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.
Spinal muscular atrophy (SMA) is an inheritable cause of infant mortality that is characterized by the loss of lower motor neurons and skeletal muscle atrophy. The degeneration of motor neurons is caused by insufficient levels of survival motor neuron (SMN) protein, which is encoded by two nearly identical genes SMN1 and SMN2. Most cases of SMA harbour homozygous deletions of the SMN1 gene and retain at least one copy of SMN2.READ MORE