A low-voltage activated,transient calcium current is responsible for the time-dependent depolarizing inward rectification of rat neocortical neurons in vitro

Intracellular recordings were obtained from rat neocortical neurons in vitro. The current-voltage-relationship of the neuronal membrane was investigated using current- and single-electrode-voltage-clamp techniques. Within the potential range up to 25 mV positive to the resting membrane potential (RMP: –75 to –80 mV) the steady state slope resistance increased with depolarization (i.e. steady state inward rectification in depolarizing direction). Replacement of extracellular NaCl with an equimolar amount of choline chloride resulted in the conversion of the steady state inward rectification to an outward rectification, suggesting the presence of a voltage-dependent, persistent sodium current which generated the steady state inward rectification of these neurons. Intracellularly injected outward current pulses with just subthreshold intensities elicited a transient depolarizing potential which invariably triggered the first action potential upon an increase in current strength. Single-electrode-voltage-clamp measurements reveled that this depolarizing potential was produced by a transient calcium current activated at membrane potentials 15–20 mV positive to the RMP and that this current was responsible for the time-dependent increase in the magnitude of the inward rectification in depolarizing direction in rat neocortical neurons. It may be that, together with the persistent sodium current, this calcium current regulates the excitability of these neurons via the adjustment of the action potential threshold.     

The influence of visual illusions on grasp position

 Visual size illusions have been shown to affect perceived object size but not the aperture of the hand when reaching to those same objects. Thus, vision for perception is said to be dissociated from vision for action. The present study examines the effect of visual-position and visual-shape illusions on both the visually perceived center of an object and the position of a grasp on that object when a balanced lift is required. The results for both experiments show that although the illusions influence both the perceived and the grasped estimates of the center position, the grasp position is more veridical. This partial dissociation is discussed in terms of its implications for streams of visual processing. Received: 17 November 1997 / Accepted: 11 September 1998     

Survival and immunogenicity of dissociated allogeneic fetal neural dopamine-rich grafts when implanted into the brains of adult mice

Summary The survival of grafts of dissociated allogeneic fetal neural dopamine (DA) rich tissue in the striatum has been studied after transplantation between inbred strains of mice differing at defined immunogenetical loci between donor and recipient. Six to 7 weeks and 15 weeks after grafting, surviving grafted DA neurons were found in the brains of all the recipients, albeit with a large variation in numbers, located either within the striatum or within the adjacent lateral ventricle. The mean number of surviving DA neurons did not differ between the syngeneic controls and the histoincompatible donor-host combinations, and there was no difference in survival between grafts that differed at single or multiple major histocompatibility complex (MHC) loci, and those that differed at multiple non-MHC loci. The amount of inflammatory cells in the graft area did not differ between the groups, and none of the animals showed massive infiltration of inflammatory cells. The in situ immunogenicity of the grafted neural tissue after intracerebral implantation was monitored by means of Simonsen's alloimmunization test, at 6–7 weeks after transplantation, which provides a sensitive measure primarily of the cellular immunological response. Most, but not all, graft recipients showed immunization with a Spleen Index (S.I.) close to that seen in recipients of an orthotopical skin graft of the same histoincompatibility combination. In contrast to the prolonged survival of the intracerebral neural transplants, none of the skin grafts survived longer than 3 weeks, thus demonstrating the immunologically privileged status of the brain. We conclude that intracerebrally grafted allogeneic neural tissue is capable of provoking a cellular immune response. Despite host immunization, however, the dissociated fetal neural allografts survived for at least 15 weeks without any overt signs of rejection, regardless of the donor-host combination used.     

The role of the monkey sensory cortex in the recovery from cerebellar injury

Summary The aim of the study was to investigate the contribution of the primary sensory cortex in the compensation of cerebellar deficits during self-paced movements. For this purpose, monkeys were trained on motor tasks which required goal-reaching and independent finger movements. The intermediate and lateral deep cerebellar nuclei and the sensory cortex were lesioned in isolation and in sequence and the course of motor recovery was studied on the test performances. The deep nuclei were lesioned by kainic acid injections, the sensory cortex was removed by ablation. Cerebellar lesions in isolation produced obvious deficits at proximal and distal joints, affecting both slow and fast motor adjustments. Only lesions of the anterior portions of the intermediate and lateral deep nuclear complexes produced deficiencies in voluntary movements. Lesions of the posterior portions produced postural disturbances. The process of recovery following cerebellar lesions was slow and, depending on the nature of the task, was found to be differentially disruptive for motor performances requiring fast and slow motor adjustments. The deficits at distal joints appeared to be more enduring than those at proximal joints. Sensory cortical lesions in isolation produced much less severe and more transient motor deficits. They consisted of hand clumsiness and their recovery was fast and reached higher levels of performance than following cerebellar lesions. When the sensory cortex was removed secondarily to a cerebellar lesion and after recovery from the cerebellar deficits, the initially recovered motor performance became much worse again (decompensation). Removal of the sensory cortex prior to a cerebellar lesion exaggerated the cerebellar deficits and severely limited their recovery. Slow and fast motor performances were completely abolished for three weeks following sequential lesions. Signs of recovery subsequently appeared and stabilized at low levels of performance by five to seven weeks. The effects of combined, sequential cerebellar and sensory cortical lesions were much worse than expected if the effects from the two lesions were merely additive. This indicates that there is some functional interrelationship between the sensory cortex and the cerebellum, which promotes compensation. The somatosensory cortex appears to play a crucial role in the process of recovery from cerebellar motor deficits and it is likely that sensation is an important component in the process of recovery. It is suggested that the sensory cortex exerts its compensatory actions via a structure or structures which receives convergent cerebellar and sensory cortical inputs.     

Extensive monosynaptic inhibition of ventral respiratory group neurons by augmenting neurons in the Bötzinger complex in the cat

Summary Axonal projections and synaptic connectivity of expiratory B?tzinger neurons with an augmenting firing pattern (Bot-Aug neurons) to neurons in the ipsilateral ventral respiratory group (VRG) were studied in anaesthetized cats. Antidromic mapping revealed extensive axonal arborizations of Bot-Aug neurons (24 of 45) to the rostral or caudal VRG, with some having arbors in both regions. Of 234 pairs of neurons studied with intracellular recording and spike-triggered averaging, monosynaptic inhibitory postsynaptic potentials (IPSPs) were evoked in 49/221 VRG neurons by 38/98 Bot-Aug neurons. The highest incidence of monosynaptic inhibition was found in inspiratory bulbospinal neurons (10 of 23 tested). Evidence was also found for monosynaptic inhibition, by a separate group of Bot-Aug neurons, of expiratory bulbospinal neurons (12/58), while excitatory postsynaptic potentials (EPSPs) were identified in another two of these neurons. In addition, monosynaptic IPSPs were recorded from 13 of 53 identified laryngeal motoneurons, and from 14 of 100 respiratory propriobulbar neurons. Presumptive disynaptic IPSPs were recorded from 11 of the 221 VRG neurons. We conclude that Bot-Aug neurons exert widespread inhibition on all major neuron categories in the ipsilateral VRG, and should be regarded as an important element in shaping the spatiotemporal output pattern of both respiratory motoneurons and premotor neurons.     

Deceleration affects anticipatory and reactive components of triggered postural responses

Understanding the physiological and psychological factors that contribute to healthy and pathological balance control in man has been made difficult by the confounding effects of the perturbations used to test balance reactions. The present study examined how postural responses were influenced by the acceleration–deceleration interval of an unexpected horizontal translation. Twelve adult males maintained balance during unexpected forward and backward surface translations with two different acceleration–deceleration intervals and presentation orders (serial or random). “SHORT” perturbations consisted of an initial acceleration (peak acceleration 1.3 m s⁻²; duration 300 ms) followed 100 ms later by a deceleration. “LONG” perturbations had the same acceleration as SHORT perturbations, followed by a 2-s interval of constant velocity before deceleration. Surface and intra-muscular electromyography (EMG) from the leg, trunk, and shoulder muscles were recorded along with motion and force plate data. LONG perturbations induced larger trunk displacements compared to SHORT perturbations when presented randomly and larger EMG responses in proximal and distal muscles during later (500–800 ms) response intervals. During SHORT perturbations, activity in some antagonist muscles was found to be associated with deceleration and not the initial acceleration of the support surface. When predictable, SHORT perturbations facilitated the use of anticipatory mechanisms to attenuate early (100–400 ms) EMG response amplitudes, ankle torque change and trunk displacement. In contrast, LONG perturbations, without an early deceleration effect, did not facilitate anticipatory changes when presented in a predictable order. Therefore, perturbations with a short acceleration–deceleration interval can influence triggered postural responses through reactive effects and, when predictable with repeated exposure, through anticipatory mechanisms.     

The development of goal-directed reaching in infants: hand trajectory formation and joint torque control

Nine young infants were followed longitudinally from 4 to 15 months of age. We recorded early spontaneous movements and reaching movements to a stationary target. Time-position data of the hand (endpoint), shoulder, and elbow were collected using an optoelectronic measurement system (ELITE). We analyzed the endpoint kinematics and the intersegmental dynamics of the shoulder and elbow joint to investigate how changes in proximal torque control determined the development of hand trajectory formation. Two developmental phases of hand trajectory formation were identified: a first phase of rapid improvements between 16 and 24 weeks of age, the time of reaching onset for all infants. During that time period the number of movement units per reach and movement time decreased dramatically. In a second phase (28–64 weeks), a period of fine-tuning of the sensorimotor system, we saw slower, more gradual changes in the endpoint kinematics. The analysis of the underlying intersegmental joint torques revealed the following results: first, the range of muscular and motiondependent torques (relative to body weight) did not change significantly with age. That is, early reaching was not confined by limitations in producing task-adequate levels of muscular torque. Second, improvements in the endpoint kinematics were not accomplished by minimizing amplitude of muscle and reactive torques. Third, the relative timing of muscular and motion-dependent torque peaks showed a systematic development toward an adult timing profile with increasing age. In conclusion, the development toward invariant characteristics of the hand trajectory is mirrored by concurrent changes in the control of joint forces. The acquisition of stable patterns of intersegmental coordination is not achieved by simply regulating force amplitude, but more so by modulating the correct timing of joint force production and by the system's use of reactive forces. Our findings support the view that development of reaching is a process of unsupervised learning with no external or innate teacher prescribing the desired kinematics or kinetics of the movement.     

Trajectory control in targeted force impulses

Summary This study was undertaken in order to determine the time course of the process by which information derived from a visual target is used to accurately set the amplitude of a simple motor response. We refer to this process as response specification. Separate auditory and visual cues were given to the subjects in order to independently control the moment of response initiation and the time available for processing amplitude information from the target. Six subjects initiated impulses of isometric force in synchrony with the last of predictable series of regular tones. Response amplitudes were to match one of three visual target steps occurring at random times between 0 and 400 ms before the response-synchronizing tone. Using these separate auditory and visual cues, we were able to systematically vary the time interval between target presentation and response onset, termed here Stimulus-Response or S-R interval. Target steps were presented in blocks of either predictable (simple condition) or unpredictable (choice condition) amplitudes. The peak forces and the peaks of their time derivatives were analyzed to determine how subjects achieved accuracy under the different conditions and at different S-R intervals. The trajectories of responses produced in the simple condition were independent of the S-R interval. In contrast, when targets were presented in unpredictable order, the distribution of the peak forces of the subjects' responses depended on the S-R interval. At short S-R intervals (<125 ms), subjects made responses whose peak forces were distributed around the center of the range of target steps. These responses formed a unimodal, but broad distribution which was independent of actual target amplitude. With increasing S-R interval (>125 ms), the distributions of peak forces gradually shifted toward the correct target amplitudes, with the means reaching the appropriate amplitudes at S-R intervals of 250–400 ms. At S-R intervals comparable to a reaction time, the range of peak forces was constricted to a similar extent as previously observed in a reaction time task (Hening et al. 1988). We found that the gradual improvement of accuracy was not achieved through changes in trajectory control: at all S-R intervals, subjects utilized a pulse-height control policy (Gordon and Ghez 1987a). Different peak forces were achieved by varying the rate of rise of force, while force rise time was held relatively invariant. We did find, however, that within the constraints imposed by rise time regulation, compensatory adjustments to the force trajectories (Gordon and Ghez 1987b) were greatest during the period of specification. We conclude that (1) subjects can initiate their responses independent of the degree of specification achieved and that the normal process of specification of amplitude begins earlier and continues longer than the latency of responses in a reaction time task; (2) before target presentation, subjects prepare a default response whose amplitude is biased by prior experience with the targets presented in the task. We hypothesize that the central mechanisms that specify response amplitude do so by a progressive adjustment of the default parameters.