8 research outputs found

    Eye position modulates the electromyographic responses of neck muscles to electrical stimulation of the superior colliculus in the alert cat

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    Rapid gaze shifts are often accomplished with coordinated movements of the eyes and head, the relative amplitude of which depends on the starting position of the eyes. The size of gaze shifts is determined by the superior colliculus (SC) but additional processing in the lower brain stem is needed to determine the relative contributions of eye and head components. Models of eye-head coordination often assume that the strength of the command sent to the head controllers is modified by a signal indicative of the eye position. Evidence in favor of this hypothesis has been recently obtained in a study of phasic electromyographic (EMG) responses to stimulation of the SC in head-restrained monkeys (Corneil et al. in J Neurophysiol 88:2000-2018, 2002b). Bearing in mind that the patterns of eye-head coordination are not the same in all species and because the eye position sensitivity of phasic EMG responses has not been systematically investigated in cats, in the present study we used cats to address this issue. We stimulated electrically the intermediate and deep layers of the caudal SC in alert cats and recorded the EMG responses of neck muscles with horizontal and vertical pulling directions. Our data demonstrate that phasic, short latency EMG responses can be modulated by the eye position such that they increase as the eye occupies more and more eccentric positions in the pulling direction of the muscle tested. However, the influence of the eye position is rather modest, typically accounting for only 10-50% of the variance of EMG response amplitude. Responses evoked from several SC sites were not modulated by the eye position. \ua9 2006 Springer-Verlag

    Oculomotor areas of the primate frontal lobes: A transneuronal transfer of rabies virus and [14C]-2-deoxyglucose functional imaging study

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    We used the [14C]-2-deoxyglucose method to study the location and extent of primate frontal lobe areas activated for saccades and fixation and the retrograde transneuronal transfer of rabies virus to determine whether these regions are oligosynaptically connected with extraocular motoneurons. Fixation-related increases of local cerebral glucose utilization (LCGU) values were found around the fundus of the inferior limb of the arcuate sulcus (AS) just ventral to its genu, in the dorsomedial frontal cortex (DMFC), cingulate cortex, and orbitofrontal cortex. Significant increases of LCGU values were found in and around both banks of the AS, DMFC, and caudal principal, cingulate, and orbitofrontal cortices of monkeys executing visually guided saccades. All of these areas are oligosynaptically connected to extraocular motoneurons, as shown by the presence of retrogradely transneuronally labeled cells after injection of rabies virus in the lateral rectus muscle. Our data demonstrate that the arcuate oculomotor cortex occupies a region considerably larger than the classic, electrical stimulation-defined, frontal eye field. Besides a large part of the anterior bank of the AS, it includes the caudal prearcuate convexity and part of the premotor cortex in the posterior bank of the AS. They also demonstrate that the oculomotor DMFC occupies a small area straddling the ridge of the brain medial to the superior ramus of the AS. Our results support the notion that a network of several interconnected frontal lobe regions is activated during rapid, visually guided eye movements and that their output is conveyed in parallel to subcortical structures projecting to extraocular motoneurons

    The DAMNED Simulator for Implementing a Dynamic Model of the Network Controlling Saccadic Eye Movements

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    International audienceThe DAMNED simulator is a Distributed And Multithreaded Neural Event-Driven framework designed for implementing Spiking Neuron Networks (SNNs). This paper shows the power of DAMNED for simulating the temporal dynamics of a biologically inspired model of the system controlling saccadic eye movements. A fundamental neural structure for the saccade generation is the Superior Colliculus (SC). The proposed model relies on two pathways leaving this structure: A first one supervises the motor error and the movement initiation and a second one provides a direct drive to premotor centers. This simple model, its SNN implementation and its dynamic behaviour reproduce the evolution of movement amplitude as a function of activity location in the SC. It also accounts for classical results obtained when the SC is subjected to electrical stimulations

    Retaining the equilibrium point hypothesis as an abstract description of the neuromuscular system

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    The lambda version of the equilibrium point (EP) hypothesis for motor control is examined in light of recent criticisms of its various instantiations. Four important assumptions that have formed the basis for recent criticism are analyzed: First, the assumption that intact muscles possess invariant force-length characteristics (ICs). Second, that these ICs are of the same form in agonist-antagonist pairs. Third, that muscle control is monoparametric and that the control parameter, lambda, can be given a neurophysiological interpretation. Fourth, that reflex loop time delays and the known, asymmetric, nonlinear mechanical properties of muscles can be ignored. Mechanical and neurophysiological investigations of the neuromuscular system suggests that none of these assumptions is likely to be correct. This has been taken to mean that the EP hypothesis is oversimplified and a new approach is needed. It is argued that such an approach can be provided without rejecting the EP hypothesis, rather to regard it as an input-output description of muscle and associated segmental circuits. The operation of the segmental circuitry can be interpreted as having the function, at least in part, of compensating for a variety of nonlinearities and asymmetries such that the overall system implements the lambda-EP model equations

    Chemokines: A Potential Therapeutic Target to Suppress Autoimmune Arthritis

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