Entorhinal Inputs to Hippocampal CA1 and Dentate Gyrus in the Rat: A
Current-Source-Density Study.
Leung, Stan L., Lisa Roth and Kevin J. Canning.
Department of Physiology and Clinical Neurological Sciences, University of
Western Ontario, ondon, Canada N6A 5A5.
APStracts 2:0002N, 1995.
SUMMARY AND CONCLUSIONS
1. Laminar profiles of the average evoked potentials and current-source-
density analysis were used to study the input provided by the medial perforant
path (PP) to the hippocampus in the urethane-anesthetized rat. 2. Stimulation
of the PP activated an early latency sink in the middle molecular layer of the
dentate gyrus (DG) and in the stratum lacunosum-moleculare in CA1. The DG
current sink was generated by excitatory synaptic currents activated by the PP
on dentate granule cells. In the normal rat, the peak current sink in the DG
was typically 5 times greater than that of CA1. However, the CA1 sink could be
distinguished from the DG sink in several ways: (1) it peaked when the DG sink
was subsiding, (2) it showed paired-pulse facilitation while the DG sink did
not, (3) in rats in which the DG was lesioned by local colchicine injection,
the DG sink was reduced much more than the CA1 sink. 3. The PP afferents to
CA1 required a slightly higher stimulus threshold (>100_A) for activation than
those projecting to the DG granule cells (<30_A). The onset latency of the
early CA1 sink (2.5 +/- 0.2 ms) was also slightly longer than that of the DG
sink (1.7 +/- 0.1 ms), suggesting that the axons of entorhinal layer III cells
that project to CA1 have a slightly lower conduction velocity than the axons
of the layer II cells that project to the DG. 4. The short-latency current
sink activated by the PP in the distal dendritic layers of CA1 was likely
provided by excitatory currents at the distal apical dendrites of CA1
pyramidal cells. The accompanying current source was mainly confined to
stratum radiatum and appeared not to involve the cell body layer. Thus, the
electrotonic current spread may not be effective enough to depolarize the cell
body or axon hillock. Contribution of interneurons to the above source-sink
profile is possible, with the provision that these interneurons must have
dendritic processes that span strata radiatum and lacunosum-moleculare. 5.
Extracellular field recordings provided no evidence that PP evoked a short
latency (<9 ms) CA1-generated population spike, even with the use of
micropipettes filled with 8 mM bicuculline. Similarly, unit recordings in CA1
revealed only long latency (9-17 ms) unit firing after PP stimulation,
corresponding to a late, di/tri-synaptic excitation of CA1 via the Schaffer
collaterals. 7. High frequency tetanus of the PP readily gave long-term
potentiation (LTP) of the early- and late-latency excitation in CA1, with or
without LTP of the DG excitation. LTP of the early-latency sink in CA1 was
also found in rats with colchicine lesion of the DG. 8. In conclusion, the PP
was shown to excite CA1 cells at their distal apical dendrites in vivo. While
this excitation appeared to be weak in urethane-anesthetized rats, it showed
paired-pulse facilitation and LTP, suggesting that the temporal
characteristics of the entorhinal input may control the strength of this
synapse.
Received 29 August 1994; accepted in final form 8 February 1995.
APS Manuscript Number J541-4.
Article publication pending J. Neurophysiol.
ISSN 1080-4757 Copyright 1995 The American Physiological Society.
Published in APStracts on 3 April 1995.