Druginduced Sleep

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Setting aside the general anaesthetics, which do not directly modify the function of any particular neurotransmitter, all the drugs that are used to induce sleep, i.e. the 'hypnotics', augment the function of GABA and so directly depress neuronal function and probably facilitate cortico-thalamic synchrony. Most of them are benzodiazepines and even those that are not, like zopiclone (a cyclopyrrolone) and Zolpidem (an imidazopyridine), act on the benzodiazepine receptor (see Chapter 19). Many benzodiazepines have a long half-life (20+ h) and a similar spectrum of activity, being both anxiolytic and sedative, and unless these effects are actually required during the day after the hypnotic action (as would occur with nitrazepam and flurazepam) it is important to use those benzodiazepines with a short half-life: e.g. temazepam, lorazepam

Figure 22.9 Summary of the influence of varying factors on sleep and waking. The EEG is shown diagramatically in the typical arousal (awake) state and in both non-REM (slow wave) and REM sleep. Appropriate activity levels, high or low, are shown for the different factors such as light input, melatonin secretion or ACh, NA, and 5-HT function in the different phases

Figure 22.9 Summary of the influence of varying factors on sleep and waking. The EEG is shown diagramatically in the typical arousal (awake) state and in both non-REM (slow wave) and REM sleep. Appropriate activity levels, high or low, are shown for the different factors such as light input, melatonin secretion or ACh, NA, and 5-HT function in the different phases and lormetazepam (T^2s = 6-10 h). All hypnotics appear to increase SWS at the expense of REM sleep and this has been suggested as a cause of irritability and possibly even the cognitive deficits claimed to be associated with use of these drugs.

That hypnotic drugs do not produce a natural sleep should not be surprising in view of the fact that they merely augment GABA and depress neuronal function, when sleep is clearly a very complex phenomenon involving the integrated activity of a number of neurotransmitters. To what extent it might be possible to induce sleep by simultaneously blocking the action of ACh, noradrenaline, 5-HT and histamine is not known. It would be an interesting experiment but the peripheral and other central effects are too numerous and dangerous to contemplate its trial.

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