Priming of homosynaptic long-term depression in hippocampus by previous synaptic activity.
Mechanisms regulating long-lasting, activity-dependent decreases in synaptic strength are poorly understood. Theoretical studies have suggested that the critical level (threshold) of synaptic activity needed to induce long-term depression (LTD) versus potentiation (LTP) of synaptic transmission should vary as a function of previous synaptic activity. In order to determine whether such a 'sliding threshold' is indeed a physiological phenomenon, we stimulated Schaffer collateral afferents in area CA1 of rat hippocampal slices at frequencies from 1 to 5 Hz before or after inducing LTP.
Department of Neuroscience, Albert Einstein College of Medicine, Bronx, New York 10461.
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EM
Wexler
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PK
Stanton
D000818:Animals; D004558:Electric Stimulation; D005071:Evoked Potentials / Q000502:physiology; D006624:Hippocampus / Q000166:cytology / Q000502:physiology*; D066298:In Vitro Techniques; D008297:Male; D009473:Neuronal Plasticity / Q000502:physiology*; D051381:Rats; D017207:Rats, Sprague-Dawley; D016194:Receptors, N-Methyl-D-Aspartate / Q000502:physiology; D013569:Synapses / Q000502:physiology*; D009435:Synaptic Transmission / Q000502:physiology
D016194:Receptors, N-Methyl-D-Aspartate