Empathy is a multidimensional construct composed of several components such as emotion recognition, emotional perspective taking and affective responsiveness. Even though patients with schizophrenia demonstrate deficits in all core components of this basic social ability, the neural underpinnings of these dysfunctions are less clear. Using fMRI, we analyzed data from 15 patients meeting the DSM-IV criteria for schizophrenia and 15 matched healthy volunteers performing three separate paradigms tapping the core components of empathy, i.e. emotion recognition, perspective taking and affective responsiveness. Behavioral data analysis indicated a significant empathic deficit in patients, reflected in worse performance in all three domains. Analysis of functional data revealed hypoactivation in a fronto-temporo-parietal network including the amygdala in patients. Moreover, amygdala activation correlated negatively with severity of negative symptoms. The results suggest that schizophrenia patients not only suffer from a broad range of emotional deficits but also show cortical and subcortical abnormalities, extending previous findings on fronto-temporal cortical dysfunctions. Since empathy is related to psychosocial functioning and hence of high clinical relevance in schizophrenia, a more detailed understanding of the exact nature of these impairments is mandatory.

Cholinergic neurotransmission has been implicated in memory and attention. We investigated the effect of the non-competitive nicotinic antagonist mecamylamine on three components of attention processes (i.e. alerting, orienting and executive control) in 12 healthy male subjects whilst performing the Attention Network Task (ANT) in a magnetic resonance imaging (MRI) scanner. Participants received 15 mg mecamylamine in a single blind and placebo- controlled randomized procedure 90 min prior to obtaining functional MRI data. Our results confirm previous reports of beneficial effects of cueing (alerting and orienting) and detrimental effects of conflict (executive control) on reaction times when performing the ANT. The functional MRI data confirmed distinct neural networks associated with each of the three attention components. Alerting was associated with increased left temporal lobe activation while orienting increased bilateral prefrontal, right precuneus and left caudate activation. Executive control activated anterior cingulate and precuneus. Mecamylamine slowed overall response time and down-regulated brain activation associated with orienting and to some extent brain activation associated with executive control when compared to placebo. These findings are consistent with nicotinic modulation of orienting attention by cueing and executive control when responding to conflicting information. The latter nicotine antagonist effect may be mediated via cholinergic modulation of dopamine neurotransmission in mesolimbic pathways.

BackgroundIn-vivo observations of neural processes during human aggressive behavior are difficult to obtain, limiting the number of studies in this area. To address this gap, the present study implemented a social reactive aggression paradigm in 29 healthy men, employing non-violent provocation in a two-player game to elicit aggressive behavior in fMRI settings.ResultsParticipants responded more aggressively after high provocation reflected in taking more money from their opponents. Comparing aggression trials after high provocation to those after low provocation revealed activations in neural circuits involved in aggression: the medial prefrontal cortex (mPFC), the orbitofrontal cortex (OFC), the dorsolateral prefrontal cortex (dlPFC), the anterior cingulate cortex (ACC), and the insula. In general, our findings indicate that aggressive behavior activates a complex, widespread brain network, reflecting a cortico-limbic interaction and overlapping with circuits underlying negative emotions and conflicting decision-making. Brain activation during provocation in the OFC was associated with the degree of aggressive behavior in this task.ConclusionTherefore, data suggest there is greater susceptibility for provocation, rather than less inhibition of aggressive tendencies, in individuals with higher aggressive responses. This further supports the hypothesis that reactive aggression can be seen as a consequence of provocation of aggressive emotional responses and parallel evaluative regulatory processes mediated mainly by the insula and prefrontal areas (OFC, mPFC, dlPFC, and ACC) respectively.Electronic supplementary materialThe online version of this article (doi:10.1186/s12868-017-0390-z) contains supplementary material, which is available to authorized users.