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Benedetto, A.

Publications and source records attributed to Benedetto, A..

6 recordsLinked to original sources

Muscle-specific motor unit firing characteristics in elbow flexors and extensors after cervical spinal cord injury

Individuals with cervical spinal cord injury (SCI) often exhibit asymmetric recovery of upper-limb function, with greater weakness in elbow extensors than flexors. To determine whether muscle-specific changes in motor unit (MU) behavior contribute to this disparity, we identified MU firing instants from high-density surface electromyography to characterize MU firing characteristics in the biceps brachii (BIC) and triceps brachii (TRI) of individuals with cervical SCI (n = 20) and non-injured controls (n = 18). We quantified rate-coding behavior and metrics related to persistent inward currents (PICs), including onset-offset hysteresis ({Delta}F), ascending firing rate nonlinearity, and self-sustained firing. At the group level, BIC MUs in SCI participants showed reduced rate coding and altered ascending firing rate nonlinearity relative to controls. In contrast, TRI MUs showed no clear group-level differences. However, subgroup analysis revealed that SCI participants with low-strength during extension (n = 9) exhibited lower {Delta}F and longer self-sustained firing durations in TRI MUs than those with high-strength (n = 6). In BIC, SCI participants with low-strength during flexion (n = 8) showed reduced rate-coding behavior relative to high-strength SCI participants (n = 9), with no differences in PIC-related metrics. Together, these results demonstrate muscle-specific alterations in MU firing after cervical SCI that may relate to strength recovery or preservation and underscore the need for nuanced analyses in heterogeneous SCI populations. Key pointsO_LIRate coding and nonlinear firing behaviors are significantly altered in the biceps brachii, but not triceps brachii, of participants with cervical spinal cord injury. C_LIO_LIStrength based subgroup analyses revealed muscle-specific differences in motor unit behaviors that may be associated with strength preservation or recovery following spinal cord injury. C_LIO_LIFunctional heterogeneity following spinal cord injury may mask group differences in motor unit behaviors and warrants careful interpretation of results of future studies. C_LI

neuroscience↗

Late cortical dynamics mediate the symmetry-induced numerosity illusion

Numerosity perception enables us to quickly estimate the number of objects in a visual scene, a fundamental skill supporting efficient interaction with the environment. In this study, we tracked how the human brain transforms physical inputs into numerical percepts. Using EEG we measured the neural dynamics to assess whether numerosity is perceived directly or inferred from correlated non-numerical features, and how these signals are integrated with contextual cues that bias perception. We leveraged on a visual illusion in which dot arrays appear less numerous when arranged symmetrically rather than randomly. Participants viewed dot arrays of varying physical or perceived numerosity, illusorily altered by the dots spatial arrangement. Both univariate and multivariate analyses revealed that physical numerosity was decodable from occipitoparietal electrodes as early as [~]50 ms after stimulus onset, independently of low-level features such as dot size or convex hull. Spatial arrangement was represented later, from [~]150 ms, and perceived numerosity, biased by symmetry-induced grouping, emerged at a similar latency. These results indicate that early neural signals encode physical numerosity directly, whereas the symmetry-induced underestimation arises from later grouping processes that integrate spatial information to shape perceived numerosity.

neuroscience↗

MEYE: Web-app for translational and real-time pupillometry

Pupil dynamics alterations have been found in patients affected by a variety of neuropsychiatric conditions, including autism. Studies in mouse models have used pupillometry for phenotypic assessment and as a proxy for arousal. Both in mice and humans, pupillometry is non-invasive and allows for longitudinal experiments supporting temporal specificity, however its measure requires dedicated setups. Here, we introduce a Convolutional Neural Network that performs on-line pupillometry in both mice and humans in a web app format. This solution dramatically simplifies the usage of the tool for non-specialist and non-technical operators. Because a modern web browser is the only software requirement, this choice is of great interest given its easy deployment and set-up time reduction. The tested model performances indicate that the tool is sensitive enough to detect both spontaneous and evoked pupillary changes, and its output is comparable with state-of-the-art commercial devices.

neuroscience↗

Temporal binding of Visual and Motor cortical oscillations revealed by BOLD response in Humans

The mechanisms coordinating action and perception over time are poorly understood. The sensory cortex needs to prepare for upcoming changes contingent on action, and this requires temporally precise communication that takes into account the variable delays between sensory and motor processing. Several theorists1,2 have proposed synchronization of the endogenous oscillatory activity observed in most regions of the brain3 as the basis for an efficient and flexible communication protocol between distal brain areas2,4, a concept known as "communication through coherence". Synchronization of endogenous oscillations5,6 occurs after a salient sensory stimulus, such as a flash or a sound7-11, and after a voluntary action12-18, and this impacts directly on perception, causing performance to oscillate rhythmically over time. Here we introduce a novel fMRI paradigm to probe the neural sources of oscillations, based on the concept of perturbative signals, which overcomes the low temporal resolution of BOLD signals. The assumption is that a synchronized endogenous rhythm will modulate cortical excitability rhythmically, which should be reflected in the BOLD responses to brief stimuli presented at different phases of the oscillation cycle. We record rhythmic oscillations of V1 BOLD synchronized by a simple voluntary action, in phase with behaviourally measured oscillations in visual sensitivity in the theta range. The functional connectivity between V1 and M1 also oscillates at the same rhythm. By demonstrating oscillatory temporal coupling between primary motor and sensory cortices, our results strongly implicate communication through coherence to achieve precise coordination and to encode sensory-motor timing.

neuroscience↗

Autophagy-dependent gut-to-yolk biomass conversion generates visceral polymorbidity in aging C. elegans

Aging (senescence) is characterized by the development of numerous pathologies, some of which limit lifespan. Key to understanding aging is discovery of the mechanisms (etiologies) that cause senescent pathology. In Caenorhabditis elegans a major senescent pathology of unknown etiology is atrophy of its principal metabolic organ, the intestine. Here we identify a cause of not only this pathology, but also of yolky lipid accumulation and redistribution (a form of senescent obesity): autophagy-mediated conversion of intestinal biomass into yolk. Inhibiting intestinal autophagy or vitellogenesis rescues both visceral pathologies, and can also extend lifespan. This defines a disease syndrome leading to polymorbidity and contributing to late-life mortality. Activation of gut-to-yolk biomass conversion by insulin/IGF-1 signaling (IIS) promotes reproduction and senescence. This illustrates how major, IIS-promoted senescent pathologies in C. elegans can originate not from damage accumulation, but from continued action of a wild-type function (vitellogenesis), consistent with the recently proposed hyperfunction theory of aging.

physiology↗

Monsters in the uterus: A parthenogenetic quasi-program causes teratoma-like tumors during aging in wild-type C. elegans

Many diseases whose frequency increases with advancing age are caused by aging (senescence), but the mechanisms of senescence remain poorly understood. According to G.C. Williams and M.V. Blagosklonny, a major etiological determinant of senescence is late-life, wild-type gene action and non-adaptive execution of biological programs (or quasi-programs). These generate a wide range of senescent pathologies causing illness and death. Here we investigate the etiology of a prominent senescent pathology in the nematode C. elegans, uterine tumors, in the light of the Williams Blagosklonny theory. Uterine tumors develop from unfertilized, immature oocytes which execute incomplete embryogenetic programs. This includes extensive endomitosis, leading to formation of chromatin masses and cellular hypertrophy. The starting point of pathogenesis is exhaustion of sperm stocks. The timing of this transition between program and quasi-program can be altered by blocking sperm production (causing earlier tumors) or supplying additional sperm by mating (delaying tumor onset). Other pathophysiological determinants are yolk consumption by tumors, and bacterial proliferation within tumors. Uterine tumors resemble mammalian ovarian teratomas (tera, Greek: monster) in that both develop from oocytes that fail to mature after meiosis I, and both are the result of quasi-programs. Moreover, older but not younger uterine tumors show expression of markers of later embryogenesis, i.e. are teratoma-like. These results show how uterine tumors in C. elegans form as the result of run-on of embryogenetic quasi-programs. They also suggest fundamental etiological equivalence between teratoma and some forms of senescent pathology, insofar as both are caused by quasi-programs.

developmental biology↗