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 Previous Article
Volume 17, Number 14,
Issue of July 15, 1997
pp. 5640-5650
Copyright ©1997 Society for Neuroscience
Nucleus Reuniens Thalami Modulates Activity in Hippocampal Field
CA1 through Excitatory and Inhibitory Mechanisms
Received Feb. 27, 1997; revised May 8, 1997; accepted May 8, 1997.
M. J. Dolleman-Van der Weel1, 2,
F. H. Lopes da Silva2, and
M. P. Witter1
1 Graduate School for Neurosciences Amsterdam, Research
Institute for Neurosciences, Faculty of Medicine, Department of Anatomy
and Embryology, Vrije Universiteit, 1081 BT Amsterdam, The Netherlands,
and 2 Institute of Neurobiology, Faculty of Biology,
University of Amsterdam, 1098 SM Amsterdam, The Netherlands
The nucleus reuniens thalami (RE) originates dense projections to
CA1, forming asymmetrical synapses on spines (50%) and dendrites (50%). The hypothesis that RE input modulates transmission in CA1
through excitation of both pyramidal cells and interneurons was tested
using electrophysiological methods in the anesthetized rat. The RE-CA1
afferents were selectively stimulated at their origin; evoked field
potentials and unit activity were recorded in CA1. RE-evoked depth
profiles showed a prominent negative deflection in the stratum
lacunosum-moleculare and a positive one in the stratum radiatum. The
lacunosum-moleculare sink-radiatum source configuration is compatible
with RE-elicited depolarization of apical dendrites of pyramidal cells.
Despite a consistent and robust paired pulse facilitation of RE-evoked
field potentials, population spikes in the stratum pyramidale were not
detected at any tested condition. This indicates the inability of
RE-CA1 input to discharge pyramidal cells. However, stimulation of
RE-elicited spiking of extracellularly recorded units in strata
oriens/alveus and distal radiatum, indicative of the activation of
local interneurons. Thus, RE seems to modulate transmission in CA1
through a (subthreshold) depolarization of pyramidal cells and a
suprathreshold excitation of putative inhibitory
oriens/alveus and radiatum interneurons.
RE-evoked monosynaptic or disynaptic field potentials were associated
with stimulation of rostral or caudal RE, respectively. Anatomically, a
projection from caudal to rostral RE was demonstrated that can account
for the disynaptic RE-CA1 input. Because caudal RE receives input from
the hippocampus via the subiculum, we propose the existence of a closed
RE-hippocampal circuit that allows RE to modulate the activity in CA1,
depending on hippocampal output.
Key words:
rat;
electrophysiology;
neuroanatomical tracing;
hippocampus;
midline thalamus;
limbic system;
learning and memory
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