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The Biology of Blackouts Revealed

Alcohol messes with chemical messengers responsible for memory formation.

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Brain cells aren't dead, just confused.
Photo via thinkstockphotos

By Dirk Hanson

07/07/11

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Remember all those jokes about “killing brain cells” with a drink? As it turns out, those brain cells don’t die when you drown them in alcohol. Instead, they start interfering with the transmission of glutamate, or NMDA, a crucial neurotransmitter. Too much alcohol causes NMDA receptors to go haywire. In fact, alcohol can muck up glutamate traffic so badly that the result is an increase in the manufacture of steroids that weaken the connection between brain cells involved in learning and memory. With glutamate pinwheeling around crazily in the brain—too much of it here, not enough of it there—and steroids running loose, inhibiting long-term potentiation (LTP), a signal-strengthening process considered crucial to memory formation—you're just not going to be able to form normal memories.

In animal studies at Washington University, reported in the Journal of Neuroscience, Uukitoshi Izumi, research professor of psychiatry, said “we’ve found that exposure to alcohol inhibits some receptors and later activates others, causing neurons to manufacture steroids that inhibit LTP and memory formation.” The result is familiar to almost everyone, at least once in his or her life: a period of amnesia, lasting from just a few minutes to several hours, known as a blackout. “Alcohol isn’t damaging the cells in any way that we can detect,” said one the investigators. “You still process information. You’re not anesthetized. You haven’t passed out. But you’re not forming new memories.”

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