1 sector after transient focal cerebral
ischemia, because of an insufficient expression of Cu/Zn-SOD and Mn-SOD. Our double-labeled immunohistochemical study demonstrates
that the overexpression of iNOS produced by Iba 1-immunopositive microglia may play a pivotal role in the damage of neurons
and oligodendrocytes in the ipsilateral hippocampal CA1 sector at an acute stage after transient focal cerebral ischemia. 相似文献
16.
Hwang IK Lee CH Li H Yoo KY Choi JH Kim DW Kim DW Suh HW Won MH 《Neurochemical research》2008,33(7):1309-1315
Similarities between age-related changes in the canine and human brain have resulted in the general acceptance of the canine brain as a model of human brain aging. The hippocampus is essentially required for intact cognitive ability and appears to be particularly vulnerable to the aging process. We observed changes in ionized calcium-binding adapter molecule 1 (Iba-1, a microglial marker) immunoreactivity and protein levels in the hippocampal dentate gyrus and CA1 region of adult (2-3 years) and aged (10-12 years) dogs. We also observed the interferon-gamma (IFN-gamma), a pro-inflammatory cytokine, protein levels in these groups. In the dentate gyrus and CA1 region of the adult dog, Iba-1 immunoreactive microglia were well distributed and their processes were highly ramified. However, in the aged dog, the processes of Iba-1 immunoreactive microglia were hypertrophied in the dentate gyrus. Moreover, Iba-1 protein level in the dentate gyrus in the aged dog was higher than in the adult dog. IFN-gamma expression was increased in the dentate gyrus homogenates of aged dogs than adult dogs. In addition, we found that some neurons were positive to Fluoro-Jade B (a marker for neuronal degeneration) in the dentate polymorphic layer, but not in the hippocampal CA1 region in the aged dog. These results suggest that Iba-1 immunoreactive microglia are hypertrophied in the dentate gyrus in the aged dog. 相似文献
17.
Redd1, also known as RTP801/Dig2/DDIT4, is a stress-induced protein and marked changes of Redd1 expression occurs in response to hypoxia or cerebral ischemia. In the present study, we examined the time-course changes in Redd1 protein expressions in the rat hippocampal CA1 region following chronic cerebral hypoperfusion (CCH) induced by permanent bilateral common carotid arteries occlusion (2VO). Redd1 immunoreactivity in the pyramidal neurons of the hippocampal CA1 region was increased at 7 days after 2VO surgery, and then the immunoreactivity was decreased with time. Especially, very weak Redd1 immunoreactivity was observed in the hippocampal CA1 region at 28 days after 2VO surgery. Western blot analysis showed that Redd1 level in the hippocampal CA1 region was significantly increased at 7 days following CCH and significantly decreased at 28 days after 2VO surgery, compared with that of the sham-operated group. These results indicate that Redd1 expressions is markedly changed in the hippocampal CA1 region following CCH and that change of Redd1 expression may be associated with the CCH-induced neuronal damage in the hippocampal CA1 region. 相似文献
18.
Hwang IK Yoo KY Li H Choi JH Lee CH Chung DW Lee IS Kim DW Choi SY Won MH 《Neurochemical research》2008,33(5):938-944
Adrenalectomy (ADX) has been useful for a good in vivo model for apoptosis in the hippocampus by the absence of corticosteroids
following ADX. In some neurodegenerative diseases, GABAergic neurons are more resistant to neuronal damage as compared with
glutamatergic neurons. In the present study, we observed chronological changes in three GABA degradation enzymes, e.g., GABA
transaminase (GABA-T), succinic semialdehyde dehydrogenase (SSADH) and succinic semialdehyde reductase (SSAR) immunoreactivity
and protein levels in the gerbil hippocampal CA1 region after ADX. Changes in their immunoreactivities were distinct in the
stratum pyramidale of the CA1 region. GABA-T immunoreactivity and protein level were significantly increased in the CA1 region
3 h after ADX, in contrast, SSAR and SSADH immunoreactivity and protein level were increased 12 h and 3–12 h, respectively,
after ADX. These results suggest that the increases of GABA-T, SSADH and SSAR immunoreactivity and protein levels in the hippocampal
CA1 region in ADX gerbils may be associated with the control of GABA levels in this region. 相似文献
19.
Ionized calcium-binding adapter molecule 1 (iba-1) is specifically expressed in microglia and plays an important role in the regulation of the function of microglia. We observed chronological changes of iba-1-immunoreactive cells and iba-1 level in the gerbil hippocampal CA1 region after transient ischemia. Transient forebrain ischemia in gerbils was induced by the occlusion of bilateral common carotid arteries for 5 min. Immunohistochemical and Western blot analysis of iba-1 were performed in the gerbil ischemic hippocampus. In the sham-operated group, iba-1-immunoreactive cells were detected in the CA1 region. Thirty minutes after ischemia/reperfusion, iba-1 immunoreactivity significantly increased, and its immunoreactive cells were well ramified. Three hours after ischemia/reperfusion, iba-1 immunoreactivity and level decreased, and thereafter they increased again with time after ischemia/reperfusion. Three days after ischemia/reperfusion, iba-1-immunoreactive cells had well-ramified processes, which projected to the stratum pyramidale of the CA1 region. Seven days after ischemia/reperfusion, iba-1 immunoreactivity and level were highest in the CA1 region, whereas they significantly decreased in the CA1 region 10 days after ischemia/reperfusion. Iba-1-immunoreactive cells in the ischemic CA1 region were co-localized with OX-42, a microglia marker. In brief, iba-1-immunoreactive cells change morphologically and iba-1 immunoreactivity alters in the CA1 region with time after ischemia/reperfusion. These may be associated with the delayed neuronal death of CA1 pyramidal cells in the gerbil ischemic hippocampus. 相似文献
20.