Neurobiologists have used cataplexy to help track neurological networks.
Neurobiologists have used cataplexy to help track neurological networks.
US researchers are one step closer to understanding the neurological underpinnings of sleep and waking, with histamine playing a hitherto unexpected role.
Jerome Siegel at the University of California, Los Angeles and colleagues report that studying cataplexy, a disorder similar to narcolepsy, in which people lose muscle tone but - unlike in narcolepsy - still retain awareness of their surroundings, provides an ideal route to untangling the neurological networks involved.
Muscle tone is continuously present when a person is awake, notes Siegel, but tone in the ’antigravity’ muscles is absent during both so-called REM (rapid eye movement) sleep and during cataplexy. Where cataplexy differs from sleep is that a cataplectic person is aware of his or her environment, unlike a person who is sleeping.
’Cataplexy represents a unique natural experiment in which muscle atonia is dissociated from sleep,’ write Siegel and colleagues in the journal Neuron. Despite the lack of muscle tone associated with sleep, cataplectics can visually track objects during this state and have an accurate memory of events.
Siegel’s team focused on three types of neurone - noradrenergic, serotonergic, and histaminergic. They measured the activity of these cell types during REM sleep and during cataplexy in a canine model.
The activity of all three groups was markedly reduced, or absent, during REM sleep. But the picture was different during cataplexy. The activity of noradrenergic and serotonergic neurones was similar to that seen during sleep, but histaminergic neurones continued to fire at the same - or even higher - levels than when the animal was awake.
This leaves Siegel with the hypothesis that the activity of histaminergic neurones is linked to the maintenance of waking. Interestingly, although antihistamine drugs have a history of sending people to sleep, cataplectics can take them without ill effect, he adds.
Bea Perks
References
J John et al, Neuron, 2004, 42, 619
No comments yet