Journal of Physiology

1. We used anatomical methods to examine whether the geniculocortical afferent input to dendritic spines could be gated or ‘vetoed’ by an inhibitory input to the same spine. 2. Physiologically identified X‐ and Y‐type afferents were injected intra‐axonally with horseradish peroxidase (HRP), processed, and drawn under the light microscope. Selected regions of the terminal arbors were then serially sectioned for examination under the electron microscope. 3. Three‐dimensional reconstructions of thirty‐nine HRP‐filled terminal boutons forming fifty asymmetric (type 1) synapses showed that thirty‐one synapses were on the heads of dendritic spines. Only two of thirty‐one spine heads received an additional symmetric (type 2) synapse, which is presumed to be inhibitory. 4. Examination of twenty‐three boutons from two clutch cells (a GABA (gamma‐aminobutyric acid)‐ergic smooth cell) that form symmetric (type 2) synapses on spines indicated that their preferred location was opposite the asymmetric synapse on the head of the spine. Synaptic input to the necks of spines appears rare. 5. We conclude that most of the excitation provided by the geniculocortical afferent input to the heads of spines cannot be gated or vetoed by inhibition at the level of the spine.

1. The developmental process of the monosynaptic reflex pathway was investigated morphologically and electrophysiologically in isolated lumbar spinal cords of new‐born and fetal rats. 2. Dorsal root fibres were stained with horseradish peroxidase in the fourth lumbar (L4) segment at different ages ranging from embryonic day (E) 15.5 to post‐natal day (P) 0. At E15.5, several collaterals issued from axons in the dorsal funiculus and reached the dorsal part of the dorsal horn. At E16.5, the number of collaterals entering the grey matter increased. Also, a group of collaterals extended ventralwards forming a bundle, and reached the intermediate region. At E17.5, a small number of collaterals reached the motor nuclei. The number of collaterals entering the motor nuclei increased almost linearly with age: 0 at E15.5 and at E16.5, 27 at E17.5, 184 at E18.5, 432 at E19.5 and 746 at P0. 3. The tips of collaterals and their branches had growth cones, boutons (round or oval varicosities) or other varicosities. The mean number of branches with these structures per collateral in the motor nuclei was 1.2 at E17.5, 2.5 at E18.5, 3.6 at E19.5 and 5.8 at E20.5. 4. The percentage of collaterals having growth cones in the motor nuclei was 75% at E17.5, 70% at E18.5, 38% at E19.5 and 15% at E20.5. 5. The mean number of boutons per collateral in the motor nuclei was 0.6 at E17.5, 3.2 at E18.5, 4.9 at E19.5 and 10.7 at E20.5. This increase with age was caused by both branching of collaterals and the increase in the number of boutons of the en passant type. The estimated total number of boutons in the motor nuclei of the L4 segment steeply increased after E17.5: 16 at E17.5, ca. 600 at E18.5, ca. 2000 at E19.5 and ca. 8000 at E20.5‐P0. 6. Stimulation of the L4 dorsal root evoked a reflex response in the L4 ventral root, recorded as the ventral root potential, in two out of nine preparations at E15.5 and in all preparations at and after E16.5. The onset of the ventral root potential indicated the onset of excitatory post‐synaptic potentials in motoneurones. The segmental latency of the ventral root potentials was markedly shortened between E17.5 and E18.5 (from 12.5 to 7.2 ms) and essentially unchanged at the later stages. 7. The magnitude of monosynaptic reflex responses in the L4 segment gradually increased with age during prenatal stages, becoming maximal at P2‐3 and then decreased at the following stages (P4‐P8).(ABSTRACT TRUNCATED AT 400 WORDS)

Changing the posture of the human fingers can functionally ‘disengage’ the deep finger flexor muscle from its normal action on the terminal phalanx of the fourth (or third) finger. This enables the activity of the muscle to be studied both with and without its normal proprioceptive inputs.

1. The earliest components of the developing innervation of the rabbit intestine to be detected in this study were the cholinergic excitatory and the intrinsic inhibitory innervation. These developed simultaneously in the rabbit at 17 days of gestation. Both were also present in the mouse by the 16th day of gestation. Responsiveness of rabbit tissue to exogenous acetylcholine appeared together with the advent of a functional cholinergic innervation. Since excitatory responses were potentiated by eserine, the tissue was probably able to inactivate acetylcholine through hydrolysis mediated by cholinesterase. Early relaxant responses resisted blockade by adrenergic neurone blocking agents and by antagonists active at α‐ and β‐adrenoceptors.

2. The development of the adrenergic innervation lagged far behind that of the other two components. Specific uptake of noradrenaline in the rabbit was detected for the first time at the 21st day of gestation and stores of noradrenaline could not be detected histochemically until 26‐28 days. However, relaxant responses to stimulation of the perivascular sympathetic supply, such as characterize adult tissues, had not yet developed by the time of birth. Relaxation in response to perivascular stimulation could be seen 30 days after birth.

3. Morphologic studies indicated that the longitudinal layer of smooth muscle was very primitive when an effective innervation was established. Although contractile, the cells were still myoblasts. Neural elements also appeared primitive. Thus considerable morphological maturation follows the development both of a functioning contractile machinery and innervation in the foetal gut.

4. This study helps establish that the intrinsic inhibitory innervation of the gut is not adrenergic.

1. In response to an auditory stimulus normal subjects made ballistic flexion movements of the top joint of the thumb against a lever attached to the spindle of a low‐inertia electric motor. 2. Electromyographic (e.m.g.) activity was recorded from pairs of fine wire electrodes inserted into flexor pollicis longus and extensor pollicis longus, respectively the sole flexor and extensor of the joint. 3. Movements of 5 degrees, 10 degrees and 20 degrees were made from initial angles of 10 degrees, 20 degrees and 30 degrees flexion against torques of 0.04, 0.08 and 0.16 Nm. 4. The e.m.g. activity initiating such movements was characterized by a ‘triphasic’ pattern of sequential bursts of activity in the agonist (flexor pollicis longus), then in the antagonist (extensor pollicis longus), and then in the agonist again. 5. The duration of the first agonist and first antagonist bursts ranged from about 50 to 90 ms and there was no significant change of burst length in the different mechanical conditions. 6. In movements of differing angular distance, the rectified and integrated e.m.g. activity of the first agonist burst could be correlated with the distance moved. The rectified and integrated e.m.g. activity of the first antagonist burst could not be correlated with the distance moved. 7. Responses of the muscles to perturbations either before or during the ballistic movements were studied. Current in the motor could be altered so to extend the thumb ('stretch'), to allow it to accelerate ('release'), or to prevent further movement ('halt'). 8. Suitably timed stretch increased the e.m.g. activity of the first agonist burst while release decreased it. 9. There was a small response of the agonist to stretch or halt timed to act during the interval between the first two agonist bursts; the major response was an augmentation of the second agonist burst. 10. Stretch, timed to act between the first two agonist bursts which released the antagonist, diminished the activity of the first antagonist burst while halt virtually eradicated it in all but one subject. Release, at this time, which stretched the antagonist, increased the activity of the first antagonist burst. 11. It is concluded that the individual components of a ballistic movement are relatively fixed in duration and the amount of e.m.g. activity is altered within this time interval to produce the different forces required for fast movements of different amplitude. 12. Both agonist and antagonist muscles remain under some feed‐back control during the entire course of a ballistic movement, but the amount of influence of fedd‐back depends on the supraspinal command signal and the changes in the spindle during the course of the movement.

1. Studies were made of the electromyogram (EMG) patterns associated with the performance of visually guided, step‐tracking arm movements by normal humans. Subjects were instructed to make movement either ‘accurately', ‘as fast as possible’ or ‘fast and accurately'. Movements of 16, 32, 48 and 64 deg of arc were made with each instruction. Movements had durations of approximately 250‐600 msec. 2. A ‘triphasic’ pattern of EMG activity was associated with all movements in this study. All bursts in this pattern were more clearly defined in faster movements whether the increased speed of movement was a result of increased movement amplitude or of the instruction‐related ‘intent’ of the subject. 3. The magnitudes of the two agonist EMG bursts showed identical linear dependencies on movement amplitude. The slope of this relation was instruction‐dependent, being greatest for ‘fast’ and least for ‘accurate’ movements. 4. The duration and time of onset of the initial agonist burst relative to the start of the movement were not dependent on movement amplitude or on instruction. In contrast, the time of onset of the second agonist burst depended on both movement amplitude and instruction, occurring earlier when movements were made faster. 5. The magnitude of the antagonist activity was instruction‐ but not amplitude‐dependent. Duration and onset of this burst varied with both instruction and movement amplitude.

We have examined fast flexion movements of the human thumb and fast extension movements of the elbow over three different distances at a variety of speeds in order to elucidate the function of the antagonist muscle in these circumstances. All movements were of such a velocity that they showed the typical bi‐ or triphasic pattern of muscle activation in agonist and antagonist. Slower movements, with continuous agonist activity, were not analysed. For movements made through the same angle at different velocities, there was a linear relationship between the amount of antagonist activity needed to halt the movement and the peak velocity. However, the slope of this relationship was a function of the distance moved. Movements made through large angles showed less antagonist activity than those made through small angles at the same speed. The timing of the antagonist activity also changed as a function of both distance and speed. Fast, small movements showed earlier onset of antagonist activity than slow, large ones. Movements which were halted mechanically with the subject's prior knowledge had little or no antagonist activity, since it was no longer necessary in these conditions. The complexity of these relations indicates that the triphasic pattern of muscle activity underlying these movements can no longer be regarded as a simple immutable ‘programme'. The size and timing of the bursts of muscle activity are subtly adjusted to the precise nature of the task.