Brain rhythms in the alpha frequency range [8Hz-12Hz] are present in idling conditions and sleep. They have also an important role in cognition, e.g. they modulate activity of task-irrelevant neural populations, and enhances selective attention among others. A prominent occipital alpha wave emerges in mammals when the subjects close eyes (alpha generation) and it is blocked when opening eyes (alpha blocking). This switch in alpha power is accompanied by an inverse switch in gamma activity [1]. With open eyes, the brain receives strong input from the external world and responds by strong gamma-/weak alpha-activity, whereas disappearing input at closed eyes induces the inverse strong alpha-/weak gamma-activity. Considering input as random input fluctuations, this switch may result from an alteration in exogenous fluctuations. The work proposes a mesoscopic model for the cortico-thalamic feedback (CTF) loop derived from a microscopic neuron network model. This model describes the fluctuations-induced switch as a phase transition induced by additive noise. The results suggest that the well-known emerging and blocking of occipital alpha waves may result from the alternating level of random (here exogenous) fluctuations in the brain. A related emergence of alpha-activity has been also observed in the frontal lobe under general anaesthesia. Low doses of GABAergic anaesthetics induce enhanced frontal EEG in the beta-frequency range and a further dose increase typically yields loss of consciousness (LOC) in mammalian subjects with enhanced EEG alpha-power increase and diminished beta-power [2]. Considering a similar hypothesis as in the previous study on alpha generation and blocking by exogenous fluctuations, it is assumed that anaesthetics affect endogenous brain fluctuations. A CTF model indicates that a level decrease of endogenous fluctuations modulates EEG-spectra from beta activity to alpha activity. Physiologically, endogenous fluctuations are controlled by the brain’s arousal system, that is known to be highly sensitive to anaesthetics. Hence, the endogenous fluctuations control by the arousal system permits to describe the impact of multiple anaesthetics on the brain network. These studies also link to Event-Related Synchronization and Desynchronization, which are assumed to also originate from underlying activity fluctuations. [1] Geller et al. (2014). Clin.Neurophysiol. 125(9): 1764–1773. [2] Purdon et al. (2012), PNAS 110: E1142-1