2003 Fiscal Year Final Research Report Summary
Epileptic Discharges and the neural network in the hippocampus.
| Project/Area Number |
14570050
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| Research Category |
Grant-in-Aid for Scientific Research (C)
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| Allocation Type | Single-year Grants |
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| Section | 一般 |
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| Research Field |
General physiology
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| Research Institution | KURUME UNIVERSITY |
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Principal Investigator |
HIGASHI Hideho Kurume Univ Sch of Med, Dept of Physiol, Professor, 医学部, 教授 (10098907)
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| Project Period (FY) |
2002 – 2003
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| Keywords | neural network / hippocampus / epilepsy / lidocaine / A_1 receptor / adenosine / EPSP / IPSP |
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| Research Abstract |
Extracellular recordings were made from CA1 and CA3 regions in the rat hippocampal tissue slices. Administration of various concentration (1-100μM) of lidocaine induced a transient inhibition, which was followed by an augmentation of the maximal slope of field postsynaptic potentials (fPSPs) and field excitatory postsynaptic potentials (fEPSPs). The amplitude of presynaptic volleys was simply depressed by lidocaine in a conaentration-dependent manner. Administration of adenosine 1 (A_1) receptor antagonist, DPCPX (1μM),diminished the transient inhibition of the fPSPs and fEPSPs. Intracellular recordings from CA1 neurons revealed that lidocaine suppressed the amplitude of both the evoked fast EPSPs and fast IPSP in a concentration-pendent manner, and the IC_<50> values for fast EPSPs and fast IPSP were 68μM and 7μM, respectively. Studies on evoked PSPs showed that lidocaine at low concentration (<30μM) reduced the amplitude of the fast and late IPSPs, but augmented that of the fast EPSPs. Administration of lidocaine (1-30μM) induced a DPCPX-sensitive transient hyperpolarization. In CA3 neurons, adenosine (500μM) induced a DPCPX-sensitive hyperpolarization, which was blocked by lidocaine. When the slice was incised in the stratum oriens in CA2 region, lidocaine (100μM) only augmented the fEPSPs. These results suggest that the transient inhibition of the fPSPs and fEPSPs is mainly mediated by the hyperpolarization of CA3 neurons via A_1 receptor activation. The augmentation of the fPSPs may result from the relative resistance of the fast EPSPs for the lidocaine-induced inhibition, in comparison with the fast IPSP. Thus, the intrinsic circuit of CA3 region and the synaptic inputs from CA2 and CA3 region may contribute to the transient inhibition and subsequent augmentation of the fPSPs and fEPSPs.
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