The Journal of Neurophysiology Vol. 81 No. 3 March 1999, pp. 1036-1044
Copyright ©1999 by the American Physiological Society

Long-Term Depression of Temporoammonic-CA1 Hippocampal Synaptic Transmission

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

Dvorak-Carbone, Hannah and Erin M. Schuman. Long-term depression of temporoammonic-CA1 hippocampal synaptic transmission. The temporoammonic pathway, the direct projection from layer III of the entorhinal cortex to area CA1 of the hippocampus, includes both excitatory and inhibitory components that are positioned to be an important source of modulation of the hippocampal output. However, little is known about synaptic plasticity in this pathway. We used field recordings in hippocampal slices prepared from mature (6- to 8-wk old) rats to study long-term depression (LTD) in the temporoammonic pathway. Low-frequency (1 Hz) stimulation (LFS) for 10 min resulted in a depression of the field response that lasted for 1 h. This depression was saturable by multiple applications of LFS. LTD induction was unaffected by the blockade of either fast (GABA_A) or slow (GABA_B) inhibition. Temporoammonic LTD was inhibited by the presence of the N-methyl-D-aspartate (NMDA) receptor antagonist AP5, suggesting a dependence on calcium influx. Full recovery from depression could be induced by high-frequency (100 Hz) stimulation (HFS); in the presence of the GABA_A antagonist bicuculline, HFS induced recovery above the original baseline level. Similarly, HFS or -burst stimulation (TBS) applied to naive slices caused little potentiation, whereas HFS or TBS applied in the presence of bicuculline resulted in significant potentiation of the temporoammonic response. Our results show that, unlike the Schaffer collateral input to CA1, the temporoammonic input in mature animals is easy to depress but difficult to potentiate.