Scientists discover how memories are preserved in human brain
Neuroscientists have made a significant breakthrough in understanding how memories are stored and retained in the human brain. The research, led by Todd Sacktor from SUNY Downstate Health Sciences University and Andre Fenton from New York University, has identified two molecules that play a crucial role in this process. The findings were recently published in Science Advances, marking a milestone in neuroscience.
A closer look at long-term potentiation
The concept of long-term potentiation (LTP), discovered in the early 1970s, is central to our understanding of memory storage. LTP describes how the strength of connections between neurons, known as synapses, can be enhanced through electrical stimulation. This increase in "synaptic strength" is believed to underpin memory formation and retention. Networks of these neural connections with varying strengths are thought to constitute our memories.
The role of PKMzeta and KIBRA in memory retention
The study by Sacktor and Fenton suggests that a molecule known as PKMzeta, which was previously linked to memory erasure in rats, works in tandem with another molecule called KIBRA. KIBRA attaches to synapses activated during learning, effectively "tagging" them. It then pairs with PKMzeta to keep these tagged synapses strengthened. This interaction is key for maintaining long-term memories.
Disrupting molecular interaction erases memories
The research team found that blocking the interaction between PKMzeta and KIBRA not only eliminates LTP in neurons but also disrupts spatial memories in mice. Sacktor explained, "It's not PKMzeta that's required for maintaining a memory, it's the continual interaction between PKMzeta and this targeting molecule called KIBRA." He further added, "If you block KIBRA from PKMzeta, you'll erase a memory that's a month old."
Addressing criticisms and refining understanding of memory storage
The study also addresses criticisms raised by previous research, which showed that mice that were genetically engineered to lack PKMzeta, could still form long-term memories. Sacktor and Fenton proposed that another related protein, PKCiota/lambda, took over PKMzeta's role in these cases. Their latest findings show that blocking PKMzeta but not PKCiota/lambda in normal animals erases memories, reinforcing the critical role of PKMzeta in memory storage under ordinary circumstances.
