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CBD Could Be The Next Best Option To Reduce Epileptic Seizures – New Research Reveals How

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This helps explain why cannabidiol (CBD) – a substance found in marijuana – treatment proves to be effective in reducing epileptic seizures.

A new study published by researchers at NYU Grossman School of Medicine shows how cannabidiol (CBD), a substance found in marijuana, reduces seizures in many types of hard-to-treat pediatric epilepsy.

The findings published today showed the way CBD blocks signals sent by a molecule called lysophosphatidylinositol (LPI).

LPI, which is present in brain cells known as neurons, is believed to enhance nerve impulses as part of normal function but may be taken over by illness to trigger seizures.

The research, which was published today in Neuron, supported earlier findings that CBD prevents LPI from amplifying neuronal impulses in the hippocampus, a part of the brain.

The new research shows for the first time that LPI also weakens signals that stop seizures. This helps explain why CBD treatment is so helpful.

These findings, according to corresponding author Richard W. Tsien, add to the field’s knowledge of a central seizure-inducing mechanism, with several implications for the development of novel treatment methods.

“The study also clarified, not just how CBD counters seizures, but more broadly how circuits are balanced in the brain,” adds Tsien. “Related imbalances are present in autism and schizophrenia, so the paper may have a broader impact.”

The findings of the research are based on how each neuron “fires,” sending an electrical pulse down an extension of itself until it reaches a synapse, the space that joins it to the next neuron in a neural pathway.

The pulse causes the release of substances known as neurotransmitters that float over the synapse and effect the next cell in line when it reaches the end of the cell before the synapse.

Such signals either excite the cell to fire (excitation) or put the brakes on firing when they cross (inhibition). To operate properly, there must be a balance between the two; excessive excitement may lead to seizures.

The new study looked at several models of rodents to find out how seizures work. Often, fine-tipped electrodes were used to measure the flow of electrical currents that carry information. In other experiments, the effect of LPI was studied by removing its main signaling partner genetically or by measuring how much LPI was released after seizures.

The investigations supported earlier results that LPI modifies nerve impulses by attaching to the G-coupled receptor 55 (GPR55), a protein found on the surfaces of neuronal cells.

It was discovered that this LPI-GPR55 presynaptic association led to the cell’s release of calcium ions, which in turn stimulated the release of glutamate, the primary excitatory neurotransmitter.

Also, when LPI turned on GPR55 on the other side of the synapse, it weakened inhibition by making it harder to get the right proteins in the right place. According to scientists, this combination generates a “dangerous” two-pronged strategy for increasing excitability.

The study team discovered that blocking LPI-mediated effects on both excitatory and inhibitory synaptic transmission required either genetically modifying mice to lack GPR55 or administering CBD derived from plants prior to seizure-inducing stimuli.

While earlier research had shown that CBD was a seizure-reducing target of GPR55, the present study offered a more thorough, hypothesized mechanism of action.

The authors hypothesize that CBD inhibits a “positive feedback loop” in which seizures boost LPI-GPR55 signaling, which presumably promotes additional seizures, which in turn raises LPI and GPR55 concentrations.

There are a number of possible mechanisms behind recurrent epileptic seizures, however more research is necessary to corroborate this hypothesis.

The authors emphasize that while the present research focused on the cannabinoid CBD derived from plants, LPI is a component of a signaling network that also contains “endocannabinoids” like 2-Arachidonoylglycerol (2-AG), which naturally exist in human tissues. LPI and 2-AG both act on receptors that CBD also controls, but they do so in different ways at the synapse.

Endocannabinoids like 2-AG respond to an increase in brain activity by turning down the release of neurotransmitters from nerve cells. LPI, on the other hand, makes electrical signals stronger. It’s interesting to note that enzymes can change LPI and 2-AG into one another.

Theoretically, the brain might regulate activity by switching between pro-excitatory LPI and the restorative effects of 2-AG, according to the study’s lead author, post-doctoral researcher Evan Rosenberg, PhD, of Tsein’s group. 

“Drug designers could inhibit the enzymes that underpin LPI production or promote its conversion to 2-AG, as an additional approach to control seizures. LPI could also serve as a biomarker of seizures or predictor of clinical responsiveness to CBD, providing an area of future research.”

Source: 10.1016/j.neuron.2023.01.018

Image Credit: Getty

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