Description Transcript Keywords Info Professor Seth Grant explains that long-term potentiation may last for days or weeks, but is usually studied over the course of several hours.
Related Content. Long-term Potentiation Professor Seth Grant explains that long-term potentiation is based on the principle that synapses become stronger with experience. ID: Source: G2C. Multiple Electrode Arrays Professor Tom O'Dell explains how multiple electrode arrays are being used to study electrical activity in the brain. Recording Electrical Activity in Brain Slices Researchers from the Wellcome Trust Sanger Institute demonstrate how action potentials are recorded from brain slices, and how long-term potentiation is measured.
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Four hours after washout of CHX, [ 3 H] leucine incorporation was only inhibited by That is why we have added the drug during the whole experiment Fig. On the other hand, 4 h after anisomycin washout, the protein synthesis was still reduced by In the two parts of the figure A, B , either drug was applied starting 20 min before the induction of LTP on the S1 pathway till the end of the experiment.
LTP was induced using a single high-frequency stimulation train Hz, 1 s. In each part of the figure, the time courses of the fEPSP slope in the S1 pathway and S2 pathway control , both in the presence and in the absence of the protein-synthesis inhibitor used, are displayed. Sample fEPSP traces from individual experiments are shown in the insert; they were recorded in the presence of the drug, before thin traces and 8 h30 after thick traces LTP induction.
Anisomycin is thus a powerful inhibitor of the basal protein synthesis. We put this hypothesis to the test, using a chemical induction of LTP in order to affect a great number of synapses. Thirty minutes later, the incorporation of [ 3 H] leucine was not increased Sajikumar et al. They also demonstrated that this late-LTP was dependent on de novo protein synthesis as it was blocked by anisomycin and emetine.
Fonseca et al. The more rapid the frequency of the test stimulation, the more the LTP was sensitive to protein-synthesis inhibitors.
The delivery of either drug started 20 min before the train of stimulation and was maintained during the entire experiment. The fEPSP slopes measured at the end of the experiments were not different — whether anisomycin was applied or not Similarly, the fEPSP slopes measured at the end of the experiments were not different in the presence or in the absence of cycloheximide In a methodology paper, Sajikumar et al [11] recommended to wait at least 4 h after dissection before inducing LTP. According to these authors, this long resting period provides a more stable recording but also allows the slices to reach a metabolic stability and might lead to a reduction of the level of the plasticity-related proteins PRPs close to zero.
In a recent paper, Redondo et al [15] also used this long resting period before inducing a protein synthesis-dependent LTP. We therefore applied anisomycin after a recovery period in interface of 4 h. In order to diminish the risk of side effects of weakly reversible drug, anisomycin was further applied only for 1 h after the induction of LTP. As shown in figure 5A , the potentiation reached 8 h after the train in such conditions was not different from that obtained when the recovery period lasted 1.
Eight hours after the train, the potentiation was still at For these experiments, the recovery period was extended to 4 h. LTP was triggered using a single high-frequency stimulation train Hz, 1 s. Open circles correspond to the fEPSP slopes measured on the potentiated pathway, whereas filled circles represent the fEPSP slopes measured on the control pathway.
It has been repeatedly claimed that the development of the late phase of L-LTP necessitates the synthesis of plasticity-related proteins PRPs. We demonstrated above that, in our experimental conditions, these PRPs were not synthesized during the LTP induction or after it.
A possibility remained that these PRPs would be synthesized during the recovery period. To assess the hypothesis, we pre-incubated slices during 4 h with anisomycin before inducing LTP Fig.
Here again, the level of potentiation reached 8 h after induction In our experimental conditions, the L-LTP triggered by a single train was found to be surprisingly protein synthesis-independent. We next ascertained that it shared the main properties of the L-LTP reported in the literature, i. One hour after the train, we observed a residual potentiation of As shown in figure 6A , after washing the drug, LTP could be induced normally in the same slices.
Other ACSF components were unchanged. We modified the ACSF composition to alter the ratio between calcium and magnesium concentrations from 2.
Two hours after its induction, the LTP was reduced to Four hours after the train, the potentiation was reduced to In rat hippocampal slices, Fonseca et al [18] found that the sensitivity of L-LTP to protein-synthesis inhibitors was dependent on the protocol used for the test-pulse stimulation. In their study, they showed that when the test-pulse frequency was 0. Fonseca et al [18] also demonstrated that at that test frequency 0.
Their finding is consistent with the idea that synaptic activity increases the turnover of proteins necessary for LTP, thereby modulating LTP stability.
The decay time of that t-LTP was inversely related to the frequency of stimulation during the post-tetanic test period. In this study, LTP, tested in mouse hippocampal slices, was found not to be dependent on protein synthesis.
It was thus interesting to investigate whether increasing the test-pulse frequency could modify the maintenance phase of LTP. We found that if the Schaffer collaterals were stimulated every 10 sec, the potentiated response decreased progressively.
For clarity, only the data related to the tetanized pathways are shown. In cultured cells, it has been demonstrated that these receptors are incorporated into the membrane in an activity-dependent manner for GluR1 and GluR1-GluR2 and thanks to a constitutive process for GluR2-GluR3 For a review [24].
When applied after LTP induction Fig. This effect was reversible: about 30 minutes after the washout of the drug the response came back to its initial level. Baseline was calculated on the 20 minutes prior to the drug perfusion. Only data related to the tetanized pathways are shown. To facilitate the comparison, the fEPSP slope is expressed in percentage of the mean fEPSP amplitude measured over a period of 20 min before the application of the drug.
However, this does not rule out the possibility that an L-LTP induced by repeated trains of stimulation would be protein-synthesis dependent. We thus checked the effect of a protein-synthesis inhibitor on the L-LTP induced by 4 trains Hz, 5 min apart. As shown in Figure 9 , the fEPSP slopes measured at the end of the experiments were not different — whether anisomycin was applied or not The strength of the synapses tested via S2 remained unchanged in the presence of anisomycin LTP was induced using four high-frequency stimulation trains Hz, 1 s, 5 min apart.
The time courses of the fEPSP slope in the S1 pathway and S2 pathway control , both in the presence and in the absence of the drug, are displayed. Sample fEPSP traces from an individual experiment are shown in the insert; they were recorded in the presence of the drug, before thin traces and 8 h after thick traces LTP induction.
According to the classical views about LTP, long-lasting LTP 1 necessitates the application of several trains of HFS for its induction and 2 is dependent on a synthesis of some proteins, triggered by the inductive stimulus.
In the present work, carried out in mouse hippocampal slices, we demonstrated that a long-lasting LTP could be triggered 1 by a single train of HFS and 2 in the presence of inhibitors of protein synthesis.
In order to validate our result, two different inhibitors of protein synthesis the efficacy of which had been ascertained were used with two different timings of inhibition and two different periods of recovery after dissection. This result was previously obtained in rat hippocampal slices [11] , [10] , [25] whereas in mice the group of Nguyen has repeatedly shown that a single train Hz, 1 s induced a short-term LTP lasting only between 1 and 2 h [26] — [29].
First of all, we would like to emphasize the fact that technical conditions have a great influence on the duration of the LTP induced by a single train of stimulation. In previous publications, our group showed that a short-lasting LTP can be transformed into a long-lasting one by modifying the recovery conditions of the slice [30]. We have also observed over years a lengthening of the sustained phase of the LTP induced in mouse hippocampal slices maintained in interface.
Indeed, recordings made in showed a short-lasting LTP going back to baseline within 3 hours [31]. Modifications in the dissection procedure reducing tissue stretching have made it possible to obtain an LTP sustained for 6 hours [32].
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