A decrease in firing threshold observed after induction of the EPSP-spike (E-S) component of long-term potentiation in rat hippocampal slices View Full Text


Ontology type: schema:ScholarlyArticle     


Article Info

DATE

1990-03

AUTHORS

L. E. Chavez-Noriega, J. V. Halliwell, T. V. P. Bliss

ABSTRACT

Two components of long-term potentiation (LTP) are distinguished with extracellular recording electrodes: a synaptic and an EPSP-Spike (E-S) component. The latter consists of the enhancement produced in the population spike amplitude in excess of that predicted by EPSP potentiation alone. The experiments carried out in this study were designed to investigate intracellular correlates of E-S potentiation and to examine the hypothesis that an increased postsynaptic excitability underlies E-S potentiation. CA1 pyramidal neurons were synaptically activated from stratum radiatum. LTP, defined as a stable increase in the probability of firing to afferent stimulation, was found to be related to a decrease in the intracellular PSP peak amplitude and slope required to fire the cells at a probability of 0.5. These changes were accompanied by a decrease in threshold to direct activation. No significant changes in input resistance or resting potential were recorded. These excitability changes were only observed in cells displaying LTP; they were not related to the potentiation of the synaptic component (PSP amplitude). Our results support the hypothesis that different mechanisms underlie the two components of LTP, and that a reduction in threshold for neuronal discharge accompanies tetanus-induced E-S potentiation. It is suggested that an increase in the ratio of synaptically evoked excitation/inhibition and a reduction in tonic synaptic inhibition through GABAA channels contribute to E-S potentiation. More... »

PAGES

633-641

Identifiers

URI

http://scigraph.springernature.com/pub.10.1007/bf00229331

DOI

http://dx.doi.org/10.1007/bf00229331

DIMENSIONS

https://app.dimensions.ai/details/publication/pub.1037617023

PUBMED

https://www.ncbi.nlm.nih.gov/pubmed/2340880


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