DailyDirt: How To Forget (When You Want To)

from the urls-we-dig-up dept

The movie Eternal Sunshine of the Spotless Mind is based on a fictional technology that allows people to selectively forget events in their life that they don’t want to remember. While that whole movie was dedicated to erasing memories, memory loss actually isn’t an uncommon plot device. For example, Men In Black had “neuralyzers” that zapped away a person’s memory, and the main character in Memento suffered from a complete loss of his short-term memory. (And don’t forget all the soap operas that use amnesia in various convenient situations.) In reality, it’s much harder to induce forgetfulness on demand, but some research could make it easier to do so in the future. Here are a few studies you might want to remember — and later forget.

If you’d like to read more awesome and interesting stuff, check out this unrelated (but not entirely random!) Techdirt post via StumbleUpon.

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Comments on “DailyDirt: How To Forget (When You Want To)”

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Mason Wheeler (profile) says:

I’m a bit surprised at the bit about the xenon. Xenon is a noble gas: except in highly extreme laboratory conditions that definitely don’t exist within the body of a living mammal, it’s chemically inert. It doesn’t interact with living systems or mess around with chemical processes. So how exactly does it go about changing the way brain chemistry works?

John Fenderson (profile) says:

Re: Re: Re:

Just because I have some time and an insatiable curiosity, I searched for more info about the mechanism by which a noble gas can affect living beings. The short answer is: nobody seems to know yet. The most comprehensive paper I could find quantifies the anesthetic effects, the dosage required, the receptors involved, and so forth at length. But when it comes to answering the “how” question (what is the chemical process?), it comes up empty.

Recent in vitro research has suggested that xenon acts not only on NMDA channels but also on TREK-1 channels (discussed above). TREK-1 channels are also activated by the neuroprotective agents riluzole,63 a therapeutic agent used to treat amyotrophic lateral sclerosis, and polyunsaturated fatty acids. Consequently, it has been postulated that these channels contribute to neuroprotection. As TREK-1 channels are activated by intracellular acidosis and reduce neuronal excitability, this is certainly feasible.

Xenon is not ‘inert’ with respect to cerebral haemodynamics; increased cerebral blood flow (CBF) with preserved cerebral autoregulation is thought to occur acutely with xenon administration.

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