ANALYSIS OF FIELD POTENTIALS-EVOKED IN CA1 BY ANGULAR BUNDLE STIMULATION IN THE RAT

Citation
Jl. Stringer et Cm. Colbert, ANALYSIS OF FIELD POTENTIALS-EVOKED IN CA1 BY ANGULAR BUNDLE STIMULATION IN THE RAT, Brain research, 641(2), 1994, pp. 289-294
Citations number
25
Categorie Soggetti
Neurosciences
Journal title
ISSN journal
00068993
Volume
641
Issue
2
Year of publication
1994
Pages
289 - 294
Database
ISI
SICI code
0006-8993(1994)641:2<289:AOFPIC>2.0.ZU;2-G
Abstract
Anatomical data and in vitro electrophysiological data suggest that en torhinal cortical efferents monosynaptically excite CA1 pyramidal cell s. In vivo stimulation of the angular bundle (AB) evokes an extracellu lar waveform, suggestive of a population spike. Previously, this wavef orm has been claimed to be activation of the direct entorhinal cortex to CA1 pathway and a volume-conducted response from the dentate gyrus. This study sought to distinguish between these two possibilities usin g several techniques in urethane anesthetized rats. A comparison of wa veforms evoked in the dentate gyrus (DG) and in CA1 by a single-shock test stimulus to the AB revealed that the early positive-to-negative p hase of the waveform recorded in CA1 correlated in time and amplitude to the population spike recorded in the DG. When the AB test stimulus was preceded by a single shock to the AB or to the contralateral hilus , the amplitudes of the DG population spike and the early phase of the CA1 waveform decreased equally. Current source density analysis of th e response to the AB test stimulus revealed that early current sinks l ocalized only to the DG. Finally, focal application of the local anest hetic tetracaine into CA1 did not decrease the amplitude of the wavefo rm evoked by the AB test stimulus. Tetracaine, however, greatly decrea sed the population spike evoked in CA1 by stimulating the contralatera l CA3. Together these data indicate that the early positive-to-negativ e phase of the waveform in CA1 evoked by the AB test stimulus reflects events in the DG and not direct activation of CAI by entorhinal corti cal afferents.