Epilepsy is a condition that affects 1 in 100 people. It can be caused by many factors. In some cases, there are no known causes. For others, the causes are known, but the treatments are not. The good news is that a new treatment may have arrived. It’s a synthetic drug that has been created to combat the symptoms of epilepsy. It’s even more effective than medications that are currently in widespread use.

Medications to control epileptic seizures have been around since the early 20th century, but no drug has been able to reduce both the frequency and severity of the seizures in all patients for more than a decade. Researchers have developed a new drug that harnesses the power of marijuana to stop seizures, but is completely different from the psychoactive plant.

Researchers have long been interested in the effects of cannabidiol, the non-psychoactive cannabinoid found in marijuana, on the brain. In fact, the compound has been approved by the Food and Drug Administration (FDA) to treat two rare forms of childhood epilepsy. While cannabidiol is a promising treatment, it is not without side effects. It has been found to cause mice to become lethargic, and it can also change the brain’s structure and function.. Read more about epilepsy and cannabinoids and let us know what you think.

 

“There have been many studies that show a link between seizures and endocannabinoids,” said Soltesz. “What makes our research unique is that we were able to see endocannabinoid synthesis and activity in real time.”

a halt to the thrills

Endocannabinoids are thought to have a function in the brain’s inhibition of excessive excitation. When excitatory neurons, which secrete chemical “go” signals, reach a certain threshold, they trigger the synthesis and release of endocannabinoids, which bind to CB1 on excitatory neurons and serve as a brake, causing the cell to relax.

While smoking marijuana floods the entire brain with relatively long-lasting THC, endocannabinoids are released in specific areas of the brain under specific conditions, and their rapid breakdown leaves them in place and active for extremely short periods of time, according to Soltesz, who has spent decades researching the link between endocannabinoids and epilepsy. 

However, since endocannabinoids are so delicate and degrade so rapidly, there was no method to track their fluctuating amounts in animals’ brains until recently. He said, “Existing biochemical techniques were simply too sluggish.”

Soltesz heard about a novel endocannabinoid-visualization technique developed by research co-author Yulong Li, PhD, a professor of neurology at Peking University in Beijing, while he was working on the most current study. When a cannabinoid interacts to the modified endocannabinoid receptor, the technique entails redesigning specific neurons in mice to express a modified form of CB1 that produces a luminous light. Photosensitive devices can detect the fluorescence.

The scientists were able to track and pinpoint sub-second variations in fluorescence that corresponded to endocannabinoid levels where binding was taking place using this novel technique.

focusing on 2-AG

The researchers showed that 2-AG alone is the endocannabinoid molecule whose surges and fast disappearance follow neural activity in mice by inhibiting enzymes essential for the synthesis and breakdown of various endocannabinoids. When a mouse was experiencing a seizure, hundreds of times more 2-AG was produced than when it was just running in place. 

Many neuroscientists and pharmacologists believed that anandamide, an alternative endocannabinoid, was the active molecule, but the researchers were able to rule it out. The term Anandamide comes from the Sanskrit word for “bliss.”

“This previously unknown activity-dependent increase in 2-AG levels after a seizure downregulates excitatory neurons’ excessive rhythmic firing,” Soltesz said.

However, 2-AG is quickly converted to arachidonic acid, a component of inflammatory chemicals known as prostaglandins. The researchers discovered that the subsequent rise in arachidonic acid levels resulted in the accumulation of a specific type of prostaglandin, which causes constriction of tiny blood vessels in the brain where the seizure induced the production of that prostaglandin, cutting off oxygen supply to those areas. 

The cognitive impairments — disorientation, memory loss — that occur after a seizure are known to be caused by oxygen deprivation, according to Soltesz.

Soltesz stated that a medication that prevents 2-AG from being converted to arachidonic acid will kill two birds with one stone. “It would raise 2-AG levels, reducing seizure severity, and lower arachidonic acid levels, preventing the synthesis of blood-vessel-constricting prostaglandins.”

Soltesz is a member of Stanford Bio-X, Stanford Maternal and Child Health Research Institute, and Stanford Wu Tsai Neurosciences Institute.

Barna Dudok, PhD, a postdoctoral fellow at Stanford, is another research co-author.

Other University of Calgary academics, as well as Vanderbilt University researchers, participated to the project.

The study was funded by the National Institutes of Health (grants K99NS117795, MH107435, 1S10OD017997-01A1, NS99457 and NS103558), the Canadian Institutes of Health Research, the Beijing Municipal Science & Technology Commission, the National Natural Science Foundation of China, and the Peking University School of Life Sciences.

The study was also sponsored by Stanford’s Department of Neurosurgery.

Researchers at the University of California at San Diego have found that cannabidiol, the non-psychoactive chemical in marijuana, and a compound called tetrahydrocannabivarin, which is also found in cannabis, effectively reduce the severity of epileptic seizures in lab mice, and do so without creating undesirable side effects.. Read more about cbd focal seizures and let us know what you think.

This article broadly covered the following related topics:

  • banzel package insert
  • epileptic encephalopathy pdf
  • banzel dosage
  • rare seizure disorders
  • what percentage of epilepsy is genetic?
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