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SUMMARY1. We have investigated the spatial organization of monosynaptic corticospinal projections to hind-limb motoneurones, using near threshold stimulation of the surface of the precentral gyrus to activate pyramidal tract (PT) cells and intracellular recording from motoneurones to detect the resulting e.p.s.p.s.2. Monosynaptic e.p.s.p.s of cortical origin were seen in all motoneurone species investigated, those of distal as well as of proximal hind-limb muscles. The proportion of motoneurones in which the e.s.p.s were evoked and the amplitudes of the latter indicated a more extensive cortical projection to motor nuclei for distal than for proximal muscles, as previously found for forelimb motoneurones.3. Cortical areas from which monosynaptic e.p.s.p.s were evoked in individual motoneurones were remarkably large, most often between 3 and 7 mm2. Several motoneurones appeared to have two or three separate areas within the hind-limb division of the motor cortex.4. Areas of location of pyramidal tract cells projecting to various motoneurones innervating one muscle were usually not identical. They overlapped often only partially or did not overlap at all.5. Areas of location of pyramidal tract cells projecting to motor nuclei for different muscles often showed an extensive overlap. When it occurred, various motoneurones of a given motor nucleus had common cortical projection areas with motoneurones of other motor nuclei, either to synergistic or to antagonistic muscles. Our results give further evidence for overlapping of areas of cortical projections to motoneurones and speak

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Motor control was analysed by a visuomotor tracking movement using elbow flexion both in patients with cerebellar ataxia and in normal controls. A TV screen was divided into upper and lower halves, in each of which a vertical strip was displayed. The upper strip (T, target) was moved horizontally from the centre of the screen to the left or right by ramp voltage. The lower strip (D, displacement of the handle) was moved in proportion to angular displacement of the handle by a potentiometer coupled to the handle axis. The subject, while sitting in front of the TV screen, had to make D match the movement of T by controlling the handle with his right arm. The range of T movement was 30 deg in terms of the handle's angular movement. T velocity was 7.5, 15 or 30 deg/s. The subjects were told the direction and velocity of T in advance. The process of tracking was divided into three phases (initial catch-up phase, middle pursuit phase, and terminal phase), in each of which the performance of cerebellar ataxia patients differed from that of the controls. The characteristic features of the ataxic cases were (1) prolongation of the reaction time, mainly due to the increase of premotor time; (2) difficulty in selecting an appropriate amplitude of initial peak velocity in proportion to the target velocity in the initial catch-up phase; (3) disruption of smooth continuous movement, namely, the saccadic pattern in the middle pursuit phase; (4) delay in the initiation of deceleration in the terminal phase; (5) difficulty in corrective adjustment in reaching the final target point; and (6) irregular EMG activity in the agonist muscles and/or cocontraction of the antagonistic muscles. Quantitative treatment of the second and third features, as exemplified in the relationship between initial error and initial peak velocity and in the ratio of the movement arrest period, respectively, was found to be helpful in the evaluation of disease severity. The significance of these findings is discussed and the role of the cerebellar system in the control of slow voluntary movement is stressed.

The results of the present electrophysiological investigation have shed some light on the mechanisms underlying many clinical signs, at least, in patients with capsular hemiplegia. A tentative interpretation of them is given below. Cerebral lesions due to haemorrhage or infarction in the area of the middle cerebral artery interrupt an extensive part of the corticospinal tract and disturb many other descending pathways involved in voluntary performance. In consequence, a marked reduction in the ability to drive the spinal motor apparatus occurs, resulting in weakness of motor power. Here, we refer only to muscle power but not to performance. For example, the disturbance of voluntary contraction by clonus is disregarded (cf. fig. 8). On the other hand, the same lesions also release the spinal reflexes from inhibition by the higher levels of the brain and cause increased excitability in flexors and extensors. In the lower extremity, this is much more makred in extensors and extensor spasticity becomes a dominant sign clinically. Any release effect on the flexor system is largely cancelled by the high activity of the reciprocal Ia inhibitory pathway from extensors and only a fragment of it is occasionally revealed in some patients as an H-reflex in pre-tibial muscles or as weak Ia inhibition of the triceps surae. Reduced driving power of the brain may be compensated by raised excitability in the spinal cord and spastic extensors are thus naturally in a better condition to preserve motor power. Flexor muscles are doubly crippled by reduced descending impulses and strong reciprocal inhibition by the Ia impulses from the spindles of the extensor muscles.

2. Averaged records of descending volleys in corticospinal tract fibres were taken from the surface of the lateral funiculus or from its dissected fascicles. The sensitivity of the recording was sufficient to detect responses in single fibres.3. The latencies of the earliest descending volleys evoked by weak intracortical stimuli were compared with the latencies of the antidromic spike potentials ofpyramidal tract cells evoked by stimulation ofthe lateral funiculus at a low lumbar level (same conduction distance). Only in about one third of cases these latencies were similar and compatible with a direct activation of pyramidal tract cells. In the remaining cases they indicated mono-or polysynaptic activation of pyramidal tract cells.4. Latencies of the later components of the descending volleys indicated that they were due to indirect activation of pyramidal tract cells in practically all cases.5. The components of the descending volleys attributable to the indirect activation of pyramidal tract cells were greatly increased when repetitive intracortical stimuli were applied instead of single ones.6. The investigation leads to the conclusion that a weak intracortical

Despite its importance to plant function and human health, the genetics underpinning element levels in maize grain remains largely unknown. Through a genome-wide association study in the maize Ames panel of nearly 2,000 inbred lines that was imputed with ∼7.7 million SNP markers, we investigated the genetic basis of natural variation for the concentration of 11 elements in grain. Novel associations were detected for the metal transporter genes rte2 (rotten ear2) and irt1 (iron-regulated transporter1) with boron and nickel, respectively. We also further resolved loci that were previously found to be associated with one or more of five elements (copper, iron, manganese, molybdenum, and/or zinc), with two metal chelator and five metal transporter candidate causal genes identified. The nas5 (nicotianamine synthase5) gene involved in the synthesis of nicotianamine, a metal chelator, was found associated with both zinc and iron and suggests a common genetic basis controlling the accumulation of these two metals in the grain. Furthermore, moderate predictive abilities were obtained for the 11 elemental grain phenotypes with two whole-genome prediction models: Bayesian Ridge Regression (0.33-0.51) and BayesB (0.33-0.53). Of the two models, BayesB, with its greater emphasis on large-effect loci, showed ∼4-10% higher predictive abilities for nickel, molybdenum, and copper. Altogether, our findings contribute to an improved genotype-phenotype map for grain element accumulation in maize.