On the relationships between the pedunculopontine tegmental nucleus, corticostriatal architecture and the medial reticular formation

Recent studies have established that the pedunculopontine tegmental nucleus (PPTg) is integrated into corticostriatal looped architecture through connections that include established basal ganglia output nuclei (pallidum, subthalamus and substantia nigra pars reticulata), thalamus and midbrain dopamine (DA) containing neurons in both the ventral tegmental area (VTA) and substantia nigra pars compacta (SNC). It is becoming apparent that the PPTg can be functionally dissociated internally. A simple dissociation is between posterior and anterior PPTg. The posterior PPTg contains a large proportion of cholinergic neurons, has polymodal sensory input that triggers very fast neuronal activity and projects preferentially to the VTA. In contrast, the anterior PPTg contains fewer cholinergic neurons, receives outflow from both corticostriatal systems and the extended amygdala and projects to the SNC. We suggest that this organization maps on to the spiral corticostriatal architecture such that the posterior PPTg interacts with ventromedial striatal systems (a proposed function of which is to integrate incentive salient stimuli to shape flexible goal-directed actions), whereas the anterior PPTg interacts with dorsolateral striatal circuits (which are thought to mediate the learning and execution of stimulus–response associations and the formation of habits). By these interactions, the PPTg en masse contributes to high-order decision making processes that shape action selection. In addition to this we also suggest that the PPTg integrates with medial reticular formation systems that operate as an immediate low-level action selection mechanism. We hypothesize that the PPTg has a pivotal position, bridging between higher order action selection mechanisms dealing with flexible learning of novel action patterns and lower level action selection processes that permit very fast responding to imperative stimuli.