Possible mechanisms for long‐lasting potentiation of synaptic transmission in hippocampal slices from guinea‐pigs.

Abstract

1. Long-lasting potentiation of synaptic transmission was studied in the CA1 region of guinea-pig hippocampal slices maintained in vitro. 2. Stimulating pulses were delivered alternately to two independent afferent pathways, stratum radiatum and stratum oriens. The presynaptic volleys and field e.p.s.p.s. were recorded from the same two layers, while an electrode in the pyramidal cell body layer recorded the population spike or in other experiments the extra- or intracellular potentials from a single pyramidal cell. 3. A short tetanus to either of the two input pathways produced a long-lasting enhancement of the field e.p.s.p. as well as an increased size and a reduced latency of the population spike. This long-lasting potentiation was observed for up to 110 min after tetanization. Extracellular unit recordings showed that this potentiation is accompanied by an increased probability of firing and a reduced firing latency. Intracellular recordings showed an increased e.p.s.p., through the increase was smaller and less regular than for the extracellular field e.p.s.p. 4. No corresponding changes were seen in the field potential responses to stimulation of the untetanized input path, or in the intracellularly measured soma membrane potential, resistance, or excitability. The latter two properties were measured by intracellular injection of current pulses. It is concluded that long-lasting potentiation is specific to the pathway which has received the tetanization. 5. Following tetanization there was also a short-lasting (usually 2-4 min) depression, most often seen for the control pathway but sometimes visible on the tetanized side as well, superimposed on the potentiation. It is concluded that the short-lasting depression is not confined to any particular pathway but is a generalized (unspecific) phenomenon.

Exploration-dependent modulation of evoked responses in fascia dentata: Fundamental observations and time course

“…Thus, both the spike changes mentioned above and the EPSP changes reported here have some characteristics in common with LTE and may share ovedapping mechanisms. It is possible that the high-frequency stimulation used to induce LTE actually results in several separable types of plasticity, as has been suggested by other workers (Andersen, Sundberg, Sveen, Swann, & Wigström, 1980;Bliss & Lomo, 1973;Douglas & Goddard, 1975;Taube & Schwartzkroin, 1988;Wilson, 1981;Wilson, Levy, & Steward, 1981) and that under natural circumstances these may occur in isolation, and with very different time courses. Of course, it is also possible that other, as yet unknown, processes are responsible for these environmentally induced changes.…”

Synaptic plasticity by antidromic firing during hippocampal network oscillations

“…TBS of Schaffer collaterals, which provide synaptic input to apical dendrites of CA1 neurons, produced late form of long-term potentiation (L-LTP) in CA1 stratum radiatum as expected ( Fig. 2A), which is shown to be input-specific (29). Similarly, stimulation of inputs to basal dendrites in stratum oriens reliably induces L-LTP restricted to this compartment, since no changes were observed in simultaneously recorded responses from stratum radiatum (Fig.…”

“…A hallmark of most forms of synaptic plasticity is that the changes in synaptic strength are specific to the activated synapse (29,30), but since intracellular signaling would originate from the axon during antidromic action potential firing, we hypothesized that antidromic firing might induce changes in synaptic strength that are cell-wide. TBS of Schaffer collaterals, which provide synaptic input to apical dendrites of CA1 neurons, produced late form of long-term potentiation (L-LTP) in CA1 stratum radiatum as expected ( Fig.…”

A postsynaptic transient K + current modulated by arachidonic acid regulates synaptic integration and threshold for LTP induction in hippocampal pyramidal cells

“…The suppression of I A by AA would be expected to facilitate the induction of LTP both by enhancing the postsynaptic depolarization during EPSPs, and by facilitating the dendritic back-propagation of action potentials (17,(26)(27)(28). Modulation of I A may also be involved in the increased postsynaptic responsiveness that is seen during LTP, so-called ''E-S potentiation'' (29). Because the E-S potentiation in the CA1 area is homosynaptic, i.e., specific to the tetanized pathway, it could possibly be partly due to a local suppression of I A after NMDA receptor-induced AA production (7,30).…”