AUSTIN, Texas—Researchers from The University of Texas at Austin studying electric fish have gained new insight into how memory is stored at the level of neurons.
Their finding, published in the Feb. 16 issue of Neuron, could help researchers better understand memory formation and neural disorders like epilepsy in humans.
Dr. Harold Zakon, Dr. Jörg Oestreich and colleagues show that when electric fish zap each other in dark waters, their neurons store a memory of the sizzling communiqué by turning on special cell membrane channels.
The channels give the fish neurons the ability to retain a memory long after its original stimulus is gone.
“There is short-term stimulation that results in long-term changes in excitability,” says Zakon, professor of neurobiology. “Essentially, it is memory.”
The electric fish studied by Zakon and Oestreich discharge electrical signals to survey their environment and communicate with each other.
“Every time they discharge, it’s kind of like they are opening their eyes and closing them,” says Zakon. “Each pulse of electricity is a snapshot of the environment. These guys are swimming around and discharging at a very regular frequency. They’re digitizing their environment.”
But a problem occurs when the fish are close to each other. They can jam each other’s electrical signals. In response, one of the fish will jump to a higher frequency to avoid the jamming signal, emitting more electrical pulses per second than its neighbor.
Oestreich and Zakon found that once the jamming avoidance has started, the fish’s neurons continue to discharge at a higher frequency, even after its neighbor fish may have swum away.
The researchers discovered that the neurons’ memory was not caused by increased flow of glutamate to their synapses. Glutamate is the major excitatory neurotransmitter in the nervous system and is involved in the processes of learning and memory. They blocked glutamate and found that it did not affect the memory of the neurons.
Instead, the glutamate sets off a cascade of events in the neuron that results in the activation of ion channels, called TRP channels, which then remain active for a long time.
“The long-term activation of these TRP channels,” says Zakon, “is the ‘memory.’”
Zakon, Oestreich and colleagues don’t yet understand how the stimulus leads to the long-lasting activation of the TRP channel. They are pursuing further studies.
“We’re looking at the general idea that we have long-term changes in the brain that affect the computation that neurons do,” says Zakon. “We have ion channels [in the neurons] and we know those are activated. The mystery is how a short stimulus leads to such a long-lasting activation of the TRP receptor.”
For more information contact: Lee Clippard, College of Natural Sciences, 512-232-0675.