TAU researchers solve brain mystery

Scientists discover how memory is encoded in brain cells.

brainbow nerve cells 311 (photo credit: Brainbow/Idan Segev)
brainbow nerve cells 311
(photo credit: Brainbow/Idan Segev)
The molecular mechanism that regulates the coding of memory in brain cells – a question that has puzzled neuroscientists for many years – has been discovered by researchers at Tel Aviv University, whose find was published this week in the journal Neuron.
Dr. Inna Slutsky of the university’s Sackler Medical Faculty, doctoral student Tal Laviv and post-doctoral student Inbal Riven, along with Prof. Paul Schlesinger of the Salk Institute in California, succeeded in observing the activity of neurons in a single synapse (the gap between neurons).
They realized that they understood why there were different synaptic activities and that this difference was important for coding memory within the nerve cells.
The team also discovered that the difference between the neural connections was caused by GABA, a molecule produced by the neurons that hinders their activities.
Slutsky explained that the synapses, which constitute junctures for the transmission of data from one neuron to another, are the basic units for storing memories in the brain. The differences in synaptic activity, she said, are the necessary characteristic in the brain’s learning and memory process. Previous research has shown that some of the synapses are “quiet” and don’t release chemical neurotransmitters; thus, they don’t transmit information when the synapses are at rest. Some transmit data constantly, while in most synapses, the transmissions vary. Even though the rest condition of synapses is a critical requirement for coding and processing of memory, until now the molecular mechanism that causes the differences in release of neurotransmitters was not known.
The new discovery focuses on synaptic activity in the hippocampus, a brain region known to be involved in memory and learning. The team examined the influence of the GABA neurotransmitter, which is found throughout the brain and usually hinders neural activity. The research found that the mechanism that regulates the differences among the synapses is carried out by GABA while activating GABAb receptors, which are found in the synapses and modulate individual synapse activity in a local way. Thus, the TAU researchers found out how the mechanism works at the synaptic level and not just at the level of cells and whole tissue, which had been the case before.
Slutsky said the research would not have succeeded without the “breakthrough” in scanning techniques that began in recent years.
“We succeeded in unifying two optical techniques at high resolution – one to see the activity of individual synapses and the second to understand the dynamics of interactions between proteins up to 10 nanometers in size in a single synapse,” she said.
She added that the discovery had been helped by proteins of the GABAb receptor that were attached by genetic engineering to fluorescent molecules in Schlesinger’s lab. These engineered proteins made it possible to follow the location and activities in the neurons and constituted the sensor for the level of activity of the GABAb receptor in individual synapses, she explained.
In November 2009, Slutsky published an article on amyloid beta, the protein whose excess is involved in the decline in cognitive function found in Alzheimer’s disease patients. Her study then found that it had an important physiological role in the healthy brain: It regulates the transfer of signals between synapses.
“Amyloid beta is a positive regulator that intensifies the basic activities of the synapse, while GABA is a negative regulator that minimizes its activities. These studies brought us to the hypotheses that the intensification of basic activity of the synapses constitutes the first and critical stage in the development of a decline in learning and memory in neurodegenerative diseases,” she concluded.