Although the relationship of CRH-BP to EEG is unknown, a relationship of CRH to EEG has been established in animal models, including mechanism of effect. CRH is known to increase the firing rate of LC neurons and to influence global forebrain EEG activity [37], [38]. LC activation influences the firing properties of thalamic neurons that are implicated in the generation of the alpha rhythm [27], [39] and induces fronto-cortical and hippocampal EEG changes in rats [40]. A logical possibility for the influence of CRH-BP on the EEG might involve CRH binding in the locus coeruleus (LC) and VTA (although CRH-BP mRNA has not been detected in rat LC and it is not known if it is present in human LC [31]). CRH-BP may be required for CRH to potentiate NMDAR-mediated excitatory postsynaptic currents in the VTA that herald the switch from regular firing to burst firing in dopamine neurons (41). The VTA sends dopamine containing projections to the LC that influence LC neuronal activation [42], [43]. One could therefore speculate that VTA CRH-BP variation might influence the resting EEG via the VTA dopamine–LC–thalamic neuronal oscillator pathway.
