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Acquisition was not affected by treatment (p?> 0.05; one-way ANOVA). DAB injection with vehicle disrupted long-term memory retention, confirming our previous results (Figure?1B). Conversely, 100, but not 10?nmol of L-lactate coadministered with DAB significantly rescued the memory loss. Retesting check details the rats 7?days after training revealed that the effects of?treatments persisted (p?Autophagy a rapid glycogenolysis and consequent efflux of lactate in the hippocampus, which is critical for long-term memory formation. Long-term potentiation (LTP) is a leading cellular model for memory formation and is induced at CA1 synapses by IA (Whitlock et?al., 2006). Accordingly, we next tested the effect of blocking glycogen metabolism on LTP in area CA1 of anesthetized young adult rats. After establishing a baseline of responses at Schaffer collateral-area CA1 (SC-CA1) synapses, LTP of SC-CA1 synapses was induced by a high-frequency tetanic stimulation protocol in the absence or presence of DAB delivered locally to the CA1 neuropil through the recording pipette. In the absence of DAB (the control group), robust LTP was induced (fEPSP slope: 133.85 �� 7.9% of baseline at 120?min posttetanus; Figure?3A, closed circles) as expected (Bozdagi et?al., 2007). In contrast, in the presence of DAB, tetanic stimulation produced a strong initial potentiation, but thereafter, potentiation decayed rapidly to baseline by 75?min in the DAB injected group (Figure?3A, open circles), indicating Etoposide solubility dmso that DAB blocks the maintenance but not the induction of LTP. To rule out that the effect of DAB on LTP maintenance resulted from non-specific general metabolic demands of the high-frequency tetanic stimulation per se, we tested the effect of DAB on baseline neurotransmission in a group of rats in which LTP was blocked by an i.p. injection of the N-methyl-D-aspartate receptor (NMDAR) antagonist MK-801 prior to stimulation. Figure?3A shows that when LTP was blocked by MK-801, DAB had no effect on baseline over 120?min following stimulation, supporting the ides that DAB blocked LTP maintenance selectively. We verified that DAB alone, in the absence of tetanic stimulation, had no effects on basal synaptic transmission by examining parameters that reflect normal synaptic function, including the relationship between stimulus strength and the size of the postsynaptic response (input-output relationship; Figure?3B) or paired-pulse facilitation (PPF, Figure?3C).