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Abstract:
Noradrenergic modulation has been hypothesized to contribute to memory consolidation by promoting synaptic plasticity in recently activated neural circuitries [1]. Behavioral studies identified a time window of ~ 2h after learning when noradrenergic influence on memory consolidation is most pronounced. Behavioral data are complemented with studies of long-term potentiation (LTP) or long-term depression (LTD), a cellular models of memory formation. One important outcome of these studies is that noradrenaline (NA) is required for late, protein-dependent phase of synaptic plasticity. According to the consolidation hypothesis, memory formation is a long-lasting process and thus continues after actual learning experience, i.e. off-line. Recently, sleep-mediated mechanisms of off-line information processing has drawn a lot of attention. A number of human and animal studies have convincingly shown the beneficial role of slow wave sleep (SWS) for memory consolidation. The activity of brain stem nucleus Locus Coeruleus (LC) - a major source of NA in the forebrain - is low, but not absent during SWS. By directly monitoring spiking activity of LC in behaving rats, we have recently revealed a transient surge of LC activity that occurred during SWS at around 2h after learning. In the present study we aimed to characterize LC activity in relation to SWS-associated cortical oscillations. Both slow waves (~ 1Hz) and spindles (~12Hz) are modulated by learning. LC activity is highly synchronized during SWS. Firing of LC neurons mostly occurs during the transition from cortical down to up state defined by a phase of slow oscillations. The LC activity is elevated immediately after the spindle onset. Taking into account experience-dependent replay of neuronal assemblies in multiple brain regions time-locking of LC activity to major cortical rhythms suggests synchronous noradrenergic modulation promoting synaptic plasticity in multiple and functionally connected brain sites.
