Friday, January 29, 2010

December 2009: Cannabinoid receptor-1 activation in the spinal cord leads to an inhibition of nerve cell damage and death. (Cleveland Clinic, Clevelan

First some background:
in conditions known as neurodegenerative diseases, such as Huntington’s disease, Alzheimer’s disease, Parkinson’s disease, multiple sclerosis, and Lou Gehrig’s disease (ALS, amylotrophic lateral sclerosis), one of the major problems is what is
referred to as excitotoxicity. Excitotoxicity is when cells in our brain are overexcited by natural signals, leading to cell damage and eventually death. A well-known mechanism for the development of the aforementioned neurodegenerative diseases is the excitotoxicity of glutamate receptors on brain cells (glutamate is one of our body’s natural signals). These glutamate receptors have two main subtypes, NMDA and AMPA, with their names referring to an artificial substance that can perform the same role as the natural signal, glutamate.

The new information:
Within the spinal cord, nerve cells that send signals to the brain can be prevented from damage and death due to excitotoxicity. Within these nerve cells, excitotoxicity is mediated through NMDA glutamate receptors. This new research involved exposing the spinal cord nerve cells to NMDA (N-methyl-D-aspartic acid) in the presence of cannabinoids. It was found that the toxic effects of NMDA (and therefore the natural signal, glutamate) were blocked when the cannabinoids were present.

What this means:
This research simply provides more evidence for what is already generally known, that cannabinoids can slow down and even potentially stop the progression of neurodegenerative diseases. Bhat, M, WD Bowen, J Cheng, and Q Liu.

“Signaling pathways from cannabinoid receptor-1 activation to inhibition of N-methyl-D-aspartic acid mediated calcium influx and neurotoxicity in dorsal root ganglion neurons.” The Journal of pharmacology and experimental therapeutics. 331.3 (2009): 1062-70.

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