Neuroscience

Current hypotheses on the mechanisms underlying the development and plasticity of the ocular dominance system through competitive interactions between pathways serving the two eyes strongly suggest the involvement of neurotrophins and their high affinity receptors. In the cat, infusion of the tyrosine kinase B ligand (trkB), neurotrophin-4/5 (NT-4/5), abolishes ocular dominance plasticity that follows monocular deprivation (Gillespie et al., 2000), while tyrosine kinase A and C ligands (trkA and trkC) do not have this effect. One interpretation of this finding is that NT-4/5 causes overgrowth and sprouting of thalamocortical and/or corticocortical terminals, leading to promiscuous neuronal connections which override the experience-dependent fine tuning of connections based on correlated activity. The present study tested whether neurons in cortical regions infused with NT-4/5 showed anatomical changes compatible with this hypothesis. Cats at the peak of the critical period received chronic infusion NT-4/5 into visual cortical areas 17/18 via an osmotic minipump. Visual cortical neurons were labeled in fixed slices using the DiOlistics methods (Gan et al., 2000) and analyzed in confocal microsco-py. Infusion of NT-4/5 induced a significant increase of spine-like processes on primary dendrites and a distinctive sprouting of protuberances from neuronal somata in all layers. The increase of neuronal membrane was paralleled by an increase in density of the presynaptic marker synaptophysin in infused areas, suggesting an increase in the numbers of synapses. A contingent of these newly formed synapses may feed into inhibitory circuits, as suggested by an increase of GAD-65 immunostaining in NT-4/5 affected areas. These anatomical changes are consistent with the physiological changes in such animals, suggesting that excess trkB neurotrophin can stimulate the formation of promiscuous connections during the critical period.

The central nervous system (CNS) is thought to use motor strategies that minimize several criteria, such as end-point variability or effort, to plan optimal motor patterns. In the case of vertical arm movements, a large body of literature demonstrated that the brain uses a motor strategy that takes advantage of the mechanical effects of gravity to minimize muscle effort. Results from other studies suggested that the relative importance of each criterion may vary according to the tasks constraints. For example, it could be hypothesized that reduced end-point variability driven by high accuracy demands is detrimental to effort minimization. The present study probes this specific hypothesis using the framework of gravity-related effort minimization. We asked twenty young healthy participants to perform vertical arm reaching movements towards targets whose size varied across conditions. We recorded the arm kinematics and electromyographic activities of the anterior deltoid to study two well-known motor signatures of the gravity-related optimization process; i.e., directional asymmetries on velocity profiles and negative epochs on phasic muscular activities. The results showed that both indices were reduced as target size decreased, demonstrating that the gravity-related optimization process was reduced under high accuracy constraints. This phenomenon is consistent with the use of a trade-off strategy between effort and end-point variability. More generally, it suggests that the CNS is able to appropriately modulate the relative importance of varied motor costs when facing varying task demands.

Corticostrial or cortico-basal ganglia circuitry plays an important role in integrating sensory and motor information, developing appropriate goal-directed behavior, promoting the maturation of GABAergic interneurons in the striatum, and regulating the nigrostriatal pathways. Dysfunction of this circuitry has been seen in some movement disorders. However, the dynamic changes of this circuitry in early life are not fully elucidated. Previous studies demonstrated that projections from motor cortices of caudal forelimb and jaw-lip-tongue areas to the striatum developed postnatally with terminal-like fibers evident at postnatal day 7. Here we report the development of the projections from the motor cortex governing whisker and neck movements to the striatum. Corticostriatal projections from this area were mainly ipsilateral and also underwent a progressive, postnatal development. The pyramidal tract and its collaterals to the dorsal striatum appeared on the day of birth (postanatal day 0 (P0)), peaked on P6 in density, and continued to be tuned until P36. The intertelencephalic projections in the dorsolateral striatum were established between P6 and P12 and continued to be refined between P20 and P36. Neurons in this motor cortex sent their axons to the contralateral motor cortex via the corpus callosum at the age between P6 and P12. Our results suggest that the time window between P6 and P12 is critical for the development of the projections from the motor cortex governing whisker and neck movement to the striatum in the rat. The overall process of the development of this circuitry appears to correspond to the functional development of whisker movement and locomotor activities.

The medial habenula (MHb)-interpeduncular nucleus (IPN) pathway plays an important role in information transferring between the forebrain and the midbrain. The MHb-IPN pathway has been implicated in the regulation of fear behavior and nicotine addiction. The synapses between the ventral MHb and the IPN show a unique property, i.e., an enhancement of synaptic transmission upon activation of GABAB receptors. This GABAB receptor-mediated potentiation of ventral MHb-IPN synaptic transmission has been implicated in regulating fear memory. Although IPN is known to contain parvalbumin (PV) and somatostatin (SST) GABAergic neurons and vesicular glutamate transporter 3 (VGLUT3)-expressing neurons, it is unknown how GABAB receptor activation affects ventral MHb-mediated glutamatergic transmission onto these three subtypes of IPN neurons. Our studies show robust glutamatergic connectivity from ventral MHb to PV and SST neurons in the IPN, while the ventral MHb-mediated glutamatergic transmission in IPN VGLUT3 neurons is weak. Although activation of GABAB receptors produces a robust potentiation of ventral MHb-mediated glutamatergic transmission in PV neurons, we observed a modest effect in IPN SST neurons. Despite the diminished basal synaptic transmission between ventral MHb and IPN VGLUT3 neurons, activation of GABAB receptors causes transient conversion of non-responding ventral MHb synapses into active synapses in some IPN VGLUT3 neurons. Thus, our results show strong ventral MHb connectivity to GABAergic IPN neurons compared to VGLUT3-expressing IPN neurons. Furthermore, GABAB receptor activation produces a differential effect on ventral MHb-mediated glutamatergic transmission onto PV, SST, and VGLUT3 neurons in the IPN.

Several sensorimotor control studies have provided evidence supporting that the central nervous system optimizes gravitys effects to minimize muscle effort. Recently, this hypothesis has been supported by the consistent observation of direction-specific negative epochs in the phasic electromyographic signal of antigravity muscles during vertical arm movements. This suggests that gravity torque is harvested to produce some of the arms motion. However, further investigation is needed to more finely understand how the CNS integrates gravity effects into muscle commands. Here, we aimed to analyze the phasic muscular activity across varying movement speeds during horizontal and vertical arm movements. We quantified the amount of negativity during acceleration and deceleration phases for all movement directions during fast, natural, and slow movements. We found that the negativity was more important during the acceleration phase of downward movements and during the deceleration phase of upward movements, resulting in diminished phasic activity compared to horizontal movements. Concomitantly, we found direction-specific effects of movement speed on phasic EMG activity of gravity muscles. This resulted in altered EMG to kinematics relationships in vertical movements compared to horizontal ones. These results support the Effort-minimization hypothesis and confirm that the negativity of phasic EMG is an important aspect of the motor command. Furthermore, the present results reveal that the CNS finely tunes this feature across a range of movement speeds and directions.

Caldendrin is a calmodulin-like Ca2+ binding protein that is expressed primarily in neurons and regulates multiple effectors including Cav1 L-type Ca2+ channels. Here, we tested the hypothesis that caldendrin regulates Cav1-dependent pathways that repress neurite growth in dorsal root ganglion neurons (DRGNs). By immunofluorescence, caldendrin was localized in medium- and large-diameter DRGNs. Consistent with an inhibitory effect of caldendrin on neurite growth, neurite initiation and growth was enhanced in dissociated DRGNs from caldendrin knockout (KO) mice compared to those from wild type (WT) mice. In an in vitro axotomy assay, caldendrin KO DRGNs grew longer neurites via a mechanism that was more sensitive to inhibitors of transcription as compared to WT DRGNs. Strong depolarization, which normally represses neurite growth through activation of Cav1 channels, had no effect on neurite growth in DRGN cultures from female caldendrin KO mice. Remarkably, DRGNs from caldendrin KO males were no different from those of WT males in terms of depolarization-dependent neurite growth repression. We conclude that caldendrin opposes neurite regeneration and growth, and this involves coupling of Cav1 channels to growth-inhibitory pathways in DRGNs of females but not males. Our findings suggest that caldendrin KO mice represent an ideal model in which to interrogate the transcriptional pathways controlling neurite regeneration and how these pathways may differ in males and females.

Reorganization of the sensorimotor cortex following amputation and other interventions has revealed large-scale plastic changes between the hand and face representations. To investigate whether hand-face interactions are also present in the normal state of the system we measured sensorimotor interactions between these two areas using an afferent inhibition transcranial magnetic stimulation (TMS) protocol in which the TMS motor evoked potential (MEP) is inhibited when it is preceded by an afferent stimulus. We hypothesized that if hand-face interactions exist in the normal state of the system then stimulation of the face would inhibit hand MEPs. In two separate experiments we delivered an electrocutaneous stimulus to either the right upper lip (Experiment 1) or right cheek (Experiment 2) and recorded muscular activity from the right first dorsal interosseous (FDI). Both lip and cheek stimulation inhibited FDI MEPs. To investigate the specificity of this effect we conducted two additional experiments in which cutaneous stimulation was applied to either the right forearm (Experiment 3) or right arm (Experiment 4). Neither forearm nor arm stimulation inhibited FDI MEPs. These data provide the first evidence for face-to-hand afferent inhibition and we suggest that the mechanisms underlying these sensorimotor interactions could contribute to face/hand interactions observed following sensorimotor reorganisation.

A long-lasting GABA-dependent increase in the excitability of afferent fibres, and thus modulation of the sensory input to the spinal cord, may be evoked by epidural polarization. However, the direct effects of fibre polarization are short-lasting and the sustained increase in their excitability appears to be secondary to the release of GABA from nearby astrocytes. We have now investigated whether the modulation of spinal sensory input by stimulation of a peripheral nerve, previously attributed to synaptically evoked intraspinal field potentials, is evoked in a similar way. However, as neither its dependence on GABA nor its relays have been investigated, we addressed the question of whether the increase in the excitability of epidurally stimulated afferent fibres following a peripheral nerve stimulation does or does not depend on GABA and whether it might be mediated by astrocytes. The effects of conditioning stimulation of the tibial nerve were evaluated from changes in the excitability of both group I and group II muscle afferents, estimated from action potentials recorded in peripheral nerves and in field potentials recorded in the dorsal horn respectively in acute experiments on deeply anaesthetized rats. The excitability of the afferents was increased by stimulation of group II and/or cutaneous but not group I muscle afferents. The effects were significantly weakened by blocking GABA channels by gabazine, and by astrocyte toxin L-alpha-aminoadipic acid (L-AAA), indicating that the excitability of both group I and group II afferent fibres may be modulated by GABAergic astrocytes, the new role played by astrocytes.

Exposure to nicotine in utero, often due to maternal smoking, significantly elevates the risk of auditory processing deficits in offspring. This study investigated the effects of chronic nicotine exposure during a critical developmental period on the functional expression of nicotinic acetylcholine receptors (nAChRs), glutamatergic synaptic transmission, and auditory processing in the mouse auditory brainstem. We evaluated the functionality of nAChRs at a central synapse and explored the impact of perinatal nicotine exposure (PNE) on synaptic currents and auditory brainstem responses (ABR) in mice. Our findings revealed developmentally regulated changes in nAChR expression in the medial nucleus of the trapezoid body (MNTB) neurons and presynaptic Calyx of Held terminals. PNE was associated with enhanced acetylcholine-evoked postsynaptic currents and compromised glutamatergic neurotransmission, highlighting the critical role of nAChR activity in the early stages of auditory synaptic development. Additionally, PNE resulted in elevated ABR thresholds and diminished peak amplitudes, suggesting significant impairment in central auditory processing without cochlear dysfunction. This study provides novel insights into the synaptic disturbances that contribute to auditory deficits resulting from chronic prenatal nicotine exposure, underlining potential targets for therapeutic intervention.

Mechanisms of specific memory deficits associated with Rett syndrome are poorly understood, at least in part because mutations of MECP2 have confounding effects on nervous system development and basal synaptic transmission. To mitigate such empirical uncertainties, this study exploited technical advantages of the Aplysia sensorimotor synapse to examine the potential role of MeCP2 in long-term synaptic plasticity. The results indicate MeCP2 may act as an inhibitory constraint on gene expression required for formation as well as maintenance of plasticity.

AO_SCPLOWBSTRACTC_SCPLOWThe laminins are a family of extracellular matrix proteins that regulate numerous cellular processes, including adhesion, neurite outgrowth, and axon guidance. However, it remains unclear whether laminin regulates axon guidance through local translation. Here, we show that laminin is necessary for local translation in axonal growth cones. Local translation is significantly increased in growth cones of embryonic day 17 mouse cortical neurons, either cultured on or acutely stimulated with soluble laminin 111, in the presence of BDNF. When cultured on laminin isoforms 211 or 221 in the presence of BDNF, there was a remarkable decrease in local translation in growth cones. Using a puromycin-proximity ligation assay to examine newly synthesized {beta}-actin specifically, we find a significant increase in growth cones of neurons cultured on laminin 111 in the presence of BDNF. However, soluble laminin 111 alone results in a significant reduction in nascent {beta}-actin protein synthesis. These results indicate that laminin isoforms can act in multiple ways, including synergistically with guidance cues and independently, to modulate local mRNA translation, thereby differentially influencing axon growth and guidance during development. SO_SCPLOWUMMARYC_SCPLOW SO_SCPLOWTATEMENTC_SCPLOWLocal translation in axons is critical for axon guidance. Laminin, a key component of the extracellular matrix, is necessary to induce local translation and thus mediate axon growth and guidance.

Sensorimotor integration is critical for generating skilled, volitional movements. While stroke tends to impact motor function, there are also often associated sensory deficits that contribute to overall behavioral deficits. Because many of the cortico-cortical projections participating in the generation of volitional movement either target or pass-through primary motor cortex (in rats, caudal forelimb area; CFA), any damage to CFA can lead to a subsequent disruption in information flow. As a result, the loss of sensory feedback is thought to contribute to motor dysfunction even when sensory areas are spared from injury. Previous research has suggested that the restoration of sensorimotor integration through reorganization or de novo neuronal connections is important for restoring function. Our goal was to determine if there was crosstalk between sensorimotor cortical areas with recovery from a primary motor cortex injury. First, we investigated if peripheral sensory stimulation would evoke responses in the rostral forelimb area (RFA), a rodent homologue to premotor cortex. We then sought to identify whether intracortical microstimulation-evoked activity in RFA would reciprocally modify the sensory response. We used seven rats with an ischemic lesion of CFA. Four weeks after injury, the rats forepaw was mechanically stimulated under anesthesia and neural activity was recorded in the cortex. In a subset of trials, a small intracortical stimulation pulse was delivered in RFA either individually or paired with peripheral sensory stimulation. Our results point to post-ischemic connectivity between premotor and sensory cortex that may be related to functional recovery. Premotor recruitment during the sensory response was seen with a peak in spiking within RFA after the peripheral solenoid stimulation despite the damage to CFA. Furthermore, stimulation evoked activity in RFA modulated and disrupted the sensory response in sensory cortex, providing additional evidence for the transmission of premotor activity to sensory cortex and the sensitivity of sensory cortex to premotor cortexs influence. The strength of the modulatory effect may be related to the extent of the injury and the subsequent reshaping of cortical connections in response to network disruption.

AbstractThe somatosensory cortex processes information hierarchically, transforming sensory input into appropriate responses. This hierarchy, in turn, provides a fundamental principle for the organization of anatomical and functional properties across the somatosensory cortex. While the local somatosensory hierarchy has been studied, a comprehensive model that fully illustrates somatosensory information transmission in fine detail remains lacking. In this study, we examine multimodal connectivity patterns of the entire macaque somatosensory cortex by integrating the information from receptor covariance (RC) and structural (SC) or functional connectivity (FC). Our findings not only reveal the hierarchical relationships but also propose a model of somatosensory processing streams. In this model, area 3bl serves as the initial cortical stage for somatosensory signals, projecting to areas 3al, 1, and 2. From there, somatosensory signals follow three major pathways: ventrally to the SII complex, medially to the medial SI and TSA, and posteriorly to somatosensory association areas in the parietal lobe. Further analysis shows that RC is not only closely linked to SC and FC but in addition displays unique characteristics that likely relate to the hierarchical processing across sensory modalities. This study deepens our understanding of brain connectivity patterns across different modalities and links the structural, chemoarchitectonic, and functional organization of the macaque somatosensory cortex.

Stimulus-driven responses in the cortex reduce due to prior exposure to sensory stimuli, a phenomenon called sensory adaptation. Depression of synaptic supplies and afterhyperpolarization (AHP) following each action potential are the main proposed mechanisms for adaptation. In vitro studies have shown that the neuronal adaptation in the barrel cortex depends on slow AHPs. Such AHPs can be affected by neuromodulators, such as noradrenaline. This evidence suggests that Locus Coeruleus (LC) noradrenergic system may reduce sensory adaptation through this cellular mechanism. We proposed that LC stimulation before whisker deflection can affect the degree of adaptation in the barrel cortex, depending on the nature of noradrenergic interactions in the barrel cortex. We coupled adapted or non-adapted whisker deflections with LC phasic stimulation with a 400 ms interval. A 50ms sinusoidal vibration was applied to the whisker immediately before the test deflection. Neuronal activity was recorded from the barrel cortex (BC) in a urethane anesthetized rat. We quantified the effect of LC stimulation on the degree of adaptation in BC; a lower adaptation index shows lower adaptation. Our result showed that LC stimulation significantly modulated adapted response in 30 % of units with insignificant modulation on the adaptor or non-adapted response. This modulation was in two directions; adaptation decreased in 5 % of units and increased in 25 % of units. In addition to LC modulation on adaptor response in the level of individual units, adaptor response was lower modulated in around 70 % of units, on average. This modulation was not correlated by LC modulation on non-adapted response. Although sensory adaptation in BC was attenuate by LC stimulation in the majority of units, there was a limited number of units that showed significant modulation.

Previous research on movement preparation identified a period of corticospinal suppression about 200 ms prior to movement initiation. This phenomenon has been observed for different types of motor tasks typically used to investigate movement preparation (e.g., reaction time, self-initiated, and anticipatory actions). However, we recently discovered that this phenomenon is not observed when actions must be initiated under time pressure. In the present study, we investigated urgency effects on corticospinal suppression throughout the time course of an anticipatory timing task. Participants were required to perform timing actions under two urgency scenarios, high and low, and we applied single-pulse transcranial magnetic stimulation at different times during the time course of preparation. We analysed the time course of excitability under high and low scenarios in relation to expected and actual movement onset times. Our results confirmed our earlier findings that corticospinal suppression is not observed when participants perform actions under high urgency scenarios. In addition, we found no evidence that this preparatory suppression could be shifted in time to occur later under high urgency scenarios. Moreover, we found evidence that responses prepared under high urgency are more likely to be disrupted by external events (e.g., TMS pulses). These results suggest that preparatory suppression might be a strategy employed by the central nervous system to shield motor actions from interference of external events (e.g., loud sounds) when time allows. Given these data, we propose conceptual models that could account for the absence of preparatory suppression under time pressure to act.

The mouse primary somatosensory cortex (S1) processes tactile sensory information and is the largest neocortex area emphasizing the importance of this sensory modality for rodent behavior. Most of our knowledge regarding information processing in S1 stems from studies of the whisker-related barrel cortex (S1-BC), yet the processing of tactile inputs from the hind-paws is poorly understood. We used in vivo whole-cell patch-clamp recordings from layer (L) 2/3 pyramidal neurons (PNs) of the S1 hind-paw (S1-HP) region of anaesthetized wild type (WT) mice to investigate their evoked sub- and supra-threshold activity, intrinsic properties, and spontaneous activity. Approximately 45% of these L2/3 PNs responded to brief contralateral HP stimulation in a subthreshold manner, ~5% fired action potentials, and ~50% of L2/3 PNs did not respond at all. The evoked subthreshold responses had long onset- (~23 ms) and peak-latencies (~61 ms). The majority (86%) of these L2/3 PNs responded to prolonged (stance-like) HP stimulation with both on- and off-responses. HP stimulation responsive L2/3 PNs had a greater intrinsic excitability compared to non-responsive ones, possibly reflecting differences in their physiological role. Similar to S1-BC, L2/3 PNs displayed up- and down-states, and low spontaneous firing rates (~0.1 Hz). Our findings support a sparse coding scheme of operation for S1-HP L2/3 PNs and highlight both differences and similarities with L2/3 PNs from other somatosensory cortex areas. KEY POINTSO_LIResponses of layer (L) 2/3 pyramidal neurons (PNs) of the primary somatosensory hind-paw cortex (S1-HP) to contralateral hind-paw stimulation reveal both differences and similarities compared to those of somatosensory neurons responding to other tactile (e.g. whiskers, forepaw, tongue) modalities. C_LIO_LISimilar to whisker-related barrel cortex (S1-BC) and forepaw cortex (S1-FP) S1-HP L2/3 PNs show a low spontaneous firing rate and a sparse action potential coding of evoked activity. C_LIO_LIIn contrast to S1-BC, brief hind-paw stimulus evoked responses display a long latency in S1-HP neurons consistent with their different functional role. C_LIO_LIThe great majority of L 2/3 PNs respond to prolonged hind-paw stimulation with both on- and off-responses. C_LIO_LIThese results help us to better understand sensory information processing within layer 2/3 of the neocortex and the regional differences related to various tactile modalities. C_LI

Capacitance of biological membranes is determined by the properties of the lipid portion of the membrane, as well as morphological features of a cell. In neurons, membrane capacitance is a determining factor of synaptic integration, action potential propagation speed and firing frequency due to its direct effect on the membrane time constant. Besides slow changes associated with increased morphological complexity during postnatal maturation, neuron membrane capacity is largely considered a stable, non-regulated constant magnitude. Here we report that in two excitatory neuronal cell types, pyramidal cells of mouse primary visual cortex and granule cells of the hippocampus, the membrane capacitance significantly changes between the start and the end of a daily light cycle. The changes are large, nearly two-fold in magnitude in pyramidal cells, but are not observed in cortical parvalbumin-expressing inhibitory interneurons. We discuss potential functional implications and plausible mechanisms.

Disruption of neural tracts descending from the brain to the spinal cord after brain trauma and stroke causes postural and sensorimotor deficits. We previously showed that unilateral lesion to the sensorimotor cortex in rats with completely transected thoracic spinal cord produced asymmetry in hindlimb posture and withdrawal reflexes. Supraspinal signals to hindlimb muscles may be transmitted through the paravertebral chain of sympathetic ganglia that remain intact after the transection. We here demonstrated that prior transection of the spinal cord at the cervical level that was rostrally to segments with preganglionic sympathetic neurons, did not abolish formation of asymmetry in hindlimb posture and musculo-articular resistance to stretch after unilateral brain injury. Thus not the sympathetic system but humoral signals may mediate the effects of brain injury on the lumbar spinal circuits. The asymmetric responses in rats with transected spinal cords were eliminated by bilateral lumbar dorsal rhizotomy after the left-side brain injury, but resistant to deafferentation after the right-side brain lesion. Two mechanisms, one dependent on and one independent of afferent input may account for asymmetric hindlimb motor responses. Resistance to deafferentation may be due to sustained stretch- and effort-unrelated muscle contractions that is often observed in patients with central lesions. Left-right asymmetry is unusual feature of these mechanisms that both are activated by humoral signals. Graphical Abstract O_FIG O_LINKSMALLFIG WIDTH=200 HEIGHT=120 SRC="FIGDIR/small/488460v1_ufig1.gif" ALT="Figure 1"> View larger version (26K): org.highwire.dtl.DTLVardef@14770e6org.highwire.dtl.DTLVardef@1452343org.highwire.dtl.DTLVardef@e1aedorg.highwire.dtl.DTLVardef@9c8ea_HPS_FORMAT_FIGEXP M_FIG C_FIG

Synchrony of oscillatory brain activity has been postulated to be a binding mechanism for cognitive and motor functions. Spectral analysis of human electrocorticogram (ECoG) in sensorimotor cortex has shown that power density of gamma band activity (30-60 Hz) increased and that of alpha-beta band activity (10-20 Hz) decreased during performance of manipulative visuomotor tasks, indicating that amplitude modulation of the gamma band activity occurred in relation to the task performance. Amplitude modulation may provide evidence for synchrony of local neuronal assembly. However, it does not implement the binding mechanisms for distributed networks that are necessary for cognitive and motor functions. To prove that oscillatory activity mediates a binding mechanism, phase modulation of oscillatory activity in a wide range area should be shown. We performed coherence analysis of the ECoG signals in sensorimotor cortex to study if synchrony of the gamma band activity between these areas occurs in relation to manipulative task performance. The ECoGs were recorded from 14 sites in sensorimotor cortex including hand-arm areas with subdural grid electrodes in four subjects. Coherence estimates in all pair-wise sites were calculated in different frequency bands with 10 Hz widths from 10 to 80 Hz. In all subjects, coherence estimates increased in the lower gamma band (20-50 Hz) during the performance of the manipulative tasks. But coherence in the alpha-beta band (10-20 Hz) also increased even though amplitude modulation did not occur in this frequency band. Coherence estimates increased in site pairs within and between sensory and motor areas, many separated by intervening sites. This interregional synchrony of the alpha-beta and the lower gamma activities may play a role in integration of sensorimotor information. Task-dependent increases in coherence estimates, i.e., greater increases during performance of the manipulative tasks than during the simple tasks, suggest another role of synchrony in attention mechanism. Time-series coherence analysis showed that phase modulation occurred in different timings for activities in the alpha-beta and the lower gamma bands. For the activity in higher gamma band (50-80 Hz), power density increased but coherence estimates decreased. Thus, only amplitude modulation occurred in this frequency band. Altogether these results suggest that oscillatory activities in different frequency bands may reflect different functional roles by modulating neural activity in different ways.

Rapid eye movement (REM) sleep consists of phasic and tonic microstates with unique neurophysiological properties, yet their fractal characteristics remain underexplored. Using Higuchis fractal dimension (HFD) analysis of electroencephalographic (EEG) data from healthy adults, this study investigated complexity differences between REM microstates. The results showed that both phasic and tonic REM exhibited significantly lower global HFD values compared to wakefulness, while displaying similar overall complexity levels between microstates. Importantly, phasic REM demonstrated regionally specific reductions in fractal dimensionality, with pronounced decreases observed in frontocentral areas. These localized reductions exhibited a negative association with theta band power, yet remained statistically unrelated to Lempel-Ziv complexity (LZC) measures, indicating that HFD and LZC capture distinct aspects of neural signal organization. The findings reveal that although phasic and tonic REM maintain comparable global complexity, they differ in their spatiotemporal fractal patterns. The association between increased theta power and reduced fractal dimensionality suggests that phasic REM represents a neurophysiological state favoring rhythmic regularity, potentially optimized for internal information processing. These results position HFD as a valuable complementary approach for characterizing REM microstates, with potential applications in elucidating the pathophysiology of sleep disorders.