TL;DR: In this article, an anatomically and physiologically based neuro-musculo-skeletal model was developed to emulate the actual neuro-control mechanism of human bipedal locomotion, which consists of an alpha motoneuron and proprioceptors such as a muscle spindle and a Golgi tendon organ for each muscle.
Abstract: To emulate the actual neuro-control mechanism of human bipedal locomotion, an anatomically and physiologically based neuro-musculo-skeletal model is developed. The human musculo-skeletal system is constructed as seven rigid links in a sagittal plane, with a total of nine principal muscles. The nervous system consists of an alpha motoneuron and proprioceptors such as a muscle spindle and a Golgi tendon organ for each muscle. At the motoneurons, feedback signals from the proprioceptors are integrated with the signal induced by foot-ground contact and input from the rhythm pattern generator; a muscle activation signal is produced accordingly. Weights of connection in the neural network are optimized using a genetic algorithm, thus maximizing walking distance and minimizing energy consumption. The generated walking pattern is in remarkably good agreement with that of actual human walking, indicating that the locomotory pattern could be generated automatically, according to the musculoskeletal structures and the connections of the peripheral nervous system, particularly due to the reciprocal innervation in the muscle spindles. Using the proposed model, the flow of sensory-motor information during locomotion is estimated and a possible neuro-control mechanism is discussed.
TL;DR: Pairs of head-rotating muscles, splenius and sternocleidomastoideus muscles, demonstrate reciprocal innervation, particularly for time optimal head rotations, and support the idea of higher level programmed control of head rotation in human subjects.
TL;DR: This study suggests that a muscle which develops a maximum active force of less than 45 gm would be suspect as paretic, and variations from the normal pattern of reciprocal innervation, reflected in the gradedactive force of individual muscle contraction, may help in understanding some types of oculomotor pathology.
Abstract: Actively developed horizontal muscle forces and tissue stiffnesses were measured in 29 normal orthophoric volunteer subjects (18 to 33 years old) by means of noninvasive length-tension forceps. Mean active fixation force developed at 50 deg extreme gaze was 26% greater for the medial rectus (74.8 gm) than for the lateral rectus (59.1 gm). The variation of maximum active force among individuals was 2:1 (48 to 103 gm). These muscles developed up to 25% of their maximum active force out of their field of action. Active (counter) hysteresis force differences of over 10 gm were measured between nasal and temporal gaze directions. This study suggests that a muscle which develops a maximum active force of less than 45 gm ivould be suspect as paretic. Variations from the normal pattern of reciprocal innervation, reflected in the graded, active force of individual muscle contraction, may help in understanding some types of oculomotor pathology. The mean tissue stiffness -restraining movement of the globe in the nasal direction (1.05 gm/deg) is 11 % greater than in the temporal direction (0.94 gm/deg). This is consistent with a stronger medial rectus balanced by a greater load. Variation of stiffness of 2:1 was observed among individuals; 0.8 to 1.7 gm/deg pulling nasally and 0.77 to 1.2 gm/deg temporally. Passive hysteresis and viscous force differences of over 10 gm were observed between the passive forced pull and normal spring-return of the eye. Large stiffnesses may be normal if balanced by large active forces. Abrupt changes of the length-tension curve indicate the magnitude and location of restrictions.
TL;DR: A difference does indeed exist between the reactions of the preparation in the decapitated and in the decerebrate condition; and it can be shown that the inhibitory afferent is then really producing a state of inhibition in the preparation, although that state is not made evident by any further relaxation.
Abstract: I. Reflex excitation and inhibition when brought to play simultaneously on the motoneurones of an extensor muscle can be so balanced that there results in the muscle a contraction , the degree of which evidences algebraic summation is obtainable not only in the decerebrate animal but also in the purely spinal, for instance, after decapitaion. This circumstance much facilitates the physiological study of the phenomenon. In other words, the grading (fig.1) of reflex contraction of the extensor by varying intensity of inhibition acting along with reflex excitation can be studied in the animal freshly made spinal as well as in the animal in the decerebrate condition. The muscle which I have chiefly employed in the purely spinal preparation is the isolated extensor of the knee in the decapitated cat. A difference does indeed exist between the reactions of the preparation in the decapitated and in the decerebrate condition. In the decapitated preparation, as in the decerebrate, the reflex effect of any inhibitory afferent is easily seen if stimulation of that afferent is employed concurrently with stimulation of an excitatory afferent. If however the inhibitory afferent is stimulated during the ordinary resting condition of the preparation, there is usually no change in the muscle to show that the inhibitory afferent is producing any effect at all (fig. 2). This is because the extensor muscle in the decapitated preparation is not exhibiting tonus and lies relaxed, therefore affording no background of contraction against which an inhibitory reflex can reveal itself by causing relaxation. Even in this condition it can, however, easily be shown that the inhibitory afferent is then really producing a state of inhibition in the preparation, although that state is not made evident by any further relaxation. If a stimulus sufficient to cause reflex contraction of the muscle be applied to the excitatory afferent while the inhibitory afferent, although apparently without effect, is being stimulated, the excitatory afferent is found to be ineffective (or only partially effective) then; but it, immediately becomes effective (or more effective) on withdrawal of the concurrent inhibitory stimulation (fig. 2).
TL;DR: During the peristaltic reflex, the LM and CM layers receive synchronous inhibitory neuromuscular inputs during descending inhibition and synchronous excitatory neuron inputs during ascending excitation.
Abstract: 1. Simultaneous intracellular recordings were made from longitudinal muscle (LM) and circular muscle (CM) cells of guinea-pig distal colon during the peristaltic reflex. 2. Spontaneous rhythmical depolarizations with superimposed action potentials (mean amplitude: 19 ± 2 mV) were regularly recorded from the LM (mean interval: 7 ± 1 s). In contrast, in the CM layer, spontaneous action potentials occurred with an irregular frequency. Although spontaneous action potentials in LM were rarely correlated in time with those in CM, spontaneous inhibitory junction potentials (sIJPs) were found to occur synchronously in both muscles (5 out of 27 animals; 19 %). 3. Graded inflation of an intra-luminal balloon or mucosal stimulation oral to the recording electrodes elicited gradeable compound IJPs synchronously in both LM (mean amplitude: 6 ± 1 mV) and CM (mean amplitude: 9 ± 1 mV) (descending inhibitory reflex). Evoked IJPs were often followed by action potentials in both muscle layers. 4. Mucosal stimuli applied anal to the recording electrodes elicited compound excitatory junction potentials (EJPs) synchronously in both muscles layers that were often associated with the generation of action potentials. In the LM, evoked EJP amplitudes ranged from 3 mV (subthreshold) to 31 mV (including the action potential) and in the CM from 4 mV (subthreshold) to 44 mV (including the action potential). 5. Apamin (500 n M) reduced the evoked IJP in the CM by 55 % (from 11 ± 2 to 5 ± 1 mV), but caused no significant reduction in the LM layer (from 8 ± 1 to 6 ± 1 mV). Apamin-resistant IJPs in both muscle layers were likely to be due to nitric oxide, since they were abolished by L-NA (100 µM). 6. Atropine (1 µM) abolished the ascending excitatory reflex in both muscles. 7. Injection of neurobiotin into the LM and CM confirmed that simultaneous intracellular recordings were made from different muscle layers. 8. In conclusion, during the peristaltic reflex, the LM and CM layers receive synchronous inhibitory neuromuscular inputs during descending inhibition and synchronous excitatory neuromuscular inputs during ascending excitation. No evidence was found to support reciprocal innervation.