Post by dotPost by F. BertolazziInsomma, nel sonno si fa un riversamento da RAM a ROM.
Interessante! La cerchero' in Rete.
Ti consiglio di cercare "Giulio Tononi".
La mia fonte è il "solito" Ecommunist. Ricordavo male i particolari.
Un neurone altro non è che un comparatore che ha N input collegati tramite
trimmer (sinapsi) all'ingresso non invertente ed M input coi loro trimmer
collegati a quello non invertente. Poi ci sarebbe anche un monostabile
all'uscita, ma lasciamo perdere. Se la somma degli N input è maggiore della
somma degli input M, il neurone "spara".
Durante il sonno non-REM, una volta al secondo circa, l'impedenza di
*tutti* i trimmer viene aumentata un pochino, in modo tale che il risultato
finale non cambi, salvo per i ricordi meno significativi, motivo per cui le
informazioni meno importanti vanno perdute. Chiaramente l'aumento di
impedenza di tutti i trimmer porta ad una diminuzione del consumo.
The big sleep
Jul 6th 2006 | FLORENCE
From The Economist print edition
SLEEP deprivation is an uncomfortable experience. In drivers and workers it
can lead to fatal accidents. In those under interrogation it can lead to
confession. But why it does what it does is mysterious—as, indeed, is the
purpose of sleep itself.
Many theories have been proposed to explain why the pressure to sleep
builds up until it becomes irresistible. The latest, presented at the
recent annual meeting of the Organisation for Human Brain Mapping, in
Florence, Italy, starts from the obvious proposition that the longer you
stay awake, the more you learn. Giulio Tononi of the University of
Wisconsin proposes that this extra learning makes the brain more and more
expensive to maintain. Sleep prunes back the grey matter so that, come the
morning, the brain is once again economical to run. If this pruning cannot
take place, the organ becomes less and less efficient, and dire
consequences result.
Even at rest, the brain is costly to run, consuming 20% of the body's
energy production. Most of this energy goes towards maintaining synapses,
the junctions across which impulses jump from nerve cell to nerve cell,
keeping the brain alert even when it is not doing anything. When a person
learns something new, certain synapses are strengthened relative to others.
Over the course of the day, there is a net increase in the strength and
number of the brain's synapses. And, as Dr Tononi observes, stronger
synapses consume more energy. In addition, making them requires more
protein and fats and they take up more space. Given that an organism has
limited supplies of all of these things, something must happen to prevent
the cost of having a brain from gradually spiralling out of control. That
something, Dr Tononi believes, is non-rapid eye movement (non-REM) or
slow-wave sleep.
Until recently, most sleep research focused on REM sleep. This is the time
when people dream, and dreams have had a grip on the scientific imagination
since the days of Freud, and on the popular imagination at least since
biblical times. Lately, though, researchers have started to wonder whether
they have been looking in the wrong place for the significance of sleep,
for REMming occupies only about a fifth of the night.
During the other 80% of sleep—the part that is non-REM—the firing pattern
of the brain's nerve cells sets up slow electrical waves that start at
different points in the cerebral cortex and travel across it. These
travelling waves occur hundreds of times a night, and most commonly at a
frequency, 1 cycle per second, which has been shown to depress the activity
of synapses.
Within an hour of a person falling asleep, slow waves will have covered his
entire cortex, affecting every nerve cell in it. At first, these waves are
big and powerful, but their size decreases through the night. Dr Tononi
believes that the function of these slow waves is to “downscale” synapses,
reducing their size, chemical activity and electrical activity—and thus the
strength with which they connect their nerve cells together—all over the
brain.
The trick, he thinks, is that this downscaling is done in proportion to the
existing strength of each synapse. When a sleeper awakens, the strength of
each synapse is thus the same relative to all the others, but all synapses
are weaker than they were when he went to sleep. Indeed, the weakest of
them may vanish completely, taking part of the previous day's memory with
them.
In earlier experiments, designed to replicate normal learning, Dr Tononi
found that the part of the brain showing most slow-wave activity during
sleep was the same as the part that had been activated during the
experiment. This fitted the prediction that the downscaling slow-waves
would be strongest in those parts of the brain where the most changes had
taken place during the day.
The team's latest work draws not on human subjects, but on fruit flies.
Flies, too, sleep. Their genetics—including the genetics of sleep—have been
studied for almost a century, and many of the genes that play a role in
human sleep resemble those that control sleep in fruit flies. Best of all,
experiments on fruit flies are not subject to vetting by ethics committees.
With the help of Chiara Cirelli, who also works at the University of
Wisconsin, Dr Tononi has created a mutant fruit fly that sleeps only two or
three hours a night. (A normal fly sleeps between eight and 14 hours.) The
mutation itself is in a gene for a nerve-cell protein of a type known as an
ion channel.
Ion channels sit in a cell's outer membrane and let electrically charged
atoms (ions, as they are known in chemical jargon) in and out of the cell.
In this case, the ion is potassium. It is the movement of potassium (and
also sodium) ions that causes the electrical impulses that nerve cells
carry—including the impulses found in slow-wave sleep. Moreover, the
particular protein that the flies lack is most concentrated in brain areas
involved in learning and memory. To nobody's surprise, therefore, though
the mutant fly is capable of learning things, it forgets them within
minutes. Healthy flies retain learned information for hours or even days.
The researchers' discovery finds an intriguing echo in a human disease
called Morvan's syndrome. This is a rare brain disorder that is caused by
an autoimmune response which destroys the human equivalents of the ion
channels that are affected in the mutant fruit fly. Patients with Morvan's
syndrome suffer from severe insomnia and have been known to go for months
without sleeping. Eventually, this extreme sleep deprivation kills them.
Dr Tononi's hypothesis is, it must be said, controversial. Many researchers
hold almost precisely the opposite opinion—that sleep serves to re-activate
synapses that were strengthened during the day, and thus reinforces their
strength rather than diminishing it. There is, however, a certain logical
sense to the Tononi view of the world. It is impossible to remember
everything, so a process of winnowing must take place somehow. The idea
that, after a period of expansion, the brain pares back its workforce to
become leaner and meaner is somehow rather appealing.