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A prevalence of 1% in the general population and approximately 50% concordance rate in monozygotic twins was reported for schizophrenia, suggesting that genetic predisposition affecting neurodevelopmental processes might combine with environmental risk factors. A multitude of pathways seems to be involved in the aetiology and/or pathogenesis of schizophrenia, including dopaminergic, serotoninergic, muscarinic and glutamatergic signalling. The phosphoinositide signal transduction system and related phosphoinositide‐specific phospholipase C (PI‐PLC) enzymes seem to represent a point of convergence in these networking pathways during the development of selected brain regions. The existence of a susceptibility locus on the short arm of chromosome 20 moved us to analyse PLCB1, the gene codifying for PI‐PLC β1 enzyme, which maps on 20p12. By using interphase fluorescent in situ hybridization methodology, we found deletions of PLCB1 in orbito‐frontal cortex samples of schizophrenia‐affected patients.

We often mistake an unknown person for a familiar person because of the similarities in facial features. This phenomenon, known as false memory, has been investigated mainly using words, pictures, and shapes. Previous neuroimaging studies on false memory have shown that both true and false memories trigger a similar activation in the medial temporal lobe, suggesting that it plays a common role in both. However, no study to date has investigated neural substrates of false memories for faces. In the present fMRI study, we applied a modified version of the standard false memory paradigm, using morphed pictures of faces, to induce false memory in an MRI environment. We found that activity in the amygdala and orbital cortices was associated with the degree of familiarity of items. In particular, false responses to “lure” items evoked a level of activity in the amygdala between that evoked for correct or incorrect responses to “true” items. This indicates a possible role of the amygdala in false memory. A specific region in the anterior cingulate cortex was involved in false recognition; the activity being correlated to reaction times for the response types. These results suggest that the amygdala is involved in determining the relevance of items; therefore, ambiguousness of lure items in terms of familiarity and novelty may be related to decreased activity in the amygdala. The anterior cingulate activity in false memory may be caused not only by increased effort and motor demand but also by higher mnemonic processing of lure items. ► Neural substrates of false memory for face have been investigated by using fMRI. ► Morphed face pictures successfully induced false memory in an MRI environment. ► Amygdala activity was associated with familiarity for false and true memories of faces. ► Anterior cingulate cortex played a role in false memory condition. ► Parahippocampal activation did not distinguish true and false memories for face.

Recent psychology and neuroscience studies have used tactile stimuli in patients, concluding after their experiments that touch is a sense tightly linked to emotions. In parallel, a new way of seeing films, 4D cinema, has added new stimuli to the traditional audiovisual via, including the tactile vibration. In this work, we have studied the brain activity of audience while viewing a scene filmed and directed by us and with an emotional content, under two different conditions: 1) image + sound, 2) image + sound + vibro-tactile stimulation. We have designed a glove where pulse trains are generated in coin motors at specific moments and recorded 35 viewers’ electroencephalograms (EEGs) to evaluate the impact of the vibro-tactile stimulation during the film projection. Hotelling’s T-squared results show higher brain intensity if the tactile stimulus is received during the viewing than if no tactile stimulus is injected. Condition 1 participants showed activation in left and right orbitofrontal areas, whereas Condition 2 they also showed activities in right superior frontal and right-medial frontal areas. We conclude that the addition of vibrotactile stimulus increases the brain activity in areas linked with attentional processes, while producing a higher intensity in those related to emotional processes.

According to the Reinforcement Sensitivity Theory (RST), Gray’s dimension of impulsivity, reflecting human trait reward sensitivity, determines the extent to which stimuli activate the Behavioural Approach System (BAS). The potential neural underpinnings of the BAS, however, remain poorly understood. In the present study, we examined the association between Gray’s impulsivity as defined by the RST and event-related fMRI BOLD-response to anticipation of reward in twenty healthy human subjects in brain regions previously associated with reward processing. Anticipation of reward during a Monetary Incentive Delay Task elicited activation in key components of the human reward circuitry such as the ventral striatum, the amygdala and the orbitofrontal cortex. Interindividual differences in Gray’s impulsivity accounted for a significant amount of variance of the reward-related BOLD-response in the ventral striatum and the orbitofrontal cortex. Specifically, higher trait reward sensitivity was associated with increased activation in response to cues indicating potential reward. Extending previous evidence, here we show that variance in functional brain activation during anticipation of reward is attributed to interindividual differences regarding Gray’s dimension of impulsivity. Thus, trait reward sensitivity contributes to the modulation of responsiveness in major components of the human reward system which thereby display a core property of the BAS. Generally, fostering our understanding of the neural underpinnings of the association of reward-related interindividual differences in affective traits might aid researchers in quest for custom-tailored treatments of psychiatric disorders, further disentangling the complex relationship between personality traits, emotion, and health.

Experimental mood manipulations and functional magnetic resonance imaging (fMRI) provide a unique opportunity for examining the neural correlates of mood-congruent memory formation. While prior studies in mood-disorder patients point to the medial temporal lobe in the genesis of mood-congruent memory (MCM) bias, the interaction between mood and emotional memory formation has not been investigated in healthy participants. In particular it remains unclear how regulatory structures in the pre-frontal cortex may be involved in mediating this phenomenon. In this study, event-related fMRI was performed on 20 healthy participants using a full-factorial, within-subjects repeated-measures design to examine how happy and sad moods impact memory for valenced stimuli (positive, negative and neutral words). Main effects of mood, stimulus valence and memory were examined as was activity related to successful memory formation during congruent and in-congruent moods. Behavioral results confirm an MCM bias while imaging results show amygdala and hippocampal engagement in a global mood and successful recall, respectively. MCM formation was characterized by increased activity during mood-congruent encoding of negative words in the orbito-frontal cortex (OFC) and for mood-incongruent processing of negative words in medial- and inferior-frontal gyri (MFG/IFG). These findings indicate that different pre-frontal regions facilitate mood-congruent and incongruent encoding of successfully recalled negative words at the time of learning, with OFC enhancing congruency and the left IFG and MFG helping overcome semantic incongruities between mood and stimulus valence. ► Mood-congruent memory formation marked by increased orbito-frontal activity. ► Inferior-frontal activity increased during successful mood-incongruent learning. ► A sad mood led to a general increase in amygdala activity when encoding words. ► Emotional words elicited activity in a network of frontal and posterior regions.

Chronic migraine is a relatively common disorder in neurological terms that causes very significant disability at a high cost. The precise mechanisms behind the progression of episodic migraine to chronic migraine are not well understood. Functional neuro-imaging works on the basis that neuronal activations are associated with changes in regional cerebral blood flow, and it can help us answer some of these questions. In this review, we discuss important recent studies in chronic migraine or studies relating to increasing frequency of migraine attacks. The findings show that increasing frequency of migraine attacks is associated with changes in key brainstem areas, basal ganglia and various cortical areas involved in pain.

Imaging the human orbitofrontal cortex (OFC) with fMRI is problematic due to the proximity of this region to the air-filled sinuses, which causes susceptibility artifacts. Placing a strongly diamagnetic material into the mouth (‘mouthshim’) of a human volunteer can significantly reduce the artifacts in this region. Using the same combined olfactory and visual fMRI paradigm, we compared brain activation and static B 0 field maps of participants being scanned both with and without the ‘mouthshim’. Results demonstrate that the device improves the B 0 field homogeneity within OFC, resulting in significantly stronger BOLD activation in this region. However, the device also caused both increased head motion and reduced activation in insular cortices due to more frequent swallowing and tactile stimulation of the tongue. The ‘mouthshim’ should only, therefore, be used where sensitivity in OFC regions is paramount.