Characterization of the integration time for the stabilization of long- term potentiation in area CA1 of the hippocampus

Abstract

In area CA1 of the hippocampus, synaptic activation of NMDA receptors during postsynaptic depolarization can generate either a decremental synaptic potentiation termed short-term potentiation (STP) or stable, long-term potentiation (LTP). Examining the relationship between these two forms of synaptic enhancement should provide information about the intracellular processes responsible for the stabilization of LTP. Using the hippocampal slice preparation, initial experiments confirmed that STP can be generated either by a weak tetanus or by pairing a single EPSP with postsynaptic depolarization. Following the generation of submaximal LTP, application of a weak, STP-inducing tetanus resulted in STP (not LTP), suggesting that the processes responsible for stabilizing LTP must be activated during induction and cannot be accessed at later times. To determine the interval over which processes activated during STP can be integrated and result in stable LTP (the “integration time” for the stabilization of LTP), a fixed number of afferent stimuli were given at varying intervals (5–60 sec) during postsynaptic depolarization. Using either extracellular or whole-cell recording, LTP was rarely (11% of experiments) elicited at 1 min intervals and frequently (76% of experiments) elicited at 10 sec intervals. These results indicate that following a single EPSP during postsynaptic depolarization, the processes responsible for the stabilization of LTP decay significantly within approximately 1 min, although this value may depend on the level of activation of the requisite intracellular processes.

Differential expression of short-term potentiation by AMPA and NMDA receptors in dentate gyrus.

“…Cold Spring Harbor Laboratory Press on May 12, 2018 -Published by learnmem.cshlp.org Downloaded from this estimate of time course, the STP investigated in the present experiments is the same phenomenon described and studied previously by others using experimental conditions that do not involve pharmacological blockage of second messenger kinase systems (Larson and Lynch 1988;Anwyl et al 1989;Gustafsson et al 1989;Henry and Segal 1990;Malenka 1991;Colino et al 1992;Hanse and Gustafsson 1992). Several second messenger kinases contribute to NMDA receptor-dependent LTP (Bliss and Collingridge 1993;Reymann 1993).…”

“…An initial, decremental stage is referred to as short-term potentiation (STP), and is characterized by a near-immediate increase in response magnitude followed by a rapid decay of potentiation to an asymptotic, steady-state level. STP typically has been reported to have a time course of 10 min or less, though durations as long as 90 min have been suggested (Larson and Lynch 1988;Anwyl et al 1989;Gustafsson et al 1989;Malenka 1991;Colino et al 1992;Hanse and Gustafsson 1992;Malenka et al 1992). As noted above, many previous studies have focused on the relative magnitudes of LTP expressed by AMPA and NMDA receptor subtypes, and results have been sufficiently varied so as to provide support for either a pre-or postsynaptic expression mechanism.…”

A Single Brief Burst Induces GluR1-dependent Associative Short-term Potentiation: A Potential Mechanism for Short-term Memory

“…We modified a protocol for the induction of associative LTP to induce STP (Colino, Huang, & Malenka, 1992; Malenka, 1991; Gustafsson & Wigstrom, 1986). In our protocol, a stimulus in a test pathway (33 Hz, 2 stimuli) was given together with stimulation in an independent (conditioning) pathway (100 Hz, 5 stimuli; see inset, Figure 2).…”

Interaction between intracellular tetanization and pairing-induced long-term synaptic plasticity in the rat visual cortex

“…In the CA1 area of the hippocampus, a temporal loss of ability of the pathway to undergo LTP has been observed after application of a weak tetanus which induced decremental short-term potentiation, 8 or a brief episode of lowfrequency stimulation that induced decremental short-term depression. 16 Susceptibility to LTP could be regulated by metabotropic glutamate receptors, either in a switch-like manner 4 or in a modulatory mode, 7 the latter possibility appearing more likely, since even after saturating potentiation the ability for additional potentiation is shown to recover gradually and spontaneously within 3-4 h. 9 Our data demonstrate that, also at the neocortical synapses, application of the pairing procedure or intracellular tetanization prevents induction of further potentiation with a subsequently applied protocol.…”