Neuroscience
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Is sentence structure processed by the same neural and cognitive resources that are recruited for processing word meanings, or do structure and meaning rely on distinct resources? Linguistic theorizing and much behavioral evidence suggest tight integration between lexico-semantic and syntactic representations and processing. However, most current proposals of the neural architecture of language continue to postulate a distinction between the two. One of the earlier and most cited pieces of neuroimaging evidence in favor of this dissociation comes from a paper by Dapretto and Bookheimer (1999). ⋯ Using a combination of whole-brain, group-level ROI, and participant-specific functional ROI approaches, we fail to replicate the original dissociation. In particular, whereas parts of LIFG respond reliably more strongly during lexico-semantic than syntactic processing, no part of LIFG (including in the region defined around the peak reported by Dapretto & Bookheimer) shows the opposite pattern. We speculate that the original result was a false positive, possibly driven by a small subset of participants or items that biased a fixed-effects analysis with low power.
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Coagulation factor XII (FXII) is synthesized in the liver and secreted into the circulation, where it initiates the contact activation system. Although typically thought to be restricted to the circulation, FXII protein has been found in the brain of Alzheimer's disease (AD) and multiple sclerosis patients. Moreover, activation of the contact system has been detected in the cerebrospinal fluid of these patients as well as in the brain of healthy and AD individuals. ⋯ We show that a recombinant version of this shorter FXII protein is activated by plasma kallikrein, reciprocally activates prekallikrein, and converts pro-hepatocyte growth factor (HGF) to active HGF in vitro. HGF-Met signaling plays a role in neuronal development and survival, and its dysregulation has been implicated in neurodevelopmental disorders and neurodegeneration. Taken together, our results show that a short isoform of FXII mRNA is expressed in the brain and raise the possibility that brain-derived FXII may be involved in HGF-Met signaling in neurons.
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One deficit associated with schizophrenia (SZ) is the reduced ability to distinguish self-caused sensations from those due to external sources. This reduced sense of agency (SoA, subjective awareness of control over one's actions) is hypothesized to result from a diminished utilization of internal monitoring signals of self-movement (i.e., efference copy) which subsequently impairs forming and utilizing sensory prediction errors (differences between the predicted and actual sensory consequences resulting from movement). Another important function of these internal monitoring signals is the facilitation of higher-order mechanisms related to motor learning and control. ⋯ Although adaptation was similar for SZP and controls, the extent of generalization was significantly less for SZP; movement trajectories made by patients to the furthest untrained target (135o) before and after adaptation were largely indistinguishable. Interestingly, deficits in generalization were correlated with positive symptoms of psychosis in SZP (e.g., hallucinations). Generalization was also associated with measures of SoA across both SZP and HC, emphasizing the role action awareness plays in motor behavior, and suggesting that misattributing agency, even in HC, manifests in abnormal motor performance.
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People commonly synchronize taps to rhythmic sounds and can continue tapping after the sounds stop, indicating that time intervals between sounds can be internalized. Here, we investigate what happens in the brain after simply listening to auditory beats in order to understand more about the automatic internalization of temporal intervals without tapping. Electroencephalograms were recorded while musicians attended to accelerating, decelerating, or steady click sequences. ⋯ In contrast, physical beats elicited P2 responses and early beta suppressions, likely reflecting a combination of stimulus-related processing and temporal prediction. These results suggest that the activities observed after the silent beat were not produced via sustained entrainment after the physical beats, but via automatically-formed expectation for an additional beat. Therefore, beta modulations may be generated endogenously by expectation violation, while P3a amplitudes may relate to strength of expectation, with acceleration endings causing the strongest expectations for sequence continuation.
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Genetic factors significantly contribute to the risk for developing alcoholism. To study these factors and other associated phenotypes, rodent lines have been developed using selective breeding for high alcohol preference. One of these models, the alcohol preferring (P) rat, has been used in hundreds of preclinical studies over the last few decades. ⋯ Intra-CeA infusion of NK1R antagonist attenuates yohimbine-induced reinstatement in P rats. Conversely, upregulation of NK1R within the CeA of Wistar rats increases alcohol consumption and sensitivity to yohimbine-induced reinstatement. These findings suggest that NK1R upregulation in the CeA contributes to multiple alcohol-related phenotypes in the P rat, including alcohol consumption and sensitivity to relapse.