Record Display for the EPA National Library Catalog

RECORD NUMBER: 10 OF 11

OLS Field Name OLS Field Data
Main Title Potentiation of Inhibition with Perforant Path Kindling: An NMDA-Receptor Dependent Process.
Author Gilbert, M. E. ;
CORP Author ManTech Environmental Technology, Inc., Research Triangle Park, NC.;Health Effects Research Lab., Research Triangle Park, NC.
Publisher c1991
Year Published 1991
Report Number EPA-68-02-4450; EPA/600/J-91/322;
Stock Number PB92-120468
Additional Subjects Kindling(Neurology) ; N-methyl-D-aspartate receptor ; Hippocampus ; Dizocilpine maleate ; Synapses ; Amygdala ; Rats ; Reprints ; Perforant path
Holdings
Library Call Number Additional Info Location Last
Modified
Checkout
Status
NTIS  PB92-120468 Most EPA libraries have a fiche copy filed under the call number shown. Check with individual libraries about paper copy. NTIS 02/24/1992
Collation 10p
Abstract
Kindling produces a long-lasting enhancement of excitatory and inhibitory neurotransmission. Both long-term potentiation and kindling-induced potentiation of hippocampal excitatory neurotransmission are suppressed by N-methyl-D-aspartate (NMDA) receptor antagonists. These antagonists also greatly retard the development of electrical kindling. The authors have previously reported prolonged afterdischarges (AD) in animals stimulated in the perforant path and treated with the NMDA antagonist, dizocilpine maleate (MK-801), despite a retardation in the development of kindling. In the study the potentiation of excitation and inhibition was assessed during perforant path kindling when NMDA channels were blocked with MK-801. Paired pulse inhibition at 8 interpulse intervals (IPI 20-1000 ms) was monitored before and during kindling development. MK-801 (1 mg/kg, i.p.) delivered 30 min prior to perforant path stimulation increased AD thresholds and delayed kindling development. Potentiation of the excitatory postsynaptic potential (EPSP) and of paired pulse inhibition measured 20-24 h after each drug administration/stimulation were suppressed in MK-801-treated animals. Paradoxically, AD durations were prolonged by MK-801. Longer AD durations could be accounted for by a higher incidence of secondary AD bouts in MK-801 relative to control animals. Development of potentiation of the early phase of paired pulse inhibition (IPI 20-30 ms) was delayed and the potentiation of the late phase of inhibition (IPIs of 200-1000 ms) was completely blocked by MK-801. Thus, some of the enhancement of inhibition seen with kindling is dependent upon NMDA neurotransmission. Suppression of the potentiated inhibition may account for prolonged focal ADs in the perforant path and dentate gyrus. (Copyright (c) 1991 Elsevier Science Publishers B.V.)