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Recently, researchers at Duke University and the Max Planck Florida Institute for Neuroscience revealed an unexpected molecular mechanism in memory.
the study, published online online in Nature, may explain how some diseases, such as epilepsy, are produced.
also foreshadows the secrets behind the normal brain's ability to gain memory and transform it into a brain suffering from epilepsy.
as we gain new memories, the synapses between neurons in the brain become more closely linked, especially as the synapses of neurons increase.
scientists have long suspected that a brain subject called TrkB is associated with the growth of tyb during our learning.
study confirms that this subject is in fact critical and further studies how it works.
technologies that made the discovery possible include a molecular sensor and a microscope that visualizes individual tree trout ratchets.
the team could also add small amounts of chemical signaling material and glutamate to a single detour to simulate the learning process, which can cause the desception to grow.
McNamara said: "The mouse brain has about 70 million neurons, most of which are covered with thousands of deity.
, it makes sense to study and model a single tyche.
study found that without the TrkB subject, the tyb would not have grown in response to the chemical signaling substance.
researchers suspect that brain-derived neurotrophic factors (BDNF) are also associated because it activates TrkB subjects.
scientists created a molecular sensor for BDNF and found that simulating learning-related signals causes BDNF to be released from the receiving end of the synapse.
this is surprising because previous cognitions have suggested that BDNF is released only by sender neurons.
receiver neurons not only release BDNF in the neuron gap, but also perceive BDNF.
possibility is that BDNF can regulate several surrounding cells at the same time.
although the experiments were conducted in mice, the interaction between TrkB and BDNF is also important for human learning and memory processes.
, the same mechanism exists in temporal lobe epilepsy (TLE), which works on the brain region responsible for memory and learning.
TLE is thought to be caused by early single long-term epilepsy.
during epilepsy, glutamate (memory-related neuromedicals) is released over a large period of time.
early work of McNamara showed that TrkB subjects were important for the formation of TLE.
last fall, his team found that suppressing TLE signals after the first epilepsy prevented mice from producing TLE.
McNamara's team has embarked on further experiments to explore what happens when TrkB is activated to make individual destrute ratchets bigger.
, there are other mechanisms that appear to cause TrkB to activate during memory and seizures, and McNamara's team is studying these potential mechanisms.
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