1997 Fiscal Year Final Research Report Summary
An animal of senile dementia induced by the damage of the brain vascular system
Project/Area Number |
08557005
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Research Category |
Grant-in-Aid for Scientific Research (B)
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Allocation Type | Single-year Grants |
Section | 展開研究 |
Research Field |
General physiology
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Research Institution | Kyushu University |
Principal Investigator |
HORI Nobuaki Kyushu University, raculty of Dentistry Associate Prof., 歯学部, 助教授 (60037520)
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Project Period (FY) |
1996 – 1997
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Keywords | vascular systems. / beading formation / intracellular recordings / hippocampus / senile dementia / delayd neuronal cell death / EPSP / ischemic damage |
Research Abstract |
One of possible machanisms of senile dementia may be originated by the trouble on the brain vascular systems. Neurons are not equally to ischemic damege. In the hippocampus, it is known that a transient ischemic episode can be result in an extensive delayd neuronal cell death of neurons in Ca1. We have previously reported that brief transient schemia caused loss of excitability, followed by a transient rebound, a spreading depression-like potential and beading formation at synaptic sites and finally cell death. Now we have studied the time-dependence of morphological and physiological changes that occur following transient ischemia, Hippcampal slices (400mum) were prepared from male rats (180-200g). under ether anesthesia and population EPAPs (pEPSP) from the dendrite layr and intracellular recordings were made with stimulation of the Schaffer collateral pathway. After stabilization the slices were perfused with modified Ringer solutions which lacked glucose and oxygen (LGO), had reduced K and/or with Ap-5. An iontophoretic electrode containing quisqualate and NMDA was positioned on the dendrites. The loss of excitability had the same time courses during 4.5 min of perfusion in LGO Ringer, low K (3mM) LGO and AP-5 (5X10^<-5>M) LGO Ringer. Upon reoxygenation, responses from slices with low K or AP-5 recovered almost to control but those only in LGO Ringer did not. With intracellular recording we find membrane potential to be hyperpolarized at the time of loss of excitability, and iontophoretic responses increased for a short time. We conclude that synaptic tranmission is blocked atan early stage of ischemia, but that transmitter release and NMDA receptor excitation causes damage which leads to depolarization and death.
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Research Products
(7 results)
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[Publications] Bodyrev, A.A., Stvolinsky, S.L., Tyulina, O.V., Koshelev, V.B., Hori, N.and Carpenter, D.O: "Biochemical and hysiological evidpence that carnosine is anendogenos neuroprotector against free radicas." Cellular & Molecular Neurobiolgy. 17(2). 259-71 (1997)
Description
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