ABSTRACT Sleep supports memory formation by neurophysiological mechanisms that are yet to be fully uncovered. We investigated the contribution of the direct coupling of neurons via electrical synapses (gap junctions). The administration of mefloquine (250 mg p.o. vs. placebo), an antimalarial, which blocks electrical synapses, to healthy young men before nocturnal sleep impaired the retention of word pairs learned before drug administration and disrupted the coupling of sleep spindles to EEG slow oscillations. In control experiments, in which participants received mefloquine before a consolidation interval of nocturnal wakefulness or after rather than before sleep, word‐pair memory retention was not affected by the drug, suggesting that electrical synapses specifically support the sleep‐dependent retention of verbal declarative memory. Irrespective of sleep, mefloquine enhanced the retention of sensorimotor memory assessed with a finger sequence tapping task. In supplemental experiments in rats, mefloquine administered i.p. at escalating doses of 20 and 40 mg/kg did not alter hippocampal sharp‐wave/ripple activity, a prominent mechanism of hippocampal memory replay. While mefloquine effects beyond gap junctions in the present experiments cannot be fully excluded, we conclude that electrical coupling enhances the oscillatory coordination between sleep spindles and slow oscillations and, thereby, supports systems memory consolidation.
Feld et al. (Thu,) studied this question.