Electrophysiological Changes Underlying Lapses in Memory Consolidation
Poster Dec 08, 2017
Michael Crossley, Fred Lorenzetti, Michael O'Shea, Paul R. Benjamin, Ildikó Kemenes
Memory consolidation is generally conceived as a process whereby new information sequentially moves to successively longer-term stores. In invertebrates and vertebrates, including humans, there are memory lapses during consolidation.
We previously found that in the pond snail (Lymnaea stagnalis) one-trial appetitive classical conditioning was accompanied by memory lapses at 30 min and 2h after training. Memory consolidation was disrupted when a disturbance is applied during one of these lapse periods but not when presented at any other time periods.
A second training at different times after the initial conditioning showed that training during lapse periods leads to the abolition of the memory induced by the initial training and replacement by the second memory.
Using both intracellular and extracellular (multielectrode array - MEA) we found memory lapses at times (30 min and 2h) corresponding to the times of lapses observed following in vivo training.
By recording the feeding modulatory CGC interneurons intracellularly we found that a previously described non-synaptic change, characterised by significant decrease in this neuron’s membrane potential 24h after the learning is also present after the original memory is replaced by the second memory.
Tactile sensory disturbance applied during the lapse peripods however blocked depolarization of the membrane potential when recorded at 24 hours after conditioning suggesting that memory replacement is not due to disturbance.
Early life stress (ELS) is highly associated with development of psychopathology
and mood disorders in adulthood. Genetic studies have identified variation in the gene calcium voltage-gated channel subunit alpha1C (CACNA1C) to increase risk for several psychiatric disorders. This poster assessed the expression of Cacna1c following prepubertal stress.
We found a distinct subpopulation of Tregs within BMSCs. Tregs and BMSCs in co-culture conferred neuroprotection that varied in a dose-dependent manner. Tregs minimized stem cell production of IL-6, a pro-inflammatory cytokine, and inhibited BMSC secretion of FGF-beta, a cytokine related to BMSC proliferation and differentiation. The ratio of Tregs found natively in BMSCs is optimally adapted to provide the maximum neuroprotective benefit of stem cell treatment after ischemic stroke.READ MORE