Can signals from the prefrontal cortex alone trigger a readiness potential in the pre-supplementary motor area?
The original author is not making a claim one way or another for logical AND or logical OR within this context. The statement 


  the pre-supplementary motor area (preSMA), which in turn receives inputs from the basal ganglia and the prefrontal cortex


is referring only to inputs to the preSMA; it is not making any strong statements about which inputs are causal for the readiness potential, only mentioning that those connections exist and therefore could be involved in communication of the readiness potential. 

There are in fact cortico-cortical loops that route through the basal ganglia (see for example Lopez-Paniagua &amp; Seger, 2011; there is probably a better canonical reference but not one I have in hand right now); if there is a signal from frontopolar cortex that reaches motor cortex that does not tell you the basal ganglia were not involved. A signal originating in cortex could communicate with another cortical area both via direct cortico-cortico and via basal ganglia open loops, not that a basal ganglia signal preceded both.

The only way to truly answer your title question would be to somehow inactivate either basal ganglia or PFC inputs to preSMA. I am not aware of such an experiment, it would be quite technically and ethically difficult both in humans and primates, and PFC is less developed in rodents so it's difficult to make direct analogy there.

More generally, the basal ganglia are definitely involved in voluntary movement. One can simply observe Parkinsonian patients, who have difficulties initiating voluntary movements due to basal ganglia pathology (DeLong 1990 discusses some of the motor impacts of lesions of the basal ganglia).

If you want to know whether movements can be triggered "purely by executive function and independently of primal urges/apprehensions" you will not find the answer simply by identifying whether the basal ganglia are involved or not. Although yes, the basal ganglia are often associate with more "primal" actions, that is only relevant in the absence of neocortex. In the presence of neocortex, that organization no longer applies because cortex influences the basal ganglia (and vice versa).

Furthermore, it does not seem possible to separate out the basal ganglia from neocortex in terms of cognitive control networks (Duncan 2010, Cole et al 2013), since coactivation of those areas is typically observed and not dissociable.



Cole, M. W., Laurent, P., &amp; Stocco, A. (2013). Rapid instructed task learning: A new window into the human brain’s unique capacity for flexible cognitive control. Cognitive, Affective, &amp; Behavioral Neuroscience, 13(1), 1-22.

DeLong, M. R. (1990). Primate models of movement disorders of basal ganglia origin. Trends in neurosciences, 13(7), 281-285.

Duncan, J. (2010). The multiple-demand (MD) system of the primate brain: mental programs for intelligent behaviour. Trends in cognitive sciences, 14(4), 172-179.

Lopez-Paniagua, D., &amp; Seger, C. A. (2011). Interactions within and between corticostriatal loops during component processes of category learning. Journal of cognitive neuroscience, 23(10), 3068-3083.