All bodily movements stimulate peripheral receptors that activate neurons in the brain and spinal cord through afferent feedback. How these reafferent signals are processed within the CNS during ...movement is a key question in motor control. We investigated cutaneous sensory-evoked potentials in the spinal cord, primary somatosensory and motor cortex, and premotor cortex in monkeys performing an instructed delay task. Afferent inputs from cutaneous receptors were suppressed at several levels in a task-dependent manner. We found two types of suppression. First, suppression during active limb movement was observed in the spinal cord and all three cortical areas. This suppression was induced by both bottom-up and top-down gating mechanisms. Second, during preparation for upcoming movement, evoked responses were suppressed exclusively in the motor cortical areas and the magnitude of suppression was correlated with the reaction time of the subsequent movement. This suppression could be induced by a top-down gating mechanism to facilitate the preparation and execution of upcoming movement.
Oscillatory activity in motor cortex has been observed in many experimental contexts, leading to various hypotheses about its possible behavioral function. In this issue of Neuron, Engelhard et al. ...(2013) report that oscillations can be volitionally controlled, opening new directions to explore their function and underlying mechanisms.
Successful operation of brain–computer interfaces (BCI) and brain–machine interfaces (BMI) depends significantly on the degree to which neural activity can be volitionally controlled. This paper ...reviews evidence for such volitional control in a variety of neural signals, with particular emphasis on the activity of cortical neurons. Some evidence comes from conventional experiments that reveal volitional modulation in neural activity related to behaviours, including real and imagined movements, cognitive imagery and shifts of attention. More direct evidence comes from studies on operant conditioning of neural activity using biofeedback, and from BCI/BMI studies in which neural activity controls cursors or peripheral devices. Limits in the degree of accuracy of control in the latter studies can be attributed to several possible factors. Some of these factors, particularly limited practice time, can be addressed with long‐term implanted BCIs. Preliminary observations with implanted circuits implementing recurrent BCIs are summarized.
The functional significance of electrical rhythms in the mammalian brain remains uncertain. In the motor cortex, the 12-20 Hz beta rhythm is known to transiently decrease in amplitude during ...movement, and to be altered in many motor diseases. Here we show that the activity of neuronal populations is phase-coupled with the beta rhythm on rapid timescales, and describe how the strength of this relation changes with movement. To investigate the relationship of the beta rhythm to neuronal dynamics, we measured local cortical activity using arrays of subdural electrocorticographic (ECoG) electrodes in human patients performing simple movement tasks. In addition to rhythmic brain processes, ECoG potentials also reveal a spectrally broadband motif that reflects the aggregate neural population activity beneath each electrode. During movement, the amplitude of this broadband motif follows the dynamics of individual fingers, with somatotopically specific responses for different fingers at different sites on the pre-central gyrus. The 12-20 Hz beta rhythm, in contrast, is widespread as well as spatially coherent within sulcal boundaries and decreases in amplitude across the pre- and post-central gyri in a diffuse manner that is not finger-specific. We find that the amplitude of this broadband motif is entrained on the phase of the beta rhythm, as well as rhythms at other frequencies, in peri-central cortex during fixation. During finger movement, the beta phase-entrainment is diminished or eliminated. We suggest that the beta rhythm may be more than a resting rhythm, and that this entrainment may reflect a suppressive mechanism for actively gating motor function.
Celotno besedilo
Dostopno za:
DOBA, IZUM, KILJ, NUK, PILJ, PNG, SAZU, SIK, UILJ, UKNU, UL, UM, UPUK
It has been proposed that the efficacy of neuronal connections is strengthened when there is a persistent causal relationship between presynaptic and postsynaptic activity. Such activity-dependent ...plasticity may underlie the reorganization of cortical representations during learning, although direct in vivo evidence is lacking. Here we show that stable reorganization of motor output can be induced by an artificial connection between two sites in the motor cortex of freely behaving primates. An autonomously operating electronic implant used action potentials recorded on one electrode to trigger electrical stimuli delivered at another location. Over one or more days of continuous operation, the output evoked from the recording site shifted to resemble the output from the corresponding stimulation site, in a manner consistent with the potentiation of synaptic connections between the artificially synchronized populations of neurons. Changes persisted in some cases for more than one week, whereas the output from sites not incorporated in the connection was unaffected. This method for inducing functional reorganization in vivo by using physiologically derived stimulus trains may have practical application in neurorehabilitation after injury.
Celotno besedilo
Dostopno za:
DOBA, IJS, IZUM, KILJ, NUK, PILJ, PNG, SAZU, SIK, UILJ, UKNU, UL, UM, UPUK
The functional role of cortical beta oscillations, if any, remains unresolved. During oscillations, the periodic fluctuation in excitability of entrained cells modulates transmission of neural ...impulses and periodically enhances synaptic interactions. The extent to which oscillatory episodes affect activity-dependent synaptic plasticity remains to be determined. In nonhuman primates, we delivered single-pulse electrical cortical stimulation to a “stimulated” site in sensorimotor cortex triggered on a specific phase of ongoing beta (12–25 Hz) field potential oscillations recorded at a separate “triggering” site. Corticocortical connectivity from the stimulated to the triggering site as well as to other (non-triggering) sites was assessed by cortically evoked potentials elicited by test stimuli to the stimulated site, delivered outside of oscillatory episodes. In separate experiments, connectivity was assessed by intracellular recordings of evoked excitatory postsynaptic potentials. The conditioning paradigm produced transient (1–2 s long) changes in connectivity between the stimulated and the triggering site that outlasted the duration of the oscillatory episodes. The direction of the plasticity effect depended on the phase from which stimulation was triggered: potentiation in depolarizing phases, depression in hyperpolarizing phases. Plasticity effects were also seen at non-triggering sites that exhibited oscillations synchronized with those at the triggering site. These findings indicate that cortical beta oscillations provide a spatial and temporal substrate for short-term, activity-dependent synaptic plasticity in primate neocortex and may help explain the role of oscillations in attention, learning, and cortical reorganization.
•Stimulation triggered from cortical beta oscillations induces synaptic plasticity•Synaptic potentiation or depression depends on oscillatory stimulation phase•Plasticity effects last for up to a few seconds•Effects are explained by spike-timing-dependent plasticity mechanisms
Zanos et al. demonstrate that closed-loop, phase-locked cortical stimulation from beta oscillations in the sensorimotor cortex of monkeys induces short-term, bidirectional synaptic plasticity. This effect may explain the role of oscillations in attention, learning, and cortical reorganization.
Closed-loop brain-computer interfaces have bidirectional connections that allow activity-dependent stimulation of the brain, spinal cord, or muscles. Such bidirectional brain-computer interfaces ...(BBCI) have three major applications that can be used to restore lost motor function. First, the brain could learn to incorporate a long-term artificial recurrent connection into normal behavior, exploiting the brain's ability to adapt to consistent sensorimotor conditions. The obvious clinical application for restoring motor function is to use an artificial recurrent connection to bridge a lost biological connection. Second, activity-dependent stimulation can generate synaptic plasticity on the cellular level. The corresponding clinical application is to strengthen weakened neural connections, such as occur in stroke. A third application involves delivery of activity-dependent deep brain stimulation at subcortical reward sites, which can operantly reinforce the activity that generates the stimulation. The BBCI paradigm has numerous specific applications, depending on the source of the signals and the stimulated targets.
Motor learning and functional recovery from brain damage involve changes in the strength of synaptic connections between neurons. Relevant in vivo evidence on the underlying cellular mechanisms ...remains limited and indirect. We found that the strength of neural connections between motor cortex and spinal cord in monkeys can be modified with an autonomous recurrent neural interface that delivers electrical stimuli in the spinal cord triggered by action potentials of corticospinal cells during free behavior. The activity-dependent stimulation modified the strength of the terminal connections of single corticomotoneuronal cells, consistent with a bidirectional spike-timing-dependent plasticity rule previously derived from in vitro experiments. For some cells, the changes lasted for days after the end of conditioning, but most effects eventually reverted to preconditioning levels. These results provide direct evidence of corticospinal synaptic plasticity in vivo at the level of single neurons induced by normal firing patterns during free behavior.
•Activity-dependent stimuli in spinal cord induced STDP in corticospinal terminals•Bidirectional STDP was documented at the single neuron level•A head-fixed recurrent neural interface produced STDP during free behavior
Nishimura et al. show that the strength of primate corticospinal connections can be modified by delivering intraspinal stimuli triggered from action potentials of corticospinal neurons recorded during free behavior. The synapses are strengthened or weakened, depending on the time between action potentials and stimuli.
Imagery of motor movement plays an important role in learning of complex motor skills, from learning to serve in tennis to perfecting a pirouette in ballet. What and where are the neural substrates ...that underlie motor imagery-based learning? We measured electrocorticographic cortical surface potentials in eight human subjects during overt action and kinesthetic imagery of the same movement, focusing on power in "high frequency" (76-100 Hz) and "low frequency" (8-32 Hz) ranges. We quantitatively establish that the spatial distribution of local neuronal population activity during motor imagery mimics the spatial distribution of activity during actual motor movement. By comparing responses to electrocortical stimulation with imagery-induced cortical surface activity, we demonstrate the role of primary motor areas in movement imagery. The magnitude of imagery-induced cortical activity change was ~25% of that associated with actual movement. However, when subjects learned to use this imagery to control a computer cursor in a simple feedback task, the imagery-induced activity change was significantly augmented, even exceeding that of overt movement.
PDF
