The question of how short-lived
memories (~the momentary contents of one’s consciousness) become stored in
long-term memory that lasts up to one’s lifetime is one of the most fundamental
ones in cognitive neuroscience. This process is referred to as memory
consolidation. While the underlying neural mechanisms have begun to be
understood with increasing detail, open questions have remained. As one
instance of this, there is research indicating that memory consolidation is not
a unitary one-step process, but rather that there are lapses in memory even
after the initial consolidation.
Thriving on recent advances in
understanding the behavioral and molecular mechanisms underlying memory
consolidation in Lymnaea during associative conditioning, Marra et al. (2012) studied the neural events
underlying lapses in memory that take place during consolidation. Using a
specific in vitro behavioral
one-trial conditioning approach, the authors observed lapses in memory at 30
min and 2 hours after conditioning, but not at other tested time points of 10
min, one, three, and four hours. While the lapse at 30 min marked transition
from short-term to intermediate-term memory, the lapse at two hours
post-conditioning suggested that intermediate-term memory has early and late
phases with distinct underlying molecular mechanisms. Furthre, these lapses constituted
time points during which memory consolidation was susceptible to disruption by
external stimuli. Disruption at two hours blocked long-term memory 24 hours
later, and disruption at 30 min blocked recall at three and four hours
post-conditioning. The underlying molecular mechanisms were studied by
inspecting the effects of specific pharmacological agents modulating protein
kinase activity on these different phases of consolidation.
The results suggested specific
steps in memory consolidation, with changes in properties of ion channels
resulting in increased excitability lasting for at least 10 min post-training,
followed by enhancement of synaptic efficacy by proteins synthesized from
existing RNA between 10 min and the first hour (e.g., insertion of more channel proteins) that lasts up to three
hours. New synapses are then produced over at least the first 24 hours that
correspond to consolidation to long-term memory. The long-term memory
consolidation was observed to be dependent on protein kinases C and M, with
early and late phases of long-term memory however differing in requirement of
for duration of protein kinase A activity after training. Taken together, these
results are highly exciting in illuminating specific molecular events
underlying the distinct steps that lead to consolidation of memories from
short-term through intermediate-term to long-term memory, and by showing how
the transition periods between the processes of consolidation are specifically susceptible
to disruption by distracting stimuli/events.
Reference: Marra V, O’Shea M, Benjamin PR, Kemenes I.
Susceptibility of memory consolidation during lapses in recall. Nature Communications
(2013) 4: 1578. http://dx.doi.org/10.1038/ncomms2591