生物谷報道：記憶與哪些因子有關(guān)？競爭是否有利于記憶,？最新的德國1Max-Planck Institute of Neurobiology和蘇格蘭科學(xué)家發(fā)現(xiàn),，競爭有利于LTP的形成和維持，能提高記憶,。這一研究成果揭示了競爭情況下記憶能力增強的機理,。

Figure 1. Competitive Interaction between Two Potentiated Pathways

(A) Weak and strong tetani were used to induce associative LTP in two CA3 to CA1 synaptic pathways (also see inset in the upper right corner). Four hours after the start of the experiment, the protein synthesis inhibitor anisomycin (ANI) was bath applied to the slice (yellow bar). Forty minutes later, one of the pathways (reactivated pathway [RP], red symbols) received another (weak) tetanus, while the other pathway (test pathway [TP], blue symbols) continued to receive only test pulses. Potentiation of the reactivated pathway is at the expense of persistence of LTP in the test pathway, provided the experiment is performed under anisomycin (filled symbols). In the control case (open symbols), no such effect can be observed. In this and subsequent figures, the statistical significance of the difference between test pathways in the presence or absence of anisomycin, expressed in p values, is plotted by the green triangles. The significance value of p = 0.05 is always displayed as dashed line. Repeated-measures ANOVA values: F(1,13) = 20.12; p = 0.00061. The inset in the upper right corner shows the initial hour of the experiment displayed at a more conventional time scale. The data are the same as in the main panel. Only the binning of the data is different (one data point per minute in the inset; one data point per four minutes in the main panel).

(B) Example traces of fEPSPs for the test and reactivated pathways at times indicated by the colors and the circled numbers (also see [A]).

(C) The competitive maintenance effect at an expanded time scale (synaptic transmission before the second potentiation in the test and reactivated pathways was normalized to 100%).

(D) Correlation between the potentiation of the reactivated pathway and the decrease of the test pathway are plotted for each experiment, either in the presence (filled symbols) or absence (open symbols) of anisomycin. A linear regression shows for the anisomycin experiments a clear correlation of the amount of potentiation in the reactivated pathway with the amount of decay in the test pathway while there is no correlation for the control cases.

(E) The effect only occurs on a potentiated pathway: an unpotentiated control pathway (CP, blue symbols) does not show decay in response to reactivation of the other pathway (RP, red symbols), which was subjected to an initial tetanus (filled arrow) and then a second tetanus (filled arrow) in the presence of anisomycin.

(F) Time course of the synaptic responses in two pathways that both expressed associative LTP. Anisomycin alone does not cause decay in either pathway (RP and TP only in analogy to [A]; no reactivation is applied). n, number of slices.

Figure 2. Competitive Maintenance Does Not Occur under APV but It Is Also Observed with an Alternative Protein Synthesis Blocker, Emetine

(A and B) Competitive interaction does not occur if AP-5 is present during the reactivation. (A) Experiment similar to the one shown in Figure 1A but in the presence of AP-5 and anisomycin or anisomycin alone. For clarity, only the relevant 6.5 hr of the experiment are shown (responses 20 min before the last tetanus were normalized to 100%). Under AP-5, NMDA receptors are blocked, and no further potentiation is obtained by the reactivation. No decay was observed for the test pathway in turn. Without APV, the same competitive interaction displayed in Figure 1A occurs. Repeated-measures ANOVA values: F(1,10) = 6.921; p = 0.025. (B) The experiments performed with anisomycin alone (solid circles) show a clear correlation between potentiation in the reactivated pathway and decay in the test pathway, whereas the experiments performed with anisomycin and APV yield no correlation (compare also to Figure 1D). n, number of slices.

(C and D) Competitive interactions are also induced when protein synthesis is blocked with emetine. (C) Experiment similar to the one shown in Figure 1A, only with emetine as protein synthesis blocker instead of anisomycin. Again, only the relevant 6.5 hr of the experiment are shown (responses 20 min before the last tetanus were normalized to 100%). Repeated-measures ANOVA values: F(1,4) = 30.073; p = 0.0053. (D) The emetine experiments also show a clear correlation between potentiation in the reactivated pathway and decay in the test pathway. n, number of slices.

Figure 3. Modulation of Protein Availability Influences Competitive Maintenance

(A and B) Competitive interaction is increased after prolonged application of anisomycin. (A) Experiment similar to the one shown in Figure 1A; however, anisomycin was bath applied for a period of 3 hr, presumably limiting the availability of plasticity factors even further. The decline observed in the test pathway due to the reactivation is increased. For clarity, only the relevant 6.5 hr of the experiment are shown (responses before the last tetanus were normalized to 100%). Repeated-measures ANOVA values: F(1,10) = 26.57; p = 0.00042. (B) Potentiation in the reactivated pathway plotted against the potentiation (resp. decay) in the test pathway, either in the presence (filled symbols) or absence (open symbols) of anisomycin. The correlation analysis reveals a stronger correlation between potentiation in the reactivated pathway and decay in the test pathway as well as a stronger effect (denoted by the steeper slope of the regression line).

(C and D) Competitive interaction is decreased by reducing the time period between initial LTP induction and reactivation. (C) In this case, the reactivating tetanus was applied already after 2 hr, causing the competition to vanish (p values as green triangles). For clarity, only the relevant 8.5 hr of the experiment are shown (responses 20 min before the last tetanus were normalized to 100%). Repeated-measures ANOVA values: F(1,15) = 0.625; p = 0.4416. (D) Linear regression returns no correlation. n, number of slices.

Figure 4. Competitive Interaction Is Absent when Input Pathways Are in Separate Dendritic Domains

(A) Experiment similar to the one shown in Figure 1A. This time, however, stimulation electrodes were spatially separated. Fibers in the stratum oriens served as the reactivated pathway, whereas the fibers of the stratum radiatum defined the test pathway. With this spatial separation, the competitive interaction between the two potentiated pathways vanished. For clarity, only the relevant 6.5 hr of the experiment are shown (responses 20 min before the last tetanus were normalized to 100%). Repeated-measures ANOVA values: F(1,13) = 0.294; p = 0.5966.

(B) Illustration of the positions of recording and stimulation electrodes. Two stimulation electrodes placed in the stratum oriens and the stratum radiatum were used to evoke fEPSPs. In this case, we used two recording electrodes placed within the basal and apical dendritic region of CA1 neurons to faithfully record the synaptic potentials generated on different sides of the cell body.

(C) Linear regression shows no correlation between potentiation in the reactivated pathway and decay in the test pathway. n, number of slices.

Figure 5. Competitive Interaction Is a Function of LTP Reactivation Strength

(A) Experiment similar to the one shown in Figure 1A. For clarity, only the relevant 3.5 hr of the experiment are shown (responses 20 min before the last tetanus were normalized to 100%). In contrast to the experiment in Figure 1A, high-frequency trains differing in the number of pulses were used to reactivate the second pathway. The more pulses are applied to the reactivated pathway (the “stronger” the stimulation), the more pronounced is the decay in the test pathway.

(B) Relationship between the number of pulses used for the reactivating tetanus and the subsequent decay produced in the synaptic responses of the test pathway. n, number of slices.

Figure 6. Competitive Interaction under Conditions of Prior Weak Associative Tetanization

(A) Experiment similar to the one shown in Figure 1A, but in the absence of anisomycin. Associative LTP was induced by concurrently applying weak tetanus to both pathways (see inset). Four hours later, one of the pathways (P1) received a second weak tetanus, this time in the absence of anisomycin. This results in potentiation of the reactivated pathway, again at the expense of a decay in the test pathway. In the control experiments (open symbols), no second tetanus was applied. For clarity, only the relevant 4 hr of the experiment are shown (responses 20 min before the last tetanus were normalized to 100%). Repeated-measures ANOVA values: F(1,12) = 27.28; p = 0.00021.

(B) Linear regression shows a clear correlation between potentiation in the reactivated pathway and decay in the test pathway. n, number of slices.

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