Marijuana's impairment of short-term memory has always been thought to be caused by its interaction with neurons (nerve cells). New research shows that it's actually due to interaction with another type of cell, glial cells called astrocytes.
This opens up the possibility that with a little molecular tinkering, the medical benefits of marijuana – pain and nausea relief, as well as lowering eye pressure – can be obtained without the accompanying memory problems. It also adds to the picture that's emerged in the last decade of glial cells playing a much more prominent role in the nervous system than they've previously been given credit for.
Astrocytes also contain cannabinoid receptors, and researchers set out to test their function by observing mutant mice that lack these receptors.
Glial cells surround neurons and have always been thought of as primarily acting as housekeepers for them, providing protection, support and nutrients as well removing debris.
THC, the active ingredient in marijuana, has long been known to bind to specific sites on the brain's neurons called cannabinoid receptors, causing many metabolic changes. Its effects on memory were thought to be one of them. But astrocytes also contain cannabinoid receptors, and researchers set out to test their function by observing mutant mice that lack these receptors.
By testing the mice' ability to navigate a water maze, the researchers found that mice lacking astrocyte cannabinoid receptors did not show the normal decline in short term memory found after THC exposure, while mice lacking cannabinoid receptors on their nerve cell did. This strongly implies that THC's impairment of short term memory comes from its binding to astrocytes, not to neurons.
This means that somewhere down the road, it may be possible to block the interaction of THC with astrocytes while still allowing it to bind to neurons, hopefully preserving its therapeutic benefits while eliminating its detrimental effect on short term memory.
An article on the study appears in the journal, Cell.