User:Boydena/sandbox

In the brain
As stated previously, FFA1 has an affinity for long chain fatty acids. Such fatty acids are also present in the brain, where FFA1 has also been found in high abundance. FFA1 receptors are present over the entire brain, but in highest numbers in the medulla oblongata and the substantia nigra. Recent studies have also observed that FFA1 was present in the olfactory bulb, striatum, hippocampus, midbrain, hypothalamus, cerebellum, cerebral cortex and in the spinal cord.

Fatty acids play an important role in normal brain development as well as maintaining proper neuronal function. It has been found that certain fatty acids that are in abundance in the brain may be linked with FFA1. These fatty acids likely activate FFA1, inducing an intracellular response. It has been found that docosahexaenoic acid (DHA) has a higher affinity than other fatty acids for FFA1. DHA makes up 30% and arachidonic acid, another fatty acid found in the brain, makes up 20% of the fatty acids in the brain. Both of these fatty acids must be obtained from the diet because the body cannot make them. A correct balance of these fatty acids is vital to normal brain function and structure. DHA is supplied to the brain via astrocytes, which release DHA so that it reaches a high enough concentration to act as an extracellular signal on FFA1.

The abundance of FFA1 in the brain and the high affinity for DHA suggest that FFA1 may play a role in neuronal function in the brain. It is hypothesized that DHA and arachidonic acid could improve memory function by interacting with FFA1 in the hippocampus neurons. This hypothesis is based on the idea that once FFA1 is activated by these fatty acids, the resulting signal is related to progenitor cell proliferation. This implies that FFA1 signaling could stimulate the production of new memory cells in the brain. More research needs to be done in proving these suggestions, but if proven to be true FFA1 could be a target in producing new memory cells that are destroyed by diseases like Alzheimer’s and Parkinson’s disease.

Additionally, FFA1 abundance in the brain has been suggested to play a role in pain. DHA has been reported to induce an increased tolerance for pain without binding to opioid receptors. Researchers have hypothesized that stimulation of FFA1 by DHA could accelerate the release of endorphins, which is how DHA could induce an increased tolerance to pain. DHA binds to FFA1, which could activate a signaling cascade that leads to Ca 2+ influx, which then leads to accelerated endorphin release and novel pain control. Again, additional research must be done to fully understand the mechanism and to prove these hypotheses, but the implications could provide additional targets for pain control in individuals.