Despite popular belief that saturated fats must be avoided at all times, recent research led by Richard Huganir of the Department of Neuroscience at Hopkins shows that palmitate, a fatty acid that is present in the brain, plays a significant role in memory retention.
Nerve cells, or neurons, communicate with each other via synapses (the gaps between two neurons). Neurotransmitters, which are chemical signals, are sent from the terminal branches of one neuron, and are received by the receptors on the dendrites of the second neuron.
Long-term potentiation and synapse plasticity, phenomenas that show how the connection between two neurons can change in strength, suggest that long term memory is stored in synapses. Continuous sculpting of synaptic connections creates new memories, strengthens existing ones and erases old ones.
It has long been known that the neurotransmitter glutamate plays a key function in synaptic plasticity (the ability of synapses between neurons to strengthen and weaken over time). This chemical activates NMDA receptors, which promotes the communication between nerve cells. However, the way that NMDA receptors are put together has always been a mystery.
The Hopkins research team added radioactive palmitate to live neurons. NMDA receptors were filtered out, and radioactivity was tracked via X-ray film. The locations where palmitate attached to the NMDA receptors were pinpointed.
The researchers discovered that there are two palmitoylation sites at one end, the C-terminus, of each of the NMDA receptor subunits NR2A and NR2B. When the fat attaches to the first region near the membrane, the addition of phosphate groups to tyrosine kinase proteins is increased, thereby stabilizing NMDA receptors on neuron surfaces.
But before you gorge yourself on meat and dairy, foods that contain palmitate, you should know that the location at which the fatty acid binds is just as important as the amount of palmitate present.
Attaching a palmitate of the second site at the middle of C-terminus causes NMDA receptors to accumulate within the Golgi apparatus, a cell's protein packaging and shipping center, of the neuron. Because the receptors are stuck within the Golgi, expression of NMDA at the synapse is reduced.
Researchers suggest that palmitoylation of the second site may function to ensure the quality of NMDA receptor manufacture: if it is not assembled properly, NMDA never gets the chance to function at the neuron's surface. Directing the palmitoylation of different sites of NMDA effectively controls the strength of synapse connections, which in turn accounts for the shaping of memory circuits.
The failure of palmitoylation, researchers believe, will impair memory and learning, because communication between synapses cannot occur without NMDA activation. According to Huganir, this discovery creates the possibility of improving memory by artificially changing concentrations of palmitate.
"This new modification of the NMDA receptors . . . reveals new potential drug targets, such as the enzymes that add or remove the palmitate," Huganir said in a press release. "If we could shift the balance of palmitoylation, then perhaps we could affect and enhance learning and memory."
Please note All comments are eligible for publication in The News-Letter.