A schematic model of somatic state activation and decision-making. (a) This is the neural circuitry (in green) that represents the impulsive system, in which the amygdala is a trigger structure for emotional (somatic) states from primary inducers. It couples the features of primary inducers, which can be processed subliminally (e.g., via the thalamus) or explicitly (e.g., via primary sensory cortices), with effector structures that trigger the emotional/somatic response. However, the amygdala is also directly connected to the ventral striatum (V.S.) and its trigger can also activate classical motivational systems associated with approach of drug related cues.
(b) This is the neural circuitry (in red) that represents the reflective system, in which the ventromedial prefrontal cortex (VMPC) is a trigger structure for emotional (somatic) states from secondary inducers. It couples systems involved in memory to systems involved in processing emotions, so that memories or thoughts about drug cues are linked to their emotional attributes. Memories, information, or knowledge held temporarily in working memory, and manipulated by the executive processes of working memory are dependent on the dorsolateral prefrontal cortex (DLPFC), but these working processes also include the ventrolateral prefrontal cortex as well as the lateral region of the orbitoforntal cortex. The hippocampus is also engaged, at least in situations where the memory of a scenario exceeds 40 seconds, which is the maximum capacity of the short term memory mediated by the DLPFC). Structures involved in representing previous feeling states include the Insula and surrounding somatosensory cortices, as well as the posterior cingulate cortex (PCC) and the precuneate cortex. This coupling mediated by the VMPC can also lead to the triggering of somatic states (red lines).
(c) Somatic signals triggered simultaneously by the impulsive system and reflective system compete. We argue that this competition actually occurs in the body proper, although some authors have challenged the validity of this peripheral link (e.g., see [Dunn et al., 2006] for a critique). Even if this peripheral link proves to be invalid, neuroanatomical evidence supports neural competition at the next link of the circuitry, the neurotransmitter cell bodies in the brainstem. Whether the competition of hailing somatic signals via the impulsive and reflective systems occurs in the body or the brainstem, a “winner takes all” somatic signal emerges, either positive or negative, and this resultant ascending feedback somatic signal (blue lines) participate in two functions: in one it provides a substrate for feeling the emotional state, through the insula and surrounding somatosensory cortices; in the other, it provides a substrate for biasing decisions through motor effector structures such as the striatum (Str.), and the anterior cingulate cortex (ACC) and adjacent Supplementary Motor Area (SMA). Another highly candidate region involved in this complex motor preparation is the Cerebellum (not shown in this diagram).
In light of more recent evidence on the role of the insula in cigarette smoking, we propose that the insula has a more specific role: Especially during withdrawal or drug deprivation, homeostatic signals arising in the body are perceived in the insula as feelings of urges, which in turn act on the impulsive system and sensitize it (green line), whereas its action on the reflective system is to inhibit it or “hijack” it. It remains to be determined the mechanism by which the insular activity sensitizes the impulsive system. One possibility, for example, is that neuronal signals from the insula activate the ventral tegmental area and increase the mesolimbic dopamine surge, thereby heightening the motivation to seek drugs. Such a possible mechanism can connect the insula to the classic neural systems that have been implicated in addiction (i.e., the mesolimbic dopamine system).