Neuroscience
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In a therapeutic environment a proper regulation of the empathic response strengthens the patient-therapist relationship. Thus, it is important that psychotherapists constantly regulate their own perspective and emotions to better understand the other's affective state. We compared the empathic abilities of a group of 52 psychotherapists with a group of 92 non-psychotherapists and found psychometric differences. ⋯ Psychotherapists showed greater functional connectivity between the left anterior insula and the dorsomedial prefrontal cortex, and less connectivity between rostral anterior cingulate cortex and the orbito prefrontal cortex. Both associations correlated with Perspective Taking scores. Considering that the psychometric differences between groups were in the cognitive domain and that the functional connectivity associations involve areas related to cognitive regulation processes, these results suggest a relationship between the functional brain organization of psychotherapists and the cognitive regulation of their empathic response.
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When processing repeated stimuli, the neural response is attenuated (i.e., neural adaptation) and performance seems to be facilitated; however, this neural adaptation negatively influences the subsequent processing of novel stimuli. The present study was designed to test whether and how temporal expectations reduce neural adaptation and attenuate the negative influence of neural adaptation on subsequent novel problem solving. Temporal expectations were experimentally manipulated by asking participants to solve a novel problem following three to five repeated problems, generating the expectation of repeated events in the first three serial positions as well as that of novel events in the fourth to sixth serial positions. ⋯ Regarding the novel events, the conflict monitoring- and resolution-related N400, P600 and LNC amplitudes decreased with decreased neural adaptation. These results indicate that the expectation of novel events attenuate the negative influence of neural adaptation on the subsequent processing of novel events. This study provides new insight into alleviating the constraints imposed by frequently used knowledge on the processing of novel stimuli.
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Silent myocardial infarction (MI) is critical for clinical practice with increasing risk for women and the cause remains a medical mystery. Upon the discovery of female-specific Ah-type baroreceptor neurons (BRNs), we hypothesize that glutamate mediates depressor response through afferent-specific expression of particular glutamate receptors (mGluRs) leading descending inhibition of cardiac nociception. In vivo, tail-flick reflex and electromyography were assessed to evaluate glutamate-mediated blood pressure regulation, peripheral and cardiac nociception. ⋯ Glutamate in serum, NG and nucleus tractus solitary (NTS) was raised significantly in the model rats of both sexes vs. sham-controls. Female-specific expression of mGluR7 in the baroreflex afferent pathway, especially higher expression in Ah-type BRNs, contributes significantly to cardiac analgesia, which may explain that the pathogenesis of silent MI occurs mainly in female patients. Therefore, higher expression of mGluR7 in female-specific subpopulation of Ah-type BRNs plays a critical role in cardiac analgesia and peripheral nociception.
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A number of studies has explored a positive correlation between low levels of serum Vitamin D3 (VD; cholecalciferol) and development of neurodegenerative diseases including Huntington's disease (HD). In the present study, the prophylactic effect of VD on motor dysfunction was studied in an experimental model of HD. An HD-like syndrome was induced in male C57BL/6 mice through an intraperitoneal injection (i.p) of 3-NP for 3 consecutive doses at 12 h interval of time as described previously (Amende et al. 2005). ⋯ VD administration rescued locomotor dysfunction and neuromuscular impairment in HD mice with no change in gait dynamics. In addition, administration of VD to 3-NP treated mice led to a significant enhancement in the expression of key neurotrophic factors including brain-derived neurotrophic factor (BDNF) and nerve-growth factor (NGF), the Vitamin D receptor (VDR), and antioxidant markers (catalases [Cat] and glutathione peroxidase [GpX4]) in the striatum, suggesting a detoxification effect of VD. Altogether, our results show that VD supplementation induces survival signals, diminishes oxidative stress, and reduces movement and motor dysfunction in HD.
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Amantadine and clozapine have proved to reduce abnormal involuntary movements (AIMs) in preclinical and clinical studies of L-DOPA-Induced Dyskinesias (LID). Even though both drugs decrease AIMs, they may have different action mechanisms by using different receptors and signaling profiles. Here we asked whether there are differences in how they modulate neuronal activity of multiple striatal neurons within the striatal microcircuit at histological level during the dose-peak of L-DOPA in ex-vivo brain slices obtained from dyskinetic mice. ⋯ The results show that while both drugs reduce LIDs scores behaviorally in a similar way, they have several different and specific actions on modulating the dyskinetic striatal microcircuit. The extracted features were highly accurate in separating amantadine and clozapine effects by means of principal components analysis (PCA) and support vector machine (SVM) algorithms. These results predict possible synergistic actions of amantadine and clozapine on the dyskinetic striatal microcircuit establishing a framework for a bioassay to test novel antidyskinetic drugs or treatments in vitro.