[20][21][22][23] In the early 1980s, Robinson initiated studies using the amphetamine-induced rotational behavior model to explore the mesostriatal dopamine system's function and the influence of sex and gonadal hormones with Jill Becker.
[40] Collaborating with Bryan Kolb, Robinson hypothesized that long-lasting behavioral effects of drug exposure involve changes in synaptic connectivity, which would be reflected by changes in dendritic structure.
[42] They also established patterns of changes in brain regions (e.g., dorsal vs. ventral striatum, prefrontal cortical subregions, other areas of the neocortex), their similarity after experimenter- or self-administered drugs (2002),[43] and the impact of past experience (2003),[44] and context (2004),[45] along with other features.
Initial studies, with Shelly Flagel, showed that only some animals (sign-trackers) attribute incentive salience to reward cues, which makes them attention-grabbing and desirable in their own right.
It is established that only if reward cues act as incentive stimuli do they come to attract, incite, provoke, spur, and motivate, leading to potentially maladaptive behavior.
Furthermore, Martin Sarter and colleagues have shown that sign-trackers have deficient choline transporters leading to poor executive/attentional control over behavior, relative to goal-trackers.
Robinson has speculated that the combination of enhanced "bottom-up" motivational processes and poor "top-down" inhibitory control may render sign-trackers especially prone to addiction.
[47] Finally, Robinson has initiated an investigation into the impact of pharmacokinetic factors on the emergence of addiction-like behavior, using the Intermittent Access (IntA) self-administration procedure.
Their findings have demonstrated IntA cocaine self-administration is especially effective in inducing addiction-like behavior, psychomotor, incentive, and dopamine sensitization, consistent with Incentive-Sensitization Theory.