The study of human consciousness has demonstrated that there are both conscious and unconscious systems. Other work, particularly in animals, has shown that there are habit and nonhabit systems and that these involve different brain regions and memory processes. Here we argue that habits can be equated with unconscious behavior and nonhabits with conscious behavior. This equation makes the extensive physiological literature on habit/nonhabit relevant to the less tractable issue of consciousness. On the basis of this line of reasoning, it appears that different parts of the BG and different memory structures mediate conscious and unconscious processes. It is further argued here that the unconscious system is highly capable; it can both process sensory information and produce behavior. The benefit of such a dual system is multitasking: The unconscious system can execute background tasks, leaving the conscious system to perform more difficult tasks.

Recent work showed that short-term memory (STM) is selectively reduced in GluR1 knockout mice. This raises the possibility that a form of synaptic modification dependent on GluR1 might underlie STM. Studies of synaptic plasticity have shown that stimuli too weak to induce long-term potentiation induce short-term potentiation (STP), a phenomenon that has received little attention. Here we examined several properties of STP and tested the dependence of STP on GluR1. The minimal requirement for inducing STP was examined using a test pathway and a conditioning pathway. Several closely spaced stimuli in the test pathway, forming a single brief burst, were sufficient to induce STP. Thus, STP is likely to be induced by the similar bursts that occur in vivo. STP induction is associative in nature and dependent on the NMDAR. STP decays with two components, a fast component (1.6 ± 0.26 min) and a slower one (19 ± 6.6 min). To test the role of GluR1 in STP, experiments were conducted on GluR1 knockout mice. We found that STP was greatly reduced. These results, taken together with the behavioral work of D. Sanderson et al. [Sanderson, D., Good, M. A., Skelton, K., Sprengel, R., Seeburg, P. H., Nicholas, J., et al. Enhanced long-term and impaired short-term spatial memory in GluA1 AMPA receptor subunit knockout mice: Evidence for a dual-process memory model. Learning and Memory , 2009], provide genetic evidence that STP is a likely mechanism of STM.