Marcella La Cioppa A recent study has given a biological explanation for the formation and maintenance of long-term memory, centered on a molecule called KIBRA. This molecule, according to scholars, acts like a "glue" in the sense that it adheres to strong synapses and helps maintain the connections necessary for memories to last for years, even decades.
It has long been known that neurons store information in memory as a pattern of strong and weak synapses, which in turn determines the connectivity and function of neural networks.
However, the molecules within synapses are unstable, continuously diffusing around neurons, degraded, and replaced within hours or days. This of course raises the question: how can memories remain stable over years or even decades?
The study, published in Science Advances, led by an international team of researchers, identified the role a molecule called KIBRA plays in acting like “glue” for other molecules to consolidate memory formation.
The study
The function of a protein in the kidneys and brain, referred to as KIBRA, was investigated by the scientists. Variants of this gene in humans are associated with good and poor memory.
They focused on interactions of KIBRA with other key molecules in the process of memory formation, especially a protein called protein kinase Mzeta, or PKMzeta.
This enzyme is considered to be the most important molecule known for the strengthening of typical synapses within mammals but degrades after just a few days.
Their experiments show that KIBRA constitutes a sort of “missing link” in long-term memories – a kind of “persistent synaptic tag,” or glue, which latches onto the strong synapses and the PKMzeta while avoiding the weak synapses.
During memory formation, the synapses involved are tagged by being activated, and KIBRA is selectively positioned at these synapses. PKMzeta then binds with the synaptic tag KIBRA, keeping those synapses strong. The synapse would thus stick to newly synthesized KIBRA, attracting more newly synthesized PKMzeta.
Earlier work had shown that a random brain increase of PKMzeta boosted weak or fading memories—an implausible outcome, as it should have disrupted memory instead, acting in random locations. The persistent synaptic tagging by KIBRA explains why the additional PKMzeta was improving memory—by acting only at the sites marked by KIBRA.
Source: Science Advances
