It would be interesting to find out whether the brain state switches triggered by single neuron burst in vivo is related to the bidirectional effects of cortical stimulation on the occurrence of UP states in slices (Rigas see more and Castro-Alamancos, 2007) (Figure 5B). Cortical neurons are also highly interconnected with thalamic neurons, and those from the prefrontal cortex provide strong descending inputs to the neuromodulatory circuits in the basal forebrain (Golmayo et al., 2003; Sarter et al., 2005; Zaborszky et al., 1997) and brainstem (Jodo and Aston-Jones, 1997). Thus, the brain state switch triggered by single-neuron stimulation could also be mediated by the activation

of thalamic neurons or the neuromodulatory circuits. In addition to the areas reviewed above, which are core components of the neural www.selleckchem.com/products/MDV3100.html machinery controlling sleep and wake states, many other brain structures also play modulatory roles. For example, sleep is strongly regulated by the circadian rhythms, which are controlled by the suprachiasmatic nucleus (SCN) in the hypothalamus. Dissecting the

synaptic pathways between these structures and the core components described above will be essential for understanding how sleep-wake transitions are regulated by both internal and environmental factors. Wakefulness is not a unitary brain state, and the ensemble neural activity exhibits clear changes at different levels of vigilance. When the animal is drowsy or quietly resting, there is considerable delta-band activity in EEG and LFP, although the power is generally lower than that during NREM sleep. When the animal is in an aroused/attentive state (e.g., actively engaged in sensory processing or motor tasks), the cortical activity is highly desynchronized, as measured by both LFP (Bezdudnaya et al., 2006; Niell and Stryker, 2010) and intracellular recordings (Crochet and Petersen, 2006; Okun et al., 2010; Poulet and Petersen, 2008) (Figures 1A and

1B). In addition to the general arousal, selective attention to specific STK38 stimuli is also associated with changes in ensemble cortical activity, although at a more local level. Attention to visual stimuli within the receptive fields of recorded neurons is accompanied by decreases in the low-frequency LFP activity (Fries et al., 2001; Khayat et al., 2010), and it can cause either increase or decrease in gamma activity (30–80 Hz), depending on the cortical area (Chalk et al., 2010; Fries et al., 2001). The subcortical neuromodulatory circuits involved in sleep-wake control also play important roles in the regulation of arousal and attention, and malfunctioning of these circuits causes a variety of cognitive impairments. Both the monoaminergic and cholinergic neurons in the brainstem and basal forebrain receive inputs from the prefrontal cortex (Berridge, 2008; Jodo and Aston-Jones, 1997; Sarter et al., 2005), a key circuit exerting cognitive control of behavior (Miller and Cohen, 2001) (Figure 6).