Cortico-thalamic synchrony

Figure 22.5 Pathways involved in cortico-thalamic synchrony and EEG arousal. The ascending reticular activating system (ARAS) extends from the cephalic medulla through the pons and midbrain to the thalamus (see Moruzzi and Mayoun 1949). It is activated by impulses in collaterals of the spinothalamic sensory pathway running to specific thalamic nuclei (SpThNc) and in turn activates much of the cortex, partly through the non-specific thalamic nuclei (NspThNc), which also receive inputs from SpThNc and also via the nucleus basalis (NcB). Its stimulation is followed by EEG arousal. It is probable that reciprocal links between cortical areas and the thalamus, particularly NspThN, lead to slow-wave (8 Hz) cortical EEG synchrony and, in the absence of appropriate sensory input and ARAS activity, a sleep state...

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... 

Augment, or more probably, break up thalamic-cortico synchrony and its tendency to promote slow-wave EEG activity and non-REM sleep. Whether this results in full arousal, or merely a temporary disruption of sleep to give REM periods without full awaking, will depend on the balance of inputs and the overall state of cortical activity. 

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