A natural molecule that occurs in the brain, GABA (?-Aminobutyric acid), could be the main factor in regulating how many new memories we can generate, say researchers at Tel Aviv University.
The new study by Dr. Inna Slutsky of the Sackler School of Medicine at Tel Aviv University describes what makes some memories stick.
The understanding of these mechanisms might lead to the development of new memory enhancers and new treatments for neurodegenerative diseases such as Alzheimer's.
Memories are stored in synaptic connections between neurons in our brain, said. Slutsky.
In the past, other teams, including her own, have demonstrated that the strength of individual synapses is highly variable, even at the single neuron level.
This variability ultimately determines if and how new memories are stored, and the key to this variability is GABA, a naturally-occurring chemical found in the brain.
The researchers applied advanced nanotechnology methods in optical imaging to track how proteins engineered by Prof. Paul Slesinger and his team at The Salk Institute interact with GABA at the single-synapse level.
In the hippocampus, one of the main areas of the brain involved in learning and memory, the strength of neuronal connections is known to be highly variable.
Some neurons are tightly connected to others, while some appear to be "lone rangers."
The new paper, which examines individual synapses in the hippocampus, demonstrated that this process is regulated by GABA- the main inhibitory neurotransmitter in our brain.
"We determined that variations in the local level of GABA in the vicinity of individual synapses are responsible for the differences or 'heterogeneity' of synaptic strength. And this heterogeneity may facilitate the formation of new memories," explained Slutsky.
The researchers found that higher concentrations of GABA near a synapse induced a stronger activation of its receptors, weakening basal synapse strength.
Thus, GABA makes this synapse more liable to the formation of new memories, proposed the researchers.
Slutsky said that the research may also have implications for treating diseases of the mind.
"We found that amyloid-beta, a well-known hallmark of Alzheimer's disease, regulates basal synapse strength in an opposite way to GABA," she noted.
She suggested that an increase in the basal activity of synapses might initiate memory decline in Alzheimer's and other neurodegenerative disorders.
The study has been published in the prestigious science journal Neuron.