Delay of punishment highlights differential vulnerability to developing addiction-like behavior toward sweet food.

Resistance to punishment is commonly used to measure the difficulty in refraining from rewarding activities when negative consequences ensue, which is a hallmark of addictive behavior. We recently developed a progressive shock strength (PSS) procedure in which individual rats can titrate the amount of punishment that they are willing to tolerate to obtain food rewards. Here, we investigated the effects of a range of delays (0-12 s) on resistance to punishment measured by PSS break points. As expected from delay discounting principles, we found that delayed shock was less effective as a punisher, as revealed by higher PSS breakpoints. However, this discounting effect was not equally distributed in the population of rats, and the introduction of a delay highlighted the existence of two populations: rats that were sensitive to immediate punishment were also sensitive to delayed shock, whereas rats that were resistant to immediate punishment showed strong temporal discounting of delayed punishment. Importantly, shock-sensitive rats suppressed responding even in subsequent non-punishment sessions, and they differed from shock-resistant rats in anxiety-like behavior, but not in sensitivity to pain. These results show that manipulation of temporal contingencies of punishment in the PSS procedure provides a valuable tool to identify individuals with a double vulnerability to addiction: low sensitivity to aversion and excessive discounting of negative future consequences. Conversely, the shock-sensitive population may provide a model of humans who are vulnerable to opportunity loss due to excessive anxiety.

EEG microstate co-specificity in schizophrenia and obsessive-compulsive disorder.

The past 20 years of research on EEG microstates has yielded the hypothesis that the imbalance pattern in the temporal dynamics of microstates C (increased) and D (decreased) is specific to schizophrenia. A similar microstate imbalance has been recently found in obsessive-compulsive disorder (OCD). The aim of the present high-density EEG study was to examine whether this pathological microstate pattern is co-specific to schizophrenia and OCD. We compared microstate temporal dynamics using Bayesian analyses, transition probabilities analyses and the Topographic Electrophysiological State Source-Imaging method for source reconstruction in 24 OCD patients and 28 schizophrenia patients, respectively, free of comorbid psychotic and OCD symptoms, and 27 healthy controls. OCD and schizophrenia patients exhibited the same increased contribution of microstate C, decreased duration and contribution of microstate D and greater D → C transition probabilities, compared with controls. A Bayes factor of 4.424 for the contribution of microstate C, 4.600 and 3.824, respectively, for the duration and contribution of microstate D demonstrated that there was no difference in microstate patterns between the two disorders. Source reconstruction further showed undistinguishable dysregulations between the Salience Network (SN), associated with microstate C, and the Executive Control Network (ECN), associated with microstate D, and between the ECN and cognitive cortico-striato-thalamo-cortical (CSTC) loop in the two disorders. The ECN/CSTC loop dysconnectivity was slightly worsened in schizophrenia. Our findings provide substantial evidence for a common aetiological pathway in schizophrenia and OCD, i.e. microstate co-specificity, and same anomalies in salience and external attention processing, leading to co-expression of symptoms.