In a new study, scientists found that the release of the brain’s “equivalent of THC”, can actually reduce seizure activity, however, it may also lead to some serious side effects.
According to Stanford researchers, epileptic seizures – a central nervous system disorder in which brain activity becomes abnormal, causing seizures and a number of serious, life-threatening conditions – trigger the brain to release a cannabis-like chemical, 2-arachidonoylglycerol, or 2-AG.
This compound is the most abundant endocannabinoid found in the body. It is a member of a group of molecules that play a complex and important role in various bodily processes, including immune responses and inflammation.
2-AG is thought to help regulate appetite, immune system function, and pain management by interacting with the body’s endocannabinoid system receptors.
While the benefit of creating 2-AG by the brain helps to reduce seizure intensity, research shows that it may also also increase the likeliness of memory loss.
As Ivan Soltesz, PhD, professor of neurosurgery says, the majority of epileptic seizures originate in the hippocampus – the hippocampus plays a massive role in several ways, including processing and retrieving short-term memory or learning.
Soltesz said: “There have been lots of studies providing evidence for a connection between seizures and endocannabinoids.
“What sets our study apart is that we could watch endocannabinoid production and action unfold in, basically, real time.
“While smoking cannabis floods the entire brain with relatively long-lasting THC, endocannabinoids are released in precise spots in the brain under precise circumstances, and their rapid breakdown leaves them in place and active for extremely short periods of time.”
In the study, scientists examined these processes in mice. As endocannabinoids break down rather quickly, researchers couldn’t measure their level in animals’ brains.
It turned out that, according to the report, “several hundred times as much 2-AG was released when a mouse was having a seizure compared with when it was merely running in place.”
However, as 2-AG could be converted to arachidonic acid, it can lead to the “build-up of a particular variety of prostaglandin that causes constriction of tiny blood vessels in the brain where the seizure has induced that prostaglandin’s production, cutting off the oxygen supply to those brain areas.”
Soltesz added: “A drug that blocks 2-AG’s conversion to arachidonic acid would kill two birds with one stone.
“It would increase 2-AG’s concentration, diminishing seizure severity, and decrease arachidonic acid levels, cutting off the production of blood-vessel-constricting prostaglandins.”
