196,197 research outputs found

    Cortical rhythms induced by TMS stimulation: analysis with a neural mass model

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    Knowledge of cortical rhythms represents an important aspect of modern neuroscience, to understand how the brain realizes its functions. Recent data suggest that different regions in the brain may exhibit distinct rhythms when perturbed by Transcranial Magnetic Stimulation (TMS) (Rosanova et al., 2009) and that these rhythms can change due to the connectivity among regions. In this context, neural mass models can be very useful to simulate specific aspects of electrical brain activity and, above all, to analyze and identify the overall frequency content of EEG in a cortical region of interest (ROI). In this work we implemented a model of connectivity among cortical regions (Ursino, Cona and Zavaglia, 2010) to fit the impulse responses in three ROIs during an experiment of TMS stimulation. In particular we investigated Brodmann Area (BA) 19 (occipital lobe), BA 7 (parietal lobe) and BA 6 (frontal lobe). Results show that the model can reproduce the natural rhythms of the three regions quite well, acting on a few internal parameters. Moreover, model can explain most rhythm changes induced by stimulation of another region, by using just a few long-range connectivity parameters among ROIs.

    Yolk Proteins in Vertebrate: A Review

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    In all the oviparous vertebrates, also showing different reproductive modes, that is, oviparity, ovoviviparity, and viviparity, the oocytes always contain yolk proteins that represent the nourishment store for the developing embryo. Yolk proteins derive from the cleavage of a large maternal serum lipoglycophosphoprotein called vitellogenin (VTG) produced by the liver under estrogen stimulation (Wallace, 1985 and references therein; Rosanova et al., 2002). The mammalian (eutherian) liver lost the ability tomakeVTGbut the genetic bases of this acquired inability are still unknown (Rothchild, 2003). Once synthesized by the liver, VTG reaches the ovarian follicles through the bloodstream, crosses between the granulosa cells and is incorporated into the oocytes by micropinocytosis, a mechanism of receptor-mediated endocytosis (Opresko and Wiley, 1987; Schneider, 1996; Romano and Limatola, 2000). VTG internalization occurs in coated pits of the oocyte plasma membrane; they rapidly detach and give rise to coated vesicles in the cortical oocyte cytoplasm; the latter rapidly lose their clathrin coat and coalesce to form the primordial yolk globules subsequently transformed into yolk platelets (Ghiara et al., 1968, 1970; Neaves, 1972; Wallace, 1985; Limatola and Filosa, 1989). Similar ultrastructural features were described also in the mosquito oocytes (Roth and Porter, 1964). In the platelets, VTG are enzymatically cleaved in lipovitellins and phosvitins that represent the two principal classes of yolk proteins. Lipovitellins are high molecular-weight proteins with a strongly hydrophobic nature; phosvitins show a lower molecular weight and are highly phosphorylated. The cleavage of VTG in yolk proteins is generally indicated as primary degradation; furthermore, in almost all vertebrates studied, a secondary degradation of yolk proteins occurs at oocyte maturation or later during embryo development. This review represents an attempt to summarize the numerous data of the literature about the VTG derived yolk proteins during the oogenesis and their utilization during the embryogenesis

    Yolk Proteins in Vertebrate: A Review

    No full text
    In all the oviparous vertebrates, also showing different reproductive modes, that is, oviparity, ovoviviparity, and viviparity, the oocytes always contain yolk proteins that represent the nourishment store for the developing embryo. Yolk proteins derive from the cleavage of a large maternal serum lipoglycophosphoprotein called vitellogenin (VTG) produced by the liver under estrogen stimulation (Wallace, 1985 and references therein; Rosanova et al., 2002). The mammalian (eutherian) liver lost the ability tomakeVTGbut the genetic bases of this acquired inability are still unknown (Rothchild, 2003). Once synthesized by the liver, VTG reaches the ovarian follicles through the bloodstream, crosses between the granulosa cells and is incorporated into the oocytes by micropinocytosis, a mechanism of receptor-mediated endocytosis (Opresko and Wiley, 1987; Schneider, 1996; Romano and Limatola, 2000). VTG internalization occurs in coated pits of the oocyte plasma membrane; they rapidly detach and give rise to coated vesicles in the cortical oocyte cytoplasm; the latter rapidly lose their clathrin coat and coalesce to form the primordial yolk globules subsequently transformed into yolk platelets (Ghiara et al., 1968, 1970; Neaves, 1972; Wallace, 1985; Limatola and Filosa, 1989). Similar ultrastructural features were described also in the mosquito oocytes (Roth and Porter, 1964). In the platelets, VTG are enzymatically cleaved in lipovitellins and phosvitins that represent the two principal classes of yolk proteins. Lipovitellins are high molecular-weight proteins with a strongly hydrophobic nature; phosvitins show a lower molecular weight and are highly phosphorylated. The cleavage of VTG in yolk proteins is generally indicated as primary degradation; furthermore, in almost all vertebrates studied, a secondary degradation of yolk proteins occurs at oocyte maturation or later during embryo development. This review represents an attempt to summarize the numerous data of the literature about the VTG derived yolk proteins during the oogenesis and their utilization during the embryogenesis

    Pattern-specific associative long-term potentiation induced by a sleep spindle-related spike train

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    Spindles are non-rapid eye movement (non-REM) sleep EEG rhythms (7-14 Hz) that occur independently or in association with slow oscillations (0.6-0.8 Hz). Despite their proposed function in learning and memory, their role in synaptic plasticity is essentially unknown. We studied the ability of a neuronal firing pattern underlying spindles in vivo to induce synaptic plasticity in neocortical pyramidal cells in vitro. A spindle stimulation pattern (SSP) was extracted from a slow oscillation upstate that was recorded in a cat anesthetized with ketamine-xylazine, which is known to induce a sleep-like state. To mimic the recurrence of spindles grouped by the slow oscillation, the SSP was repeated every 1.5 s (0.6 Hz). Whole-cell patch-clamp recordings were obtained from layer V pyramidal cells of rat somatosensory cortex with infrared videomicroscopy, and composite EPSPs were evoked within layers II-III. Trains of EPSPs and action potentials simultaneously triggered by the SSP induced an NMDA receptor-dependent short-term potentiation (STP) and an L-type Ca2+ channel-dependent long-term potentiation (LTP). The number of spindle sequences affected the amount of STP-LTP. In contrast, spindle trains of EPSPs alone led to long-term depression. LTP was not consistently induced by a regular firing pattern, a mirrored SSP, or a randomized SSP; however, a synthetic spindle pattern consisting of repetitive spike bursts at 10 Hz reliably induced STP-LTP. Our results show that spindle-associated spike discharges are efficient in modifying excitatory neocortical synapses according to a Hebbian rule. This is in support of a role for sleep spindles in memory consolidation. Copyrigh

    Neuronal mechanisms mediating the variability of somatosensory evoked potentials during sleep oscillations in cats

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    The slow oscillation (SO) generated within the corticothalamic system is composed of active and silent states. The studies of response variability during active versus silent network states within thalamocortical system of human and animals provided inconsistent results. To investigate this inconsistency, we used electrophysiological recordings from the main structures of the somatosensory system in anaesthetized cats. Stimulation of the median nerve (MN) elicited cortical responses during all phases of SO. Cortical responses to stimulation of the medial lemniscus (ML) were virtually absent during silent periods. At the ventral-posterior lateral (VPL) level, ML stimuli elicited either EPSPs in isolation or EPSPs crowned by spikes, as a function of membrane potential. Response to MN stimuli elicited compound synaptic responses and spiked at any physiological level of membrane potential. The responses of dorsal column nuclei neurones to MN stimuli were of similar latency, but the latencies of antidromic responses to ML stimuli were variable. Thus, the variable conductance velocity of ascending prethalamic axons was the most likely cause of the barrages of synaptic events in VPL neurones mediating their firing at different level of the membrane potential. We conclude that the preserved ability of the somatosensory system to transmit the peripheral stimuli to the cerebral cortex during all the phases of sleep slow oscillation is based on the functional properties of the medial lemniscus and on the intrinsic properties of the thalamocortical cells. However the reduced firing ability of the cortical neurones during the silent state may contribute to impair sensory processing during sleep

    EEG slow (approximately 1 Hz) waves are associated with nonstationarity of thalamo-cortical sensory processing in the sleeping human

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    Intracellular studies reveal that, during slow wave sleep (SWS), the entire cortical network can swing rhythmically between extremely different microstates, ranging from wakefulness-like network activation to functional disconnection in the space of a few hundred milliseconds. This alternation of states also involves the thalamic neurons and is reflected in the EEG by a slow (<1 Hz) oscillation. These rhythmic changes, occurring in the thalamo-cortical circuits during SWS, may have relevant, phasic effects on the transmission and processing of sensory information. However, brain reactivity to sensory stimuli, during SWS, has traditionally been studied by means of sequential averaging, a procedure that necessarily masks any short-term fluctuation of responsiveness. The aim of this study was to provide a dynamic evaluation of brain reactivity to sensory stimuli in naturally sleeping humans. To this aim, single-trial somatosensory evoked potentials (SEPs) were grouped and averaged as a function of the phase of the ongoing sleep slow (<1 Hz) oscillation. This procedure revealed a dynamic profile of responsiveness, which was conditioned by the phase of the spontaneous sleep EEG. Overall, the amplitude of the evoked potential changed sistematically, increasing and approaching wakefulness levels along the negative slope of the EEG oscillation and decaying below SWS average levels along the positive drift. These marked and fast changes of stimulus-correlated electrical activity involved both short (N20) and long latency (P60 and P100) components of SEPs. In addition, the observed short-term response variability appeared to be centrally generated and specifically related to the evolution of the spontaneous oscillatory pattern. The present findings demonstrate that thalamo-cortical processing of sensory information is not stationary in the very short period (approximately 500 ms) during natural SWS

    A neural mass model of interconnected regions simulates rhythm propagation observed via TMS-EEG

    No full text
    Knowledge of cortical rhythms represents an important aspect of modern neuroscience, to understand how the brain realizes its functions. Recent data suggest that different regions in the brain may exhibit distinct electroencephalogram (EEG) rhythms when perturbed by Transcranial Magnetic Stimulation (TMS) and that these rhythms can change due to the connectivity among regions. In this context, in silico simulations may help the validation of these hypotheses that would be difficult to be verified in vivo. Neural mass models can be very useful to simulate specific aspects of electrical brain activity and, above all, to analyze and identify the overall frequency content of EEG in a cortical region of interest (ROI). In this work we implemented a model of connectivity among cortical regions to fit the impulse responses in three ROIs recorded during a series of TMS/EEG experiments performed in five subjects and using three different impulse intensities. In particular we investigated Brodmann Area (BA) 19 (occipital lobe), BA 7 (parietal lobe) and BA 6 (frontal lobe). Results show that the model can reproduce the natural rhythms of the three regions quite well, acting on a few internal parameters. Moreover, the model can explain most rhythm changes induced by stimulation of another region, and inter-subject variability, by estimating just a few long-range connectivity parameters among ROIs

    General indices to characterize the electrical response of the cerebral cortex to TMS

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    Transcranial magnetic stimulation (TMS) combined with simultaneous high-density electroencephalography (hd-EEG) represents a straightforward way to gauge cortical excitability and connectivity in humans. However, the analysis, classification and interpretation of TMS-evoked potentials are hampered by scarce a priori knowledge about the physiological effect of TMS and by lack of an established data analysis framework. Here, we implemented a standardized, data-driven procedure to characterize the electrical response of the cerebral cortex to TMS by means of three synthetic indices: significant current density (SCD), phase-locking (PL) and significant current scattering (SCS). SCD sums up the amplitude of all significant currents induced by TMS, PL reflects the ability of TMS to reset the phase of ongoing cortical oscillations, while SCS measures the average distance of significantly activated sources from the site of stimulation. These indices are aimed at capturing different aspects of brain responsiveness, ranging from global cortical excitability towards global cortical connectivity. We analyzed the EEG responses to TMS of Brodmann's area 19 at increasing intensities in five healthy subjects. The spatial distribution and time course of SCD, PL and SCS revealed a reproducible profile of excitability and connectivity, characterized by a local activation threshold around a TMS-induced electric field of 50 V/m and by a selective propagation of TMS-evoked activation from occipital to ipsilateral frontal areas that reached a maximum at 70-100 ms. These general indices may be used to characterize the effects of TMS on any cortical area and to quantitatively evaluate cortical excitability and connectivity in physiological and pathological conditions
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