Emerging research reveals that our brains remember specific events via physical changes in synapses, the tiny connections between neurons.
Researchers at Duke University and the Max Planck Florida Institute for Neuroscience say the discovery of the molecular mechanisms by which these changes take place was unexpected.
Investigators believe the findings could also shed light on how some diseases develop, including certain forms of epilepsy.
The study appears online in the journal Nature.
“We’re beginning to unlock some of the mysteries underlying both the acquisition of a memory in the normal brain, as well as how a normal brain is transformed into an epileptic brain,” said James McNamara, M.D., a professor in the departments of neurobiology and neurology at Duke University.
As we acquire a new memory, the connections, or synapses, between certain sets of neurons strengthen. In particular, the receiving end of a pair of these neurons — consisting of a little nub called a spine — gets a little larger.
Researchers have long suspected that a brain receptor called TrkB was involved with the growth of spines when we learn, but the new study confirms that the receptor is indeed crucial and delves further into how it works.
Investigators say new technologies enabled the research as they used a molecular sensor (which they developed) to track activity of TrkB, and microscopes that allowed them to visualize a single spine in the area of living mouse brain tissue, all in real time.
The group also was able to add a tiny amount of signaling chemical, glutamate, at the single spine in order to mimic what happens during learning. This caused the spines to grow.
“The mouse brain has approximately 70 million neurons, and most of them are dotted with thousands of spines,” McNamara said. “So, to be able to model and study the events occurring in a single spine in a single neuron is remarkable.”
Without the TrkB receptor, spine growth did not occur in response to the signaling chemical, the group found.
The team suspected that yet another player, brain-derived neurotrophic growth factor (BDNF), was involved because it is the molecular key to TrkB’s lock.
The scientists created a molecular sensor for BDNF and showed that mimicking the signal associated with learning caused the release of BDNF from the receiving end of the synapse. This was surprising because conventional wisdom holds that BDNF is only released from the sending neuron, not the receiving neuron.
The fact that the receiving neuron both discharges BDNF into the gap between neurons and also senses it is “extremely unique, biologically,” said co-senior investigator Ryohei Yasuda. “One possibility is that BDNF is regulating several surrounding cells at once. We’re interested in following up to understand the exact process.”
Although the experiments were conducted in mice, the interaction between TrkB and BDNF is likely to be important for learning and memory in people, McNamara said.
Source: Duke University/ScienceDaily