Anaesthetic agents are known to affect extra-synaptic GABAergic recep- tors, which induce tonic inhibitory currents. Since these receptors are very sensitive to small concentrations of agents, they are supposed to play an important role in the underlying neural mechanism of general anaesthesia. Moreover anaethetic agents modulate the encephalographic activity (EEG) of patients and hence show an ef- fect on neural populations. To understand better the tonic inhibition effect in single neurons on neural populations and hence how it affects the EEG, the work consid- ers single neurons and neural populations in a steady-state and studies numerically and analytically the modulation of its firing rate and nonlinear gain with respect to different levels of tonic inhibition. We consider populations of both type-I (Leaky Integrate-and-Fire model) and type-II (Morris-Lecar model) neurons. The work re- veals a strong subtractive and divisive effect of tonic inhibition in type-I neurons, i.e. a shift of the firing rate to higher excitation levels accompanied by a change of the nonlinear gain. Tonic inhibition shortens the excitation window of type-II neu- rons and their populations while retaining the nonlinear gain. To bridge the single neuron description to the population description analytically, a recently proposed sta- tistical approach is employed which allows to derive new analytical expressions for the population firing rate for type-I neurons. In addition, the work derives a novel transfer function for type-I neurons as considered in neural mass models and studies briefly the interaction of synaptic and extra-synaptic inhibition. The gained results are interpreted in the context of recent experimental findings under propofol-induced anaesthesia.