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J Neurophysiol 82: 3213-3222, 1999;
0022-3077/99 $5.00
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The Journal of Neurophysiology Vol. 82 No. 6 December 1999, pp. 3213-3222
Copyright ©1999 by the American Physiological Society

Patterned Activity in Stratum Lacunosum Moleculare Inhibits CA1 Pyramidal Neuron Firing

Hannah Dvorak-Carbone and Erin M. Schuman

Howard Hughes Medical Institute and Division of Biology 216-76, California Institute of Technology, Pasadena, California 91125

Dvorak-Carbone, Hannah and Erin M. Schuman. Patterned Activity in Stratum Lacunosum Moleculare Inhibits CA1 Pyramidal Neuron Firing. J. Neurophysiol. 82: 3213-3222, 1999. CA1 pyramidal cells are the primary output neurons of the hippocampus, carrying information about the result of hippocampal network processing to the subiculum and entorhinal cortex (EC) and thence out to the rest of the brain. The primary excitatory drive to the CA1 pyramidal cells comes via the Schaffer collateral (SC) projection from area CA3. There is also a direct projection from EC to stratum lacunosum-moleculare (SLM) of CA1, an input well positioned to modulate information flow through the hippocampus. High-frequency stimulation in SLM evokes an inhibition sufficiently strong to prevent CA1 pyramidal cells from spiking in response to SC input, a phenomenon we refer to as spike-blocking. We characterized the spike-blocking efficacy of burst stimulation (10 stimuli at 100 Hz) in SLM and found that it is greatest at ~300-600 ms after the burst, consistent with the time course of the slow GABAB signaling pathway. Spike-blocking efficacy increases in potency with the number of SLM stimuli in a burst, but also decreases with repeated presentations of SLM bursts. Spike-blocking was eliminated in the presence of GABAB antagonists. We have identified a candidate population of interneurons in SLM and distal stratum radiatum (SR) that may mediate this spike-blocking effect. We conclude that the output of CA1 pyramidal cells, and hence the hippocampus, is modulated in an input pattern-dependent manner by activation of the direct pathway from EC.




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