39 research outputs found

    A cortical mechanism linking saliency detection and motor reactivity in rhesus monkeys

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    : Sudden and surprising sensory events trigger neural processes that swiftly adjust behavior. To study the phylogenesis and the mechanism of this phenomenon, we trained two male rhesus monkeys to keep a cursor inside a visual target by exerting force on an isometric joystick. We examined the effect of surprising auditory stimuli on exerted force, scalp electroencephalographic (EEG) activity, and local field potentials (LFP) recorded from the dorso-lateral prefrontal cortex. Auditory stimuli elicited (1) a biphasic modulation of isometric force: a transient decrease followed by a corrective tonic increase, and (2) EEG and LFP deflections dominated by two large negative-positive waves (N70 and P130). The EEG potential was maximal at the scalp vertex, highly reminiscent of the human 'vertex potential'. Electrocortical potentials and force were tightly coupled: the P130 amplitude predicted the magnitude of the corrective force increase, particularly in the LFPs recorded from deep rather than superficial cortical layers. These results disclose a phylogenetically-preserved cortico-motor mechanism supporting adaptive behavior in response to salient sensory events.Significance Statement Survival in the natural world depends on an animal's capacity to adapt ongoing behavior to unexpected events. To study the neural mechanisms underlying this capacity, we trained monkeys to apply constant force on a joystick while we recorded their brain activity from the scalp and, invasively, from the prefrontal cortex contralateral to the hand holding the joystick. Unexpected auditory stimuli elicited a biphasic force modulation: a transient reduction followed by a corrective adjustment. The same stimuli also elicited EEG and LFP responses, dominated by a biphasic wave that predicted the magnitude of the behavioral adjustment. These results disclose a phylogenetically-preserved cortico-motor mechanism supporting adaptive behavior in response to unexpected events

    Deletion of the BDNF receptor TrkB.T1 rescues hippocampal parvalbumin positive interneurons in a mouse model of Amyotrophic Lateral Sclerosis

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    Deletion of the BDNF receptor TrkB.T1 rescues hippocampal parvalbumin positive interneurons in a mouse model of Amyotrophic Lateral Sclerosis

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    In addition to motoneurons degeneration, Amyotrophic Lateral Sclerosis (ALS) patients have defects in brain regions primarily associated with cognitive functions, such as the hippocampus. These defects have also been confirmed in animal models of ALS. The report that transgenic mice expressing a mutant form of the human superoxide dismutase-1 (hSOD1) with a Gly93 → Ala substitution (G93A-hSOD1), causing familial ALS, have degeneration of a subsets of spinal interneurons (Mol Neurobiol. 2012, 45: 30-42) prompted us to investigate whether this phenotype extends to other CNS interneuron populations. The calcium-binding protein parvalbumin positive interneurons (PVi), constitute the largest class of hippocampal interneurons and play essential roles in hippocampus development and plasticity. Interestingly, we found that PVi are reduced in the hippocampus of presymptomatic G93A-hSOD1 mice compared to controls. Therefore, we decided to use the hippocampal PVi as a model system to identify pathways that may affect the survival of this neuronal population in neurodegenerative conditions. Recently we have shown that deletion of the BDNF receptor TrkB.T1 lacking the intracellular tyrosine kinase domain delays the onset of motoneuron degeneration in the G93A-hSOD1 mice (PLoS One. 2012, 7:e39946). Thus, we investigated hippocampal PVi in G93A-hSOD1/TrkB.T1 deficient mice, G93A-hSOD1 animals at the presymptomatic state and wild type mice as controls. Eight-week-old brains were processed to visualize PVi. After image acquisition, hippocampal slices stained for PV were analyzed with ImageJ. Surprisingly, we found that the number of hippocampal PVi was comparable between wild type and G93A-hSOD1/TrkB.T1-/-. Statistical analysis by ANOVA performed on raw data revealed highly significant differences among the three genotypes [F(2,137)=9.077, p=0.0002]. Post-hoc tests showed that G93A-hSOD1 mice had significantly less PVi (79.05±0.56) compared to wild type (93.84±0.93) and to G93A-hSOD1/TrkB.T1-/- mice (93.10±0.54). These data suggest that BDNF/TrkB.T1 signaling affects not only motoneurons but also hippocampal PVi survival. Moreover, they unveil a new function for TrkB.T1 in a cell population essential for normal hippocampal function and suggest the relevance of targeting this pathway in neurodegenerative conditions

    A little elastic for a better performance: kinesiotaping of the motor effector modulates neural mechanisms for rhythmic movements

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    Background and Aim: A rhythmic motor performance is brought about by an integration of timing information with movements. We have recently demonstrated that the precision of an isochronous performance, defined as performance of repeated movements having a uniform duration, was insensible to auditory stimuli of various characteristics (Bravi et al. 2014). Such finding has led us to further investigate where do the determining factors of precision reside. Materials and Methods: For this purpose we used manipulation of cutaneous afferents by kinesiotaping (KT), an approach that was previously shown to improve some isokinetic performances (Kim and Lee 2013; Wong et al. 2012). Subjects, tested without KT and with KT, have participated in sessions in which sets of repeated isochronous wrist's flexion-extensions (IWFEs) were performed under various auditory conditions and during their recall. Kinematics was recorded and temporal parameters were extracted and analyzed. Results and Discussion: Various degrees of improvement in the isochronous performances were evident for the KT recordings especially in terms of temporal precision. Our results indicate that, in the precision of repetitive rhythmic movements, the manipulation of cutaneous afferents plays a significant role. Whether this increase in precision is achieved by augmentation of the efficiency in central or local neural mechanisms is to be determined, but what remains certain is that when it comes to precision, a little elastic makes the difference
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