1315 Effects of ischemic insults associated with cardiac arrest on the hippocampal neurons
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s145 13 14 DOPAMINE CONTENT AND THE METABOLISM IN THE BRAIN OF NORMAL OR MPTP-TREATED COMMON MARMOSETS -DIFFERENCES BETWEEN THE CAUDATE NUCLEUS AND THE PUTAMEN. MASAHIRO NOMOTO. SHIN-ICHI IWATA. TAKE0 FUKUDA. SHIRO NAKAGAWA. Dept. of Pharmacol. and Dept. of Anatomy. Faculty of Medicine. Kanoshima Universitv, 890, Japan. The common marmoset, a New World monkey, was employed for the study of dopamine content and the metabolism in the brain. In normal control animals dopamine(DA) content was 42.7-t 3.1 in the frontal cortex, 6478+ 417 in the nucleus accumbens, 14719+ 689 in the caudate nucleus, 15992k 857 in the putamen (rig/g, mean4 S.E.M. n=7). The ratio of DA and the metabolites [ (DOPACtHVA)/DA] was 1.47rf: 0.17 in the nucleus accumbens, 0.67 f 0.07 in the caudate nucleus, 1.13+ 0.11 in the putamen in the normal control animals. In MPTP(l-methyl-Cphenyl-l,2,3,6-tetrahydropyridine)-treated animals (10 to 15 mg/kg), DA content was 39.3 f 6.5 in the frontal cortex, 3830 + 399 in the nucleus accumbens, 423 ? 150 in the caudate nucleus, 588k 82 in the putamen (r&g, meant- S.E.M. n=4). The ratio of DA and the metabolites was 1.33+ 0.16 in the nucleus accumbens, 2.56+ 0.88 in the caudate nucleus, 5.81? 2.14 in the putarnen. MPTP trearnent reduced DA content markedly in both the caudate nucleus and the putamen, however, compensatory DA metabolic hyperactivity was induced more prominently in the putamen than in the caudate nucleus. 1315 EFFECTS OF ISCHEMIC INSULTS ASSOCIATED WITH CARDIAC ARREST ON THE HIPPOCAMPAL NEURONS. mNJ1. BE NNOBUAKI , I 2 Dpof Med. Sch. e wac ofpw FnlrnnLaw 8 14-80. 2DeDts. of Pharmacol. and PhvsinL, Fat. of Dent.. Damage to the central nervous system produced by cardiac arrest may different from only cerebral ischemia following cerebral arterial occlusion, because the brain somemany exposed to toxic substances released from some organs the ischemic insults. Therefore, we tried to compare the functional and morphological changes by occlusion of vertebral and arteries (VCAO) with those caused by cardiac arrest (CAR). Under halothane anesthesia rats (about 250g) were fastened to a warmed table and a bent metal wire was inserted underneath the bundle of cardiac blood vessels and lifted to squeeze those bundle causeing CAR. After more than 5 minutes confirming CAR or zero blood pressur monitored from the femoral artery, resuscitation was started with artificial ventilation and tapping the chest. Then hippocampal slices were cut using conventional method and intra-and extracellular recordings were performed from CA1 and CA3 areas. When field potentials and long-term potential (LTP) were recorded 1 day after CAR or VCAO treatment from both CAl, these results showed much difference from normal rats. When recorded one week after ischemia insult, in CA1 both CAR and VCAO rats had showen almost no responses. CA3 from VCAO rats, 1 day after ischemia, showed oscihatory responses to mossy fiber stimulation, but CAR rats showed no response. CA3 responses in CAR rats were gradually recovered in 2 days. In CA1 and CA3, morphological changes were not observed 1 day after ischemia but a number of CA1 pyramidal cells decreased in both of CAR and VCAO rats in a week. 1316 BlPHASIC CHANGES IN F3 EXPRESSION IN THE HIPI’OCAMI’US AFTER ISCHEMIA. _ HIROYUKI CHO’. KUNIKO SHIMAZAKI* .KOUSEI TAKEUCH13. KAZUTADA WATANABE3. KEIJI OGURO ‘. TOSHIO MASUZAWAr . NOBUFUMI KAWAI’. Dent of Surgical Neuroloev’ and Dem. of Phvsioloev’.. Jichi r M ‘c pf Gerontolorrv . Sakae-Cho, Itabashi-Ku. 173. Jarran. Axonal sprouting and synaptic reorganization play an important role in the adaptation of the CNS to injury. However, molecular mechanisms underlying this neuronal plasticity are poorly understood. We have studied expression of a neural celI adhesion molecule, F3 in the hippocampus of the gerbils after transient forebrain ischemia. Immunohistochemistry using F3 antibody and in siru hybridization with cRNA probes revealed that F3 expression in the hippocampal CA1 area decreased 1 day after 5 min of ischemia but it was increased 21 days after ischemic insult. Increase in F3 expression at later stage was parallel with increased immunoreactivity of 145 kDa neurofilament which is a marker of sprouting neurites. Our results suggest that early decrease of F3 precede delayed neuronal death in the CA1 pyramidal neurons whereas late increase in F3 protein may reflect regenerative process, including sprouting of the Schaffer collateral/ commissural axons in CA1 subfield following ischemia.
Transcript of 1315 Effects of ischemic insults associated with cardiac arrest on the hippocampal neurons
s145
13 14 DOPAMINE CONTENT AND THE METABOLISM IN THE BRAIN OF NORMAL OR MPTP-TREATED COMMON MARMOSETS -DIFFERENCES BETWEEN THE CAUDATE NUCLEUS AND THE PUTAMEN.
MASAHIRO NOMOTO. SHIN-ICHI IWATA. TAKE0 FUKUDA. SHIRO NAKAGAWA. Dept. of Pharmacol. and Dept. of Anatomy. Faculty of Medicine. Kanoshima Universitv, 890, Japan.
The common marmoset, a New World monkey, was employed for the study of dopamine content and the metabolism in the brain. In normal control animals dopamine(DA) content was 42.7-t 3.1 in the frontal cortex, 6478+ 417 in the nucleus accumbens, 14719+ 689 in the caudate nucleus, 15992k 857 in the putamen (rig/g, mean4 S.E.M. n=7). The ratio of DA and the metabolites [ (DOPACtHVA)/DA] was 1.47rf: 0.17 in the nucleus accumbens, 0.67 f 0.07 in the caudate nucleus,
1.13+ 0.11 in the putamen in the normal control animals. In MPTP(l-methyl-Cphenyl-l,2,3,6-tetrahydropyridine)-treated
animals (10 to 15 mg/kg), DA content was 39.3 f 6.5 in the frontal cortex, 3830 + 399 in the nucleus accumbens, 423 ? 150 in the caudate nucleus, 588k 82 in the putamen (r&g, meant- S.E.M. n=4). The ratio of DA and the metabolites was 1.33+ 0.16 in the nucleus accumbens, 2.56+ 0.88 in the caudate nucleus, 5.81? 2.14 in the putarnen. MPTP trearnent reduced DA
content markedly in both the caudate nucleus and the putamen, however, compensatory DA metabolic hyperactivity was induced more prominently in the putamen than in the caudate nucleus.
1315 EFFECTS OF ISCHEMIC INSULTS ASSOCIATED WITH CARDIAC ARREST ON THE HIPPOCAMPAL NEURONS. mNJ1. BE NNOBUAKI , I 2
Dpof Med. Sch. e wac ofpw FnlrnnLaw
8 14-80. 2DeDts. of Pharmacol. and PhvsinL, Fat. of Dent..
Damage to the central nervous system produced by cardiac arrest may different from only cerebral ischemia following cerebral arterial occlusion, because the brain somemany exposed to toxic substances released from some organs the ischemic insults. Therefore, we tried to compare the functional and morphological changes by occlusion of vertebral and arteries (VCAO) with those caused by cardiac arrest (CAR). Under halothane anesthesia rats (about 250g) were fastened to a warmed table and a bent metal wire was inserted underneath the bundle of cardiac blood vessels and lifted to squeeze those bundle causeing CAR. After more than 5 minutes confirming CAR or zero blood pressur monitored from the femoral artery, resuscitation was started with artificial ventilation and tapping the chest. Then hippocampal slices were cut using conventional method and intra-and extracellular recordings were performed from CA1 and CA3 areas. When field potentials and long-term potential (LTP) were recorded 1 day after CAR or VCAO treatment from both CAl, these results showed much difference from normal rats. When recorded one week after ischemia insult, in CA1 both CAR and VCAO rats had showen almost no responses. CA3 from VCAO rats, 1 day after ischemia, showed oscihatory responses to mossy fiber stimulation, but CAR rats showed no response. CA3 responses in CAR rats were gradually recovered in 2 days. In CA1 and CA3, morphological changes were not observed 1 day after ischemia but a number of CA1 pyramidal cells decreased in both of CAR and VCAO rats in a week.
1316 BlPHASIC CHANGES IN F3 EXPRESSION IN THE HIPI’OCAMI’US AFTER ISCHEMIA. _
HIROYUKI CHO’. KUNIKO SHIMAZAKI* .KOUSEI TAKEUCH13. KAZUTADA WATANABE3. KEIJI
OGURO ‘. TOSHIO MASUZAWAr . NOBUFUMI KAWAI’. Dent of Surgical Neuroloev’ and Dem. of Phvsioloev’.. Jichi
r M ‘c
pf Gerontolorrv . Sakae-Cho, Itabashi-Ku. 173. Jarran.
Axonal sprouting and synaptic reorganization play an important role in the adaptation of the CNS to injury. However,
molecular mechanisms underlying this neuronal plasticity are poorly understood. We have studied expression of a neural celI
adhesion molecule, F3 in the hippocampus of the gerbils after transient forebrain ischemia. Immunohistochemistry using F3
antibody and in siru hybridization with cRNA probes revealed that F3 expression in the hippocampal CA1 area decreased 1
day after 5 min of ischemia but it was increased 21 days after ischemic insult. Increase in F3 expression at later stage was
parallel with increased immunoreactivity of 145 kDa neurofilament which is a marker of sprouting neurites. Our results
suggest that early decrease of F3 precede delayed neuronal death in the CA1 pyramidal neurons whereas late increase in F3
protein may reflect regenerative process, including sprouting of the Schaffer collateral/ commissural axons in CA1 subfield
following ischemia.
