Motor Output In Response Research Articles

The Concept of Voluntary Motor Control in the Recent Neuroscientific Literature

The concept of voluntary motor control(VMC) frequently appears in the neuroscientific literature, specifically in the context of cortically-mediated, intentional motor actions. For cognitive scientists, this concept of VMC raises a number of interesting questions:(i) Are there dedicated, modular-like structures within the motor system associated with VMC? Or (ii) is it the case that VMC is distributed over multiple cortical as well as subcortical structures?(iii) Is there any one place within the so-calledhierarchy of motor control where voluntary movements could be said to originate? And (iv) in the current neurological literature how is the adjective voluntary in VMC being used? These questions are here considered in the context of how higher- and lower-levels of motor control, plan, initiate, coordinate, sequence, and modulate goal-directed motor outputs in response to changing internal and external inputs. Particularly relevant are the conceptual implications of current neurological modeling of VMC concerning causal agency.

Distributed processing on the basis of parallel and antagonistic pathways simulation of the femur-tibia control system in the stick insect.

In inactive stick insects, sensory information from the femoral chordotonal organ (fCO) about position and movement of the femur-tibia joint is transferred via local nonspiking interneurons onto extensor and flexor tibiae motoneurons. Information is processed by the interaction of antagonistic parallel pathways at two levels: (1) at the input side of the nonspiking interneurons and (2) at the input side of the motoneurons. We tested by a combination of physiological experiments and computer simulation whether the known network topology and the properties of its elements are sufficient to explain the generation of the motor output in response to passive joint movements, that is resistance reflexes. In reinvestigating the quantitative characteristics of interneuronal pathways we identified 10 distinct types of nonspiking interneurons. Synaptic inputs from fCO afferents onto these interneurons are direct excitatory and indirect inhibitory. These connections were investigated with respect to position and velocity signals from the fCO. The results were introduced in the network simulation. The motor output of the simulation has the same characteristics as the real system, even when particular types of interneurons were removed in the simulation and the real system.

Sensory-evoked pocket scratch motor patterns in the in vitro turtle spinal cord: reduction of excitability by an N-methyl-D-aspartate antagonist.

1. In intact turtles, tactile stimulation of the body surface in the "shell pocket" region surrounding the hindlimb elicits a pocket scratch reflex, in which the hindlimb reaches toward and rhythmically rubs the stimulated site. In the present study, we utilized reduced in vitro preparations of the turtle spinal cord with attached peripheral nerves to investigate the time course and pharmacology of sensory-evoked excitability in the pocket scratch neural network. Fictive pocket scratch motor output was elicited by electrically stimulating either the ventral-posterior pocket (VPP) cutaneous nerve or the distal D8 (d.D8) nerve. Both nerves contain afferents innervating part of the pocket scratch receptive field. 2. Six-segment (D7-S2) preparations of the spinal cord, which included the entire hindlimb enlargement, produced fictive pocket scratch motor output in response to VPP nerve stimulation (n = 6). We recorded fictive motor output as electroneurograms from up to five peripheral nerves in D7-S2 preparations, including three knee extensor muscle nerves (IT-KE, which innervates triceps femoris pars iliotibialis; AM-KE, which innervates pars ambiens; and FT-KE, which innervates pars femorotibialis), a hip flexor (protractor) muscle nerve (VP-HP, which innervates puboischiofemoralis internus, pars anteroventralis), and a mixed cutaneous-muscle nerve that exhibits hip-extensor-correlated motor output during the scratch (d.D8). The timing characteristics of activity in these nerves during in vitro motor patterns were similar to what has been observed during the in vivo pocket scratch. 3. Even a single segment of spinal cord from the anterior hindlimb enlargement (D8) contained sufficient neural circuitry to generate rhythmic motor patterns in AM-KE, VP-HP, and d.D8 nerves during repeated stimulation of VPP (n = 5) or d.D8 (n = 1). Stimulus trains delivered at 3-5 Hz for > or = 6 s elicited one or more VP-HP bursts with clear burst terminations; in some cases, these were followed by distinct hip-extensor-correlated d.D8 bursts. AM-KE timing was characteristic of a pocket scratch synergy, beginning during the VP-HP burst and continuing after VP-HP offset. Thus even isolated D8 segments were capable of expressing rhythmic alternation between hip-flexor- and hip-extensor-correlated motor bursts as well as a pocket-scratch-specific knee-hip synergy. 4. A single electrical pulse delivered to the VPP or d.D8 nerve increased the excitability of the pocket scratch network in D7-S2 and D8 preparations for > or = 5-10 s. We estimated the time course of increased excitability by observing the temporal summation of scratch motor output in response to single pulses applied to cutaneous afferents at multisecond intervals. Stimulus parameters were adjusted so that a single pulse delivered to a "rested" preparation (rested = no stimulation for > 2 min) was at or just below threshold for evoking motor output. Single pulses delivered at 5- to 10-s intervals evoked strongly summating scratch motor output in D7-S2 and D8 preparations. These results show that neural mechanisms that store sensory-evoked excitation in the pocket scratch circuit exist within the spinal hindlimb enlargement and even within the isolated D8 segment. 5. With the use of in vitro preparations, we have begun to examine the pharmacology of sensorimotor processing in the pocket scratch network. Application of the N-methyl-D-aspartate (NMDA) receptor antagonist D-2-amino-5-phosphonovaleric acid (APV) (50-100 microM) to the spinal cord greatly reduced pocket scratch excitability. APV lowered the motor burst frequency of pocket scratch responses in D7-S2 preparations elicited by 3-Hz stimulation; it also reduced the amplitude of summating motor output in D7-S2 and D8 preparations in response to single electrical stimuli delivered at 5-s intervals. These results indicate that NMDA receptors have a key role in synaptic processing and sustained excitation within the pocket scratch neura

Sleep-Induced Breathing Instability

We present a view of the neuromechanical regulation of breathing and causes of breathing instability during sleep. First, we would expect transient increases in upper airway resistance to be a major cause of transient hypopnea. This occurs in sleep because a hypotonic upper airway is more susceptible to narrowing and because the immediate excitatory increase in respiratory motor output in response to increased loads is absent in non-REM sleep. Secondly, sleep predisposes to an increased occurrence of ventilatory “overshoots”, in part because abruptly changing sleep states cause transient changes in upper airway resistance and in the gain of the respiratory controller. Following these ventilatory overshoots, breathing stability will be maintained if excitatory short-term potentiation is the prevailing influence. On the other hand, apnea and hypopnea will occur if inhibitory mechanisms dominate following the ventilatory overshoot. These inhibitory mechanisms include: a) hypocapnia—if transient, will inhibit carotid chemoreceptors and cause hypopnea, but if prolonged will inhibit medullary chemoreceptors and cause apnea; b) a persistent inhibitory effect from lung stretch; c) baroreceptor stimulation, from a transient rise in systemic blood pressure immediately following termination of apnea or hypopnea may partially suppress the accompanying hyperpnea; d) depression of central respiratory motor output via prolonged brain hypoxia. Once apneas are initiated, reinitiation of inspiration is delayed even though excitatory stimuli have risen well above their apneic thresholds, and these prolonged apneas are commonly accompanied by tonic EMG activation of expiratory muscles of the chest wall and upper airway.

Plasticity of non-giant flexion circuitry in chronically cut abdominal nerve cords of the crayfish, Procambarus clarkii.

We have investigated the pattern of neuronal activity involved in the gradual return of sensory-evoked abdominal flexions in crayfish with chronically transected nerve cords. Recordings were made from eight types of identified neurone that mediate phasic abdominal movements, in a preparation consisting of the isolated abdominal nerve cord and tailfan. Responses of the cells to pinches and dorsiflexions of the tailfan were compared in two groups of animals: animals whose cords had been cut at the thoracic-abdominal junction 4-17 weeks earlier (chronic preparations), and animals whose cords had been cut at the same site either just before the experiment or up to 6 days earlier (acute preparations). Sensory stimuli produced bursts of spikes in 73% of the fast flexor motoneurones impaled in chronic preparations, but never fired these neurones in acute preparations. However, fast flexor motoneurones in both preparations were fired with approximately equal frequency by single impulses in the giant axons, suggesting that the firing thresholds of these motoneurones had not changed. Sensory stimuli also caused spiking in the extensor inhibitor and the flexor inhibitor in chronic preparations; in contrast, responses in the fast extensor motoneurones were always subthreshold and occasionally hyperpolarizing. None of these cells was fired by similar stimuli in acute preparations. Neurones restricted to the giant axon pathways (lateral, medial, segmental and motor giants) were silent during sensory-evoked flexor discharges in chronically transected cords. Flexor discharges were accompanied by intense activity in non-giant axons recorded from the dorsal cord. Two identified, non-giant interneurones with axons in the dorsal cord were substantially depolarized but never fired by sensory input in chronic preparations. Sensory-evoked firing in the fast flexor motoneurones was not abolished by removal of the posterior stump of the nerve cord at the transection site. About 20% of chronic preparations generated cyclic motor output in response to unpatterned sensory stimulation. The pattern of motor activity that develops in chronically transected cords resembles that seen in normal crayfish during non-giant tailflips. Because cord transection permanently isolates the abdomen from rostral neural centres normally required for the generation of such tailflips, the return of co-ordinated motor output in chronically cut cords may result from the sensory activation of non-giant circuitry within the abdominal nervous system.

The functional neuroanatomy of infantile autism.

Infantile autism is a behavioral syndrome consisting of specific disturbances of social relating and communication, language, response to objects, sensory sensitivity and motility. The uniqueness of this syndrome suggests one underlying pathophysiologic mechanism, although multiple etiologies, which could activate or replicate such a mechanism, have been demonstrated. Review of considerable experimental evidence and clinical observation suggests that the symptomatology of autism, including the disturbances of social relating and communication, can best be explained as a disorder of sensory modulation. This in turn suggests a neurophysiologic mechanism consisting of dysfunction of a cascading series of neurophysiologic levels or interacting neuronal loops in the brainstem and diencephalon which subserve modulation of sensory input. Some of those same systems modulate motor output in response to sensory input, and their dysfunction may release the abnormal perseverative motility of infantile autism. Other experimental evidence and clinical observations stress the language deficits of autism and implicate dysfunction of cortical structures. Brainstem and diencephalic centers project rostrally to telencephalic structures and these, in turn, modify brainstem and diencephalic function. Theories of rostrally and caudally directed sequences of pathoneurophysiologic contributions to the system dysfunction in autism are compared. It is concluded that the symptoms of autism can best be explained in terms of dysfunction of brainstem and related diencephalic behavioral systems and their elaboration and refinement by selected higher neural structures.

Dynamic relations between natural vestibular inputs and activity of forelimb extensor muscles in the decerebrate cat. II. Motor output during rotations in the horizontal plane

Decerebrate cats with the spinal cord sectioned at low thoracic levels were submitted to rotations in the horizontal plane. The position of the animal with respect to the axis of rotation was such that horizontal canal afferents were activated either alone or in combination with macular afferents. The EMG activity from the triceps brachii muscles of both forelimbs was recorded. The main findings were as follows. (1) The motor output to each forelimb extensor is increased by an increase in the activity of the horizontal canal afferents from the contralateral labyrinth. The phase of the motor output with respect to that of the vestibular afferents shows a lag which increases with frequency, reaching about 85° at 1.0 Hz. (2) The macular and horizontal canal inputs are independently processed in the central nervous system and the motor output in response to both inputs applied simultaneously is a linear summation of the outputs expected for each of the inputs.

Dynamic relations between natural vestibular inputs and activity of forelimb extensor muscles in the decerebrate cat. III. Motor output during rotations in the vertical plane

Decerebrate cats with the spinal cord sectioned at low thoracic levels were subjected to sinusoidal rotations in the vertical plane, while recording the EMG activity of both triceps brachii muscles. The applied stimulus activated utricular and saccular receptors as well as the vertical semicircular canals. Using results presented in preceding papers 2, 3, namely the dynamic response characteristics of the motor output to macular inputs and the fact that the responses to otolith and canal stimulation summate linearly 3, it is deduced that the dynamic characteristics of the motor output in response to stimulation of the vertical canals are the same as those to horizontal canal stimulation. The implication of these findings vis-à-vis the problem of central processing of vestibular inputs and the problem of postural stability is discussed.

Control of ocular movement.

The ocular-motor system is organized to concentrate the images received by the eye upon the fovea, the most sensitive area of the retina. The acquisition and maintenance of object images upon the fovea, together with their stabilization during head movements, constitute the basic roles of human eye movement. These movements are simply motor outputs in response to sensory (primarily visual) inputs, but the precision of the system represents the most extraordinary example of sensory-motor integration carried out by the brain. This elegant system of fine movement, coupled with the accuracy with which eye position can be measured and the obvious (and potential) clinical correlation, accounts for the voluminous output of eye movement research in recent years. This deep interest is reflected in past (Bach-y-Rita, Collins and Hyde, I97I; Dichgans and Bizzi, I972), present, and future symposia (a symposium entitled Basic Mechianisms of Ocular Motility and Their Clinical Implications is planned in Stockholm in June, I974). The enormity of the subject boggles the mind of someone preparing a short talk. I will not attempt an all-encompassing basic review of the subject but will concentrate upon: (i) Single unit recordings from the brain, (2) Extraocular muscle proprioception, (3) Some of our own investigations.