Stopping a Continuous Movement: A Novel Approach to Investigating Inhibitory Control.

Flexible, adaptive behavior is critically dependent on inhibitory control. For example, if you suddenly notice you are about to step on a tack and would prefer not to, the ability to halt your ongoing movement is critical. However, this behavior is usually not probed by current inhibitory control tasks, which often focus instead on inhibiting a movement before its initiation. To address limitations in existing approaches for studying termination of an ongoing movement, we developed a novel stop task with which we can directly observe and compare prepared and reactive termination of a continuous movement. Here, we present and evaluate our novel continuous movement stop task (CMST) and compare task performance to performance on the traditional stop signal task. Our data reveal that the CMST effectively dissociates planned and unplanned stopping behaviors. We found that participants initiated and completed stopping significantly earlier on planned compared with unplanned stop trials and that the variability for each measure was greater for planned compared with unplanned stop trials. In addition, we found that the time at which participants initiated the stopping process was more variable than the time it took participants to complete the stopping process. We also found that participants slowed before stopping significantly more on planned than unplanned stop trials. Finally, our data suggest that preparatory mechanisms may be similar between the CMST and the traditional stop signal tasks, but that the tasks were not related by any other measure. The unambiguous quantification of prepared and reactive stopping behavior provided by the CMST will help support future investigation of different kinds of stopping behavior.

Nonparaphilic hypersexual behavior and depressive symptoms: a meta-analytic review of the literature.

Research on nonparaphilic hypersexual behavior and its associated characteristics has increased in recent years. In the present article, the authors review the literature on the relation between nonparaphilic hypersexual behavior and depressive symptoms. There was a moderate, positive relation between nonparaphilic hypersexual behavior and depressive symptoms (r =.34). This relation was similar across gender, sexual orientation, and age. The authors discuss the implications for researchers and clinicians working with hypersexual individuals. Future research should work to elucidate the causal direction of the relation between nonparaphilic hypersexual behavior and depressive symptoms. The authors encourage clinicians who work with hypersexual patients to assess them for depressive symptoms and consider treatment options that address concurrent depressive symptoms.

Prepared and reactive inhibition in smokers and non-smokers.

INTRODUCTION: Models of addiction have identified deficits in inhibitory control, or the ability to inhibit inappropriate or unwanted behaviors, as one factor in the development and maintenance of addictive behaviors. Current literature supports disruption of the prefrontal circuits that mediate reactive inhibitory control processes (i.e., inhibition in response to sudden, unplanned changes in environmental demands) in substance use disorders. However, the relationship between disorders of addiction, such as nicotine dependence, and planned inhibitory processes (i.e., inhibition that occurs after advance warning) is unclear. The goal of the present study was to examine the extent to which reactive and planned inhibitory processes are differentially disrupted in nicotine dependent individuals. METHOD: We employed an internet-based novel stop signal task wherein participants were instructed to stop a continuous movement at either a predictable or unpredictable time. This task explicitly separated planned and reactive inhibitory processes and assessed group differences in task performance between smokers (N = 281) and non-smokers (N = 164). The smoker group was defined as any participant that identified as a smoker and reported an average daily nicotine consumption of at least 2 mg. The non-smoker group was defined as any participant that identified as a non-smoker and had not been a former smoker that quit within the last year. The smoker group also completed a questionnaire regarding smoking behaviors which included the Fägerstrom Test of Nicotine Dependence (FTND). We used these data to assess the continuous relation between planned stopping, unplanned stopping, and smoking behaviors. RESULTS: We found significant differences in stop times for both reactive and planned stopping between groups as well as within the smoker group. Additionally, in the smoker group, dependence as measured by the FTND was associated with longer stop times on planned stop trials. Surprisingly, greater daily average consumption of nicotine was related to faster stopping for both trial types. CONCLUSION: These results indicate the relevance of measuring both reactive and planned inhibitory processes for elucidating the relationship between nicotine addiction and mechanisms of inhibitory control.

Disparate insults relevant to schizophrenia converge on impaired spike synchrony and weaker synaptic interactions in prefrontal local circuits.

Schizophrenia results from hundreds of known causes, including genetic, environmental, and developmental insults that cooperatively increase risk of developing the disease. In spite of the diversity of causal factors, schizophrenia presents with a core set of symptoms and brain abnormalities (both structural and functional) that particularly impact the prefrontal cortex. This suggests that many different causal factors leading to schizophrenia may cause prefrontal neurons and circuits to fail in fundamentally similar ways. The nature of convergent malfunctions in prefrontal circuits at the cell and synaptic levels leading to schizophrenia are not known. Here, we apply convergence-guided search to identify core pathological changes in the functional properties of prefrontal circuits that lie downstream of mechanistically distinct insults relevant to the disease. We compare the impacts of blocking NMDA receptors in monkeys and deleting a schizophrenia risk gene in mice on activity timing and effective communication in prefrontal local circuits. Although these manipulations operate through distinct molecular pathways and biological mechanisms, we found they produced convergent pathophysiological effects on prefrontal local circuits. Both manipulations reduced the frequency of synchronous (0-lag) spiking between prefrontal neurons and weakened functional interactions between prefrontal neurons at monosynaptic lags as measured by information transfer between the neurons. The two observations may be related, as reduction in synchronous spiking between prefrontal neurons would be expected to weaken synaptic connections between them via spike-timing-dependent synaptic plasticity. These data suggest that the link between spike timing and synaptic connectivity could comprise the functional vulnerability that multiple risk factors exploit to produce disease.