I have this obsession with the visual system. If you did not know, then now you know! I also happen to believe that the visual system “talks” just as loud as other physiological systems when homeostatic mechanisms are breached. Let me  give you an example…

I recently read this novel article entitled “Subjective and Autonomic Responses to Smoking-Related Visual Cues.” Previous research has shown that when smoking-related visual cues are presented to smokers, they show an increase in autonomic nervous system activity compared to non-smokers. I suppose it looks something like this….DISCLAIMER: THIS DEPICTION IS INACCURATE BECAUSE I DO NOT SMOKE AND THE DATA IS NOT REAL!

The results were pretty clear. Smokers had significantly higher pupil diameters when a smoking-related cue was presented compared to non-smokers. My next question is if smokers show pronounced differences in pupil size then perhaps these same physiological measures can predict relapse? Here is my wild theory. Studies have shown that tobacco acts similarly to the sympathetic nervous system excitation. Thus, it causes the pupils to dilate via adrenergic activity. The parasympathetic activity causes the pupil to constrict via acetylcholine. An increase in pupil size probably means that more adrenaline is binding. Now, read the following abstract:

Title: Noradrenergic transmission in the extended amygdala: role in increased drug-seeking and relapse during protracted drug abstinence.

Abstract:

Studies reviewed here implicate the extended amygdala in the negative affective states and increased drug-seeking that occur during protracted abstinence from chronic drug exposure. Norepinephrine (NE) and corticotropin-releasing factor (CRF) signaling in the extended amygdala, including the bed nucleus of the stria terminalis, shell of the nucleus accumbens, and central nucleus of the amygdala, are generally involved in behavioral responses to environmental and internal stressors. Hyperactivity of stress response systems during addiction drives many negative components of drug abstinence. In particular, NE signaling from the nucleus tractus solitarius (NTS) to the extended amygdala, along with increased CRF transmission within the extended amygdala, are critical for the aversiveness of acute opiate withdrawal as well as stress-induced relapse of drug-seeking for opiates, cocaine, ethanol, and nicotine. NE and CRF transmission in the extended amygdala are also implicated in the increased anxiety that occurs during prolonged abstinence from chronic opiates, cocaine, ethanol, and cannabinoids. Many of these stress-associated behaviors are reversed by NE or CRF antagonists given systemically or locally within the extended amygdala. Finally, increased Fos activation in the extended amygdala and NTS is associated with the enhanced preference for drugs and decreased preference for natural rewards observed during protracted abstinence from opiates and cocaine, indicating that these areas are involved in the altered reward processing associated with addiction. Together, these findings suggest that involvement of the extended amygdala and its noradrenergic afferents in anxiety, stress-induced relapse, and altered reward processing reflects a common function for these circuits in stress modulation of drug-seeking.

So, what does it mean? Since pupil dilation also relies on epinephrine, and it is “upregulated” after smokers view smoking-cues, it is possible that pupil size might predict relapse in susceptible individuals.

Think about it!

Peace,

–Sharonda