Extracellular ACh levels are increased in the VTA during drug self-administration (You et al., 2008), that could result from an increase in ACh release from PPTg and LDTg afferents (Futami et al., 1995; Omelchenko and Sesack, 2006). Cholinergic neurons within PPTg neurons do not exhibit burst firing, and they are more active during wakefulness and REM sleep versus slow wave sleep, but show more activity during REM sleep than slow wave sleep (Datta and Siwek, 2002); however, there is currently no evidence that VTA DA neurons show circadian variations in activity, suggesting that the diurnally regulated neurons may not project to VTA. In addition, PPTg neurons change their firing rate in response to both locomotion and acquisition of reward (Datta and Siwek, 2002). These observations have led to the idea that the PPtg acts as a gate for salient sensory information associated with reward and/or requiring movement (Norton et al., 2011).
