Neuroskeptic has an interesting posting (here) on a paper, Key electrophysiological, molecular, and metabolic signatures of sleep and wakefulness revealed in primary cortical cultures, by Hinard and others.

We and other animals regularly lose our normal awake consciousness and go to sleep. Why this happens has been a question for a long time. There are many proposed reasons and many could be correct even at the same time. So we have evolutionary, psychological, and physiological scenerios. Now there is a surprising development.

The ability to mimic sleep in a random network of cultured neurons in a petri dish is surprising. The neuron cultures go to sleep on a sort of circadian timetable. When these neurons go to sleep they can be wakened with a mixture of neurotransmitters and therefore the scientists can produce sleep-deprived neurons. They can look at the difference in the chemistry of well-rested and sleep-deprived neurons.

One change is that lysolipids build up in the neuron cell membranes during the ‘awake’ time and are reduced during the ‘asleep’ time. Lysolipids are harmful to the cells.

So neurons seem to have had a problem for all of their existence. When they communicate they accumulate lysolipid and they need a period of non-communication to rid themselves of this type of chemical.

You will be relieved to know that there is no sign of dreaming in cultured neurons, just slow wave deep type sleep. Here is the abstract:

Although sleep is defined as a behavioral state, at the cortical level sleep has local and use-dependent features suggesting that it is a property of neuronal assemblies requiring sleep in function of the activation experienced during prior wakefulness. Here we show that mature cortical cultured neurons display a default state characterized by synchronized burst-pause firing activity reminiscent of sleep. This default sleep-like state can be changed to transient tonic firing reminiscent of wakefulness when cultures are stimulated with a mixture of waking neurotransmitters and spontaneously returns to sleep-like state. In addition to electrophysiological similarities, the transcriptome of stimulated cultures strikingly resembles the cortical transcriptome of sleep-deprived mice, and plastic changes as reflected by AMPA receptors phosphorylation are also similar. We used our in vitro model and sleep-deprived animals to map the metabolic pathways activated by waking. Only a few metabolic pathways were identified, including glycolysis, aminoacid, and lipids. Unexpectedly large increases in lysolipids were found both in vivo after sleep deprivation and in vitro after stimulation, strongly suggesting that sleep might play a major role in reestablishing the neuronal membrane homeostasis. With our in vitro model, the cellular and molecular consequences of sleep and wakefulness can now be investigated in a dish.