A McGill-led multi-institutional research team has discovered that in memory consolidation, there are a minimum of two distinct processes happening in two different brain networks -- the excitatory and inhibitory networks. The excitatory neurons are involved in creating a engram , and therefore the inhibitory neurons block out ground noise and permit long-term learning to require place.
The team, led by McGill University Professors Nahum Sonenberg and Arkady Khoutorsky, Université de Montréal Professor Jean-Claude Lacaille, and University of Haifa Professor Kobi Rosenblum, senior authors on the paper published today in Nature, also found that every neuronal system are often selectively manipulated to regulate LTM . The research, which answers a long-standing question about which neuronal subtypes are involved in memory consolidation, has potential implications for novel targets for medication for disorders like Alzheimer's disease and autism, which involve altered memory processes.
Looking for the neurons involved in memory consolidation
How do short-term memories (which last just a couple of hours) transform into long-term memories (which may last years)? it has been known for many years that this process, called memory consolidation, requires the synthesis of latest proteins in brain cells. But so far , it hasn't been known which subtypes of neurons were involved within the process.
To identify which neuronal networks are essential in memory consolidation, the researchers used transgenic mice to control a specific molecular pathway, eIF2α, in specific sorts of neurons. This pathway had already been shown to play a key role in controlling the formation of long-term memories and regulating protein synthesis in neurons. Moreover, earlier research had identified eIF2α as pivotal for both neurodevelopmental and neurodegenerative diseases.
Excitatory and inhibitory systems both play a task in memory consolidation
"We found that stimulation of protein synthesis via eIF2α in excitatory neurons of the hippocampus was sufficient to reinforce memory formation and modification of synapses, the sites of communication between neurons," says Dr. Kobi Rosenblum.
However, interestingly, "we also found that stimulation of protein synthesis via eIF2α during a specific class of inhibitory neurons, somatostatin interneurons, was also sufficient to reinforce LTM by tuning the plasticity of neuronal connections," says Dr. Jean-Claude Lacaille.
"It is fascinating to be ready to show that these new players -- inhibitory neurons -- have a crucial role in memory consolidation," added Dr. Vijendra Sharma, a search associate in Prof. Sonenberg's lab and therefore the first author on the paper. "It had been assumed, until now, that eIF2α pathway regulates memory via excitatory neurons."
"These new findings identify protein synthesis in inhibitory neurons, and specifically somatostatin cells, as a completely unique target for possible therapeutic interventions in disorders like Alzheimer's disease and autism," concluded Dr. Nahum Sonenberg. "We hope that this may help within the design of both preventative and post-diagnosis treatments for those that suffer from disorders involving memory deficits."
The research was funded by: Canada's International Development Research Centre (IDRC), in partnership with the Azrieli Foundation, the Canadian Institutes of Health Research (CIHR), and therefore the Israel Science Foundation (ISF) to K.R. and N.S., JCL is supported by a CIHR Project grant and a Canada Research Chair in Cellular and Molecular Neurophysiology.
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