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多くの四万十累層群分布域では北帯と南帯の間でマーストリヒチアン～暁新統が欠如しているが,四国西部の中村市-伊の岬地域にはこの年代の四万十累層群がよく露出している.本研究では,この地域の四万十累層群の地質と放散虫化石年代を検討した.岩相的特徴や堆積年代から,調査地域の四万十累層群は12の地層に区分される.調査域に分布する地層は,一部を除き南に向かって大局的に若くなる年代極性を示す.含礫頁岩中の頁岩礫の年代は,地層の堆積年代と比較的近接している.そして,地層の年代が若くなるのに従い頁岩礫の年代も大局的に若くなる.また,緑色岩と共存する岩相の放散虫化石年代は,後期カンパニアン～前・中期始新世に若い海洋プレートが沈み込んでいた可能性を示唆する.

Nephrotic syndrome (NS) associated with hematopoietic stem cell transplantation (HSCT) is usually related to chronic graft-versus-host disease (GVHD) and invariably occurs later than 100 days after transplantation. Here, we report the case of a 6-year-old boy who presented with NS only 61 days after cord blood stem cell transplantation (CBSCT). At 4 years old he was diagnosed with acute lymphoblastic leukemia and underwent bone marrow transplantation. Six months later, a recurrence was noted in the thymus, which required CBSCT at the age of 6. Acute GVHD and hemophagocytic syndrome occurred on day +13 and day +15, respectively, and were successfully treated with tacrolimus and a steroid. After tacrolimus was switched from intravenous infusion to oral administration, NS occurred on day +61. Complete remission was achieved in 3 weeks by resuming steroid treatment. Dry erythema with pigmentation and elevation of Th2 cytokine level suggest that NS in this case was also related to chronic GVHD. To our knowledge, this is the earliest occurrence of NS after HSCT. Hematologists and nephrologists should be aware that this condition may occur even in early periods after HSCT.

To understand the mechanisms underlying visual motion analyses for perceptual and oculomotor responses and their similarities/differences, we analyzed eye movement responses to two-frame animations of dual-grating 3 f5 f stimuli while subjects performed direction discrimination tasks. The 3 f5 f stimulus was composed of two sinusoids with a spatial frequency ratio of 3:5 (3 f and 5 f), creating a pattern with fundamental frequency f. When this stimulus was shifted by 1/4 of the wavelength, the two components shifted 1/4 of their wavelengths and had opposite directions: the 5 f forward and the 3 f backward. By presenting the 3 f5 f stimulus with various interstimulus intervals (ISIs), two visual-motion-analysis mechanisms, low-level energy-based and high-level feature-based, could be effectively distinguished. This is because response direction depends on the relative contrast between the components when the energy-based mechanism operates, but not when the feature-based mechanism works. We found that when the 3 f5 f stimuli were presented with shorter ISIs (100 ms), whereas perceived directions were biased toward the direction of pattern shift. These results suggest that the energy-based mechanism is dominant in oculomotor responses throughout ISIs; however, there is a transition from energy-based to feature-tracking mechanisms when we perceive visual motion.

To detect retinotopic activation in the human V5/MT, we obtained fMRI signals during optokinetic responses (OKR). We used two types of patterns, consisting of random dots plotted in either the central or peripheral regions, to stimulate the central and peripheral visual fields, respectively. These patterns moved at a constant speed of 20 degrees/s rightward and leftward alternately. Subjects were required to track the patterns with their eyes. The two types of visual stimuli elicited different patterns of brain activation; the area with the most significant response to central visual field stimuli was located posteriorly to that responding to peripheral visual field stimuli.

We examined the influence of target saliency on the initiation of smooth pursuit. The eye movements of five human subjects were recorded with the scleral search-coil technique. A video-projection system was used to create a pursuit target, consisting of a cluster of 14 red or green dots (0.5° squares) extending randomly over a 3°×3° region, and a surrounding background, consisting of stationary, random dots of the same size and density extending over an area 70°×40°. When the dots in the background and the target were of the same color, the target was indistinguishable from the background until it started to move. On the other hand, when the colors were different, the target was salient, even when stationary. We measured the changes in eye position over the 70-ms interval starting 70 ms after the onset of target motion (initial tracking response). When the target moved toward the fovea (centripetal motion), the initial tracking responses developed earlier when the dots in the target and background were of different color than when the two sets of dots were of the same color. However, in order to see this effect of target salience, it was critical that the colors be different before the onset of motion, but not afterwards. When the target moved away from the fovea (centrifugal motion), the initial tracking responses were independent of whether the colors of the target and the background were the same or different. Our data indicate that the initiation of tracking responses is very sensitive to the saliency of the target before the onset of target motion when that motion is toward the fovea.

Dent disease is an inherited tubulopathy caused by a mutation in the CLCN5 chloride channel gene. In cases of Dent disease in Japan (Japanese Dent, J-Dent), renal function is generally preserved and rarely progresses to advanced kidney dysfunction. However, the long-term prognosis of J-Dent remains unknown. We report the case of a 32-year-old man with J-Dent who developed advanced kidney dysfunction. Since the age of 3 years, he persistently exhibited proteinuria, and examination of a kidney biopsy specimen indicated focal segmental glomerulosclerosis (FSGS)-like lesions. Repeated corticosteroid treatments were found to be ineffective. After the age of 18 years, the patient was lost to follow-up and treatment was discontinued. The patient presented to our hospital again at the age of 32 years with advanced kidney dysfunction with low-molecular-weight proteinuria (LMWP), along with proximal tubular dysfunction and nephrocalcinosis. The patient’s 5-year-old nephew was also found to have LMWP from the age of 7 months. Therefore, Dent disease was suspected and genetic testing in the patient and his nephew revealed a CLCN5 mutation. Our case report suggests that J-Dent may cause advanced kidney dysfunction in adulthood, and, therefore, close collaboration between pediatricians and nephrologists is essential for the early identification of this complication. When male patients exhibit chronic kidney disease (CKD) of unknown etiology along with proximal tubular dysfunction and nephrocalcinosis, Dent disease should be considered. Investigations of undiagnosed adult J-Dent cases and further research on the natural history of J-Dent will help us better understand its clinical characteristics, prognosis, and effective treatment options.

Generally, image motion is induced all over the retina when an observer moves around. In spite of this, we can immediately detect objects moving in our surroundings. In this paper, a computational model is proposed to explain such detection using self-motion signals. First, we analyze the general characteristics of retinal image motion caused by both object motion and observer motion. Then a computational model is constructed in which true object motion is detected using signals of self-motion and depth values under the supposition that the surroundings are always stationary. It is suggested that the nervous system uses similar mechanisms.

We studied the effects of horizontal smooth pursuit on the ocular tracking responses to brief perturbations of a textured background in humans. When the subject was fixating a stationary spot, a brief perturbation (60°/s, 40 ms) of the background in any one of four directions (right, left, up, down) elicited a small tracking response. When the subject was pursuing a target moving against the stationary background, the same background perturbation elicited a larger response when in the same direction as the pursuit, but a smaller response when its direction was opposite to the pursuit; the response to vertical background perturbations was also enhanced during pursuit. When the subject was pursuing while the target and background were moving together, the same background perturbations elicited the larger responses regardless of their direction. These results indicate that the sensitivity to background motion is increased during smooth pursuit. However, when pursuit is executed against a stationary background – the usual situation in everyday life – the system is selectively insensitive to the reafferent visual input associated with pursuit, thereby reducing the potentially adverse effect of the background on pursuit performance.

In this paper, we propose a method for the detection of actual moving objects in a moving image obtained by a moving camera. First, we construct a basic method for the detection of actual moving objects by utilizing motion signals of a camera. In this method, actual moving objects are detected based on the difference between the actual image flow observed and the predicted image flow computed by utilizing motion signals of a camera. The basic method has some requirements which are difficult to satisfy, such as exact computation of depth values in the surroundings. Therefore, we improve this method to perform the correct detection of actual moving objects without depth signals. In the improved method, the detection is performed based on whether the actual image flow is involved in a subregion of the image flow which is computed as that of stationary objects or not. In this method, the exact computaion of depth values in the surroundings and the computation of a speed component for the translational motion of a camera are not required.

Dent disease is an X-linked disorder characterized by low-molecular-weight (LMW) proteinuria, hypercalciuria, nephrocalcinosis, urolithiasis and renal dysfunction. Dent disease is caused by mutations in at least two genes, i.e. CLCN5 and OCRL1, and its genetic background and phenotypes are common among European countries and the USA. However, only few studies on Dent disease in Japan, which was originally called 'low-molecular-weight proteinuric disease', have been reported thus far. In this study, we analysed genetic background and clinical phenotype and laboratory data of 86 unrelated Japanese Dent disease patients. The results demonstrated that the genetic basis of Japanese Dent disease was nearly identical to those of Dent disease in other countries. Of 86 unrelated Japanese Dent patients, 61 possessed mutations in CLCN5 (Dent-1), of which 27 were novel mutations; 11 showed mutations in OCRL1 (Dent-2), six of which were novel, and the remaining 14 patients showed no mutations in CLCN5 or OCRL1 (Dent-NI). Despite the similarity in genetic background, hypercalciuria was detected in only 51%, rickets in 2% and nephrocalcinosis in 35%. Although the patients were relatively young, six patients (8%) showed apparent renal dysfunction. Japanese Dent disease has a wider clinical spectrum than Dent disease in Europe and the USA.

Background. Mutations in the ATP6V1B1 and the ATP6V0A4 genes cause primary autosomal-recessive distal renal tubular acidosis (dRTA). Large deletions of either gene in patients with dRTA have not been described. Methods. The ATP6V1B1 and ATP6V0A4 genes were directly sequenced in 11 Japanese patients with primary dRTA from nine unrelated kindreds. Large heterozygous deletions were analyzed by quantitative real-time polymerase chain reaction (PCR). The clinical features of the 11 patients were also investigated. Results. Novel mutations in the ATP6V1B1 gene were identified in two kindreds, including frameshift, in-frame insertion and nonsense mutations. Large deletions in the ATP6V0A4 gene were identified in two kindreds. Exon 15 of ATP6V0A4 was not amplified in one patient, with a long PCR confirming compound heterozygous deletions of 3.7and 6.9-kb nucleotides, including all of exon 15. Direct DNA sequencing revealed a heterozygous frameshift mutation in ATP6V0A4 in another patient, with quantitative real-time PCR indicating that all exons up to exon 8 were deleted in one allele. Clinical investigation showed that four of the six patients with available clinical data presented with hyperammonemia at onset. Conclusions. To our knowledge, these dRTA patients are the first to show large deletions involving one or more entire exons of the ATP6V0A4 gene. Quantitative PCR amplification may be useful in detecting heterozygous large deletions. These results expand the spectrum of mutations in the ATP6V0A4 and ATP6V1B1 genes associated with primary dRTA and provide insight into possible structure–function relationships.

In the mouse retina, there are two distinct groups of direction-selective ganglion cells, ON and ON-OFF, that detect movement of visual images. To understand the roles of these cells in controlling eye movements, we studied the optokinetic responses (OKRs) of mutant mice with dysfunctional ON-bipolar cells that have a functional obstruction of transmission to ON direction-selective ganglion cells. Experiments were carried out to examine the initial and late phases of OKRs. The initial phase was examined by measurement of eye velocity using stimuli of sinusoidal grating patterns of various spatiotemporal frequencies that moved for 0.5 s. The mutant mice showed significant initial OKRs, although the range of spatiotemporal frequencies that elicited these OKRs was limited and the response magnitude was weaker than that in wild-type mice. To examine the late phase of the OKRs, the same visual patterns were moved for 30 s to induce alternating slow and quick eye movements (optokinetic nystagmus) and the slow-phase eye velocity was measured. Wild-type mice showed significant late OKRs with a stimulus in an appropriate range of spatiotemporal frequencies (0.0625-0.25 cycles/°, 0.75-3.0 Hz, 3-48°/s), but mutant mice did not show late OKRs in response to the same visual stimuli. The results suggest that two groups of direction-selective ganglion cells play different roles in OKRs: ON direction-selective ganglion cells contribute to both initial and late OKRs, whereas ON-OFF direction-selective ganglion cells contribute to OKRs only transiently.

The slit diaphragm (SD) is an intercellular junction between renal glomerular epithelial cells (podocytes) that is essential for permselectivity in glomerular ultrafiltration. The SD components, nephrin and Neph1, assemble a signaling complex in a tyrosine phosphorylation dependent manner, and regulate the unique actin cytoskeleton of podocytes. Mutations in the NPHS1 gene that encodes nephrin cause congenital nephrotic syndrome (CNS), which is characterized by the loss of the SD and massive proteinuria. Recently, we have identified the expression of the transmembrane glycoprotein signal regulatory protein α (SIRPα) at the SD. In the present study, we analyzed the expression of SIRPα in developing kidneys, in kidneys from CNS patients and in proteinuric rat models. The possibility that SIRPα interacts with known SD proteins was also investigated. SIRPα was concentrated at the SD junction during the maturation of intercellular junctions. In the glomeruli of CNS patients carrying mutations in NPHS1, where SD formation is disrupted, the expression of SIRPα as well as Neph1 and nephrin was significantly decreased, indicating that SIRPα is closely associated with the nephrin complex. Indeed, SIRPα formed hetero-oligomers with nephrin in cultured cells and in glomeruli. Furthermore, the cytoplasmic domain of SIRPα was highly phosphorylated in normal glomeruli, and its phosphorylation was dramatically decreased upon podocyte injury in vivo. Thus, SIRPα interacts with nephrin at the SD, and its phosphorylation is dynamically regulated in proteinuric states. Our data provide new molecular insights into the phosphorylation events triggered by podocyte injury.

To explore how local motion signals in the peripheral visual field are integrated, we recorded ocular following responses (OFRs) to moving vertical gratings extending across a wide horizontal width (1) of various vertical heights, (2) of a thin strip (4° height) at various vertical eccentricities, and (3) of two thin strips separated with various vertical distances (double-grating) in four monkeys. We found that the OFRs became larger and responsive more to lower spatial frequency than to higher as the vertical height of the motion stimuli increased up to 8° or 16°. This result is consistent with the incorporation of visual motion signals originating in the peripheral visual field; the OFRs to thin strips of drifting gratings were tuned for lower spatial frequency as the eccentricity increased. We also found that the OFRs to the double-gratings were quite similar to the sum of the responses to the single gratings in the initial period, but were significantly larger than the linear-sum in the final period. This result suggests that a non-linear mechanism, by which weak local motion signals are integrated into an effective ensemble, underlies the OFRs.

Optokinetic responses (OKRs) are reflexive eye movements elicited by a moving visual pattern, and have been recognized in a variety of species. Several brainstem and cortical structures are known to be implicated in the generation of OKRs in primates, while the OKRs of afoveate mammals have been posited to be dominated by subcortical structures. To understand the subcortical mechanism underlying OKRs, the initial OKRs to horizontal quarter-wavelength steps applied to vertical grating patterns were studied in adult C57BL/6J mice under the monocular viewing conditions. The initial OKRs to sinusoidal gratings showed directional asymmetry with temporal-to-nasal predominance, a common characteristic of afoveate mammals that uses the subcortical structures to elicit OKRs. We then examined whether the OKRs of afoveate mammals are driven by the same visual features of the moving images as those in primates. The OKRs in mice were elicited by using the missing fundamental (mf) stimuli and its variants that had been used to understand the mechanism(s) underlying the cortical control of eye movements in primates. We obtained the results indicating that the OKRs of mice are driven by the principal Fourier component of moving visual image as in primates despite the differences in neural circuitries.

When tracking a moving target in the natural world with pursuit eye movement, our visual system must compensate for the self-induced retinal slip of the visual features in the background to enable us to perceive their actual motion. We previously reported that the speed of the background stimulus in space is represented by dorsal medial superior temporal (MSTd) neurons in the monkey cortex, which compensate for retinal image motion resulting from eye movements when the direction of the pursuit and background motion are parallel to the preferred direction of each neuron. To further characterize the compensation observed in the MSTd responses to the background motion, we recorded single unit activities in cortical areas middle temporal (MT) and MSTd, and we selected neurons responsive to a large-field visual stimulus. We studied their responses to the large-field stimulus in the background while monkeys pursued a moving target and while fixated a stationary target. We investigated whether compensation for retinal image motion of the background depended on the speed of pursuit. We also asked whether the directional selectivity of each neuron in relation to the external world remained the same even during pursuit and whether compensation for retinal image motion occurred irrespective of the direction of the pursuit. We found that the majority of the MSTd neurons responded to the visual motion in space by compensating for the image motion on the retina resulting from the pursuit regardless of pursuit speed and direction, whereas most of the MT neurons responded in relation to the genuine retinal image motion.

Renal dysplasia associated with urinary tract obstruction comprises two distinct phenotypes, i.e., multicystic dysplastic kidney (MCDK) and obstructive renal dysplasia (ORD). MCDK is a common manifestation in infants with renal dysplasia, which is characterized by multiloculated thin-walled cysts with no functional parenchyma and an atretic ureter owing to pyelocalyceal occlusion early in fetal life. In contrast, ORD is an extremely rare condition which is caused by severe obstruction of the distal ureter or urethra. Here, we report two infants with ORD. Both patients manifested unilateral kidney enlargement with multiple cortical cysts, mild hydronephrosis, and marked dilatation of the ipsilateral ureter. Contralateral kidneys and urinary tracts revealed no apparent radiological abnormalities. Serial ultrasonographic studies of fetal and neonatal kidneys in both cases revealed that ureteral dilatation was evident at gestational week 16 and 27, respectively, and most of the cortical cysts disappeared within 1–3 months after birth. The functions of the affected kidneys were severely impaired but evident at the time of birth. These manifestations were consistent with a diagnosis of ORD, and were distinct from the features of MCDK. Our observation of fetal and infantile kidneys in these two cases provides us with a better understanding of the pathogenesis of ORD.

We report a case of Henoch-Schonlein purpura nephritis (HSPN) with acquired IgA deficiency due to parvovirus B19 infection. The patient was diagnosed as having Henoch-Schonlein purpura (HSP) at 6 years old, and subsequently developed macrohematuria and massive proteinuria of 7.4 g/day with decreased creatinine clearance of 70.2 ml/min/1.73 m(2) and significantly elevated serum IgA level of 449 mg/dl. The first kidney biopsy yielded the diagnosis of severe HSPN. After the initiation of the immunosuppressive therapy, the patient was infected with parvovirus B19 and developed virus-associated hemophagocytic syndrome (VAHS). Thereafter, the serum level of IgA selectively decreased and remained undetectable until the present time. Repeated kidney biopsies performed over a period of 14 years revealed a remarkable histological improvement in association with stabilization of the patient's kidney function. Considering the severity of initial kidney injury, persistent acquired IgA deficiency was likely to add favorable effects to the immunosuppressive therapy in this patient with HSPN.

Development of fetal kidney is a finely programmed sequence, and is regulated by many important molecules. The perturbation of normal kidney development leads to congenital anomalies of kidney and urinary tract (CAKUT). CAKUT includes hypoplastic/dysplastic kidney, obstructive nephropathy and several other anomalies. CAKUT is of clinically importance, since it could lead to end stage renal failure when its anomaly grade is severe. So far, several causative genes responsible for development of CAKUT have been identified, including genes encoding molecules related to the renin-angiotensin-aldosterone system, RAS system. In humans, maternal administration of agents with inhibitory effects on the RAS system, such as angiotensin-converting enzyme inhibitors (ACEIs) or angiotensin type 1 receptor blockers (ARBs), have been reported to cause severe renal malformation, designated as ACEI/ARB fetopathy. In this paper, we overview the development of fetal kidney and address the effects of ACEIs/ARBs on fetal kidney.

To study the initial part of the mouse optokinetic response, OKR (approximately 500 ms from the onset of visual stimulus motion), we recorded the ocular response to a vertical sinusoidal grating moving at a constant velocity. We found that the magnitude of the response monotonically increased as the stimulus contrast increased. The response showed a narrow band-pass property for the spatiotemporal frequency, with the largest sustained response observed at 0.125 cycle/deg and 1.5 Hz. We also found that temporal frequencies higher than 1.5 Hz elicited transient increase in the eye velocity, but weak or no sustained eye movements. Thus the initial OKR in mice is characterized by the spatiotemporal frequency of the visual stimuli. Our results suggest that the initial OKR contains two components: a transient that diminishes within approximately 200 ms, and a tonic that is maintained for more than 400 ms, and that the initial part of the OKR in mice is an appropriate measurement parameter for studies of the visual and motor systems, like ocular following response (OFR) in primates.

Background Essential tremor (ET) is the most common movement disorder and its pathophysiology is unknown. We hypothesize that increased membrane excitability in motor circuits has a key role in the pathogenesis of ET. Specifically, we propose that neural circuits controlling ballistic movements are inherently unstable due to their underlying reciprocal innervation. Such instability is enhanced by increased neural membrane excitability and the circuit begins to oscillate. These oscillations manifest as tremor. Methods Postural limb tremor was recorded in 22 ET patients and then the phenotype was simulated with a conductance-based neuromimetic model of ballistic movements. The model neuron was Hodgkin-Huxley type with added hyperpolarization activated cation current (Ih), low threshold calcium current (IT), and GABA and glycine mediated chloride currents. The neurons also featured the neurophysiological property of rebound excitation after release from sustained inhibition (post-inhibitory rebound). The model featured a reciprocally innervated circuit of neurons that project to agonist and antagonist muscle pairs. Results Neural excitability was modulated by changing Ih and/or IT. Increasing Ih and/or IT further depolarized the membrane and thus increased excitability. The characteristics of the tremor from all ET patients were simulated when Ih was increased to ~10× the range of physiological values. In contrast, increasing other membrane conductances, while keeping Ih at a physiological value, did not simulate the tremor. Increases in Ih and IT determined the frequency and amplitude of the simulated oscillations. Conclusion These simulations support the hypothesis that increased membrane excitability in potentially unstable, reciprocally innervated circuits can produce oscillations that resemble ET. Neural excitability could be increased in a number of ways. In this study membrane excitability was increased by up-regulating Ih and IT. This approach suggests new experimental and clinical ways to understand and treat common tremor disorders.

We recorded the initial vertical vergence eye movements elicited in monkeys at short latency (∼70 ms) when the two eyes see one-dimensional (1D) horizontal grating patterns that are identical except for a phase difference (disparity) of one-quarter wavelength. With gratings composed of single sine waves, responses were always compensatory, showing Gaussian dependence on log spatial frequency (on average: peak = 0.75 cycles/deg; SD = 0.74; r2 = 0.980) and monotonic dependence on log contrast with a gradual saturation well described by the Naka-Rushton equation (on average: n = 0.89; C50 = 4.1%; r2 = 0.978). With gratings composed of two sine waves whose spatial frequencies were in the ratio 3:5 and whose disparities were of opposite sign (the 3f5f stimulus), responses were determined by the disparities and contrasts of the two sine-wave components rather than the disparity of the features, consistent with early spatial filtering of the monocular inputs before their binocular combination and mediation by detectors sensitive to disparity energy. In addition, responses to the 3f5f stimulus showed a nonlinear dependence on the relative contrasts of the two sine waves. Thus on average, when the contrast of one sine wave was 2.3 times greater than that of the other, the one with the lower contrast was largely ineffective as though suppressed, and responses were determined almost entirely by the sine wave of higher contrast: Winner-Take-All. These findings are very similar to those published previously on the vertical vergence responses of humans, indicating that the monkey provides a good animal model for studying these disparity vergence responses.

Recurrent FSGS is a major challenge in the field of nephrology. To clarify the role of NPHS2 defects in the pathogenesis of FSGS recurrence, we sequenced all eight exons of NPHS2 in 11 Japanese pediatric FSGS patients with or without post-transplant recurrence. All patients had biopsy-proven primary FSGS, had no family history of renal diseases or consanguinity, were steroid-resistant, and received living-related renal transplantation. The mean age at onset was 5.0 +/- 3.1 yr and mean age at renal transplantation was 10.4 +/- 4.1 yr. Mutational analysis of NPHS2 was performed using polymerase chain reaction and direct sequencing. We found a synonymous T/C polymorphism at alanine 318 (GCC to GCT) in seven of 11 patients but no other causative NPHS2 mutations. FSGS recurred immediately after transplant in seven patients, while the remaining four patients had no recurrence for 3.2-5.8 yr. There were no differences between recurrent and non-recurrent patients in the onset age and the interval from onset to ESRD. In conclusion, we detected no causative NPHS2 mutations in Japanese pediatric FSGS patients with or without post-transplant recurrence. Further studies on the involvement of other genes are required to better understand recurrent FSGS.

To understand how the CNS uses past experiences to generate movements that accommodate minute-by-minute environmental changes, we studied the trial-by-trial updating of the gain for initiating smooth pursuit eye movements and how this relates to the history of previous trials. Ocular responses in humans elicited by a small perturbing motion presented 300 ms after appearance of a target were used as a measure of the gain of visuomotor transmission. After the perturbation, the target was either moved horizontally (pursuit trial) or remained in a stationary position (fixation trial). The trial sequence randomly included pursuit and fixation. The amplitude of the response to the perturbation was modulated in a trial-by-trial manner based on the immediately preceding trial, with preceding fixation and pursuit trials decreasing and increasing the gain, respectively. The effect of the previous trial was larger with shorter intertrial intervals, but did not diminish for at least 2,000 ms. A time-series analysis showed that the response amplitude was significantly correlated with the past few trials, with dynamics that could be approximated by a first-order linear system. The results suggest that the CNS integrates recent experiences to set the gain in preparation for upcoming tracking movements in a changing environment.

We examined whether there are any adaptive effects on the pursuit initiation after a prolonged exposure to moving visual stimuli. The eye movements of six human subjects were recorded with the scleral search-coil technique or a Dual Purkinje Image Eye-tracker system. A random-dot image appeared on a CRT monitor and moved coherently in one direction (rightward or leftward) at 10 deg/s for 4 s, while the subject fixated on a stationary target (conditioning stimulus). The screen was blanked for 0.2 s, and then the target stepped to the right or left of the center and moved 10 deg/s leftward or rightward. We measured change in the eye position over the open-loop period of the pursuit initiation. When the pursuit target moved in the same direction as the preceding visual stimulus, a significant reduction in the initial tracking responses (55.9% decrease on average) was found. We then studied in detail the properties of the motion adaptation in pursuit initiation by varying the visual conditions systematically and obtained the following findings. When the subjects tracked the target that moved at 10 deg/s, the pursuit initiation was affected not only by the conditioning stimulus of the same speed as the target, but also by those of different speeds. Further, the conditioning stimulus moving at 10 deg/s affected the pursuit initiation not only when the target moved with the same speed but also when it moved at different speeds (more remarkable for slower speeds). The effect of conditioning stimuli on the pursuit initiation was larger when the duration of the conditioning period was longer. The effect of conditioning stimuli decayed as the duration of the blank period became longer. The findings from the present study are consistent with the properties of neurons in the middle temporal area of monkeys.

Primates are able to track a moving target with their eyes, even when the target is seen against a stationary textured background. In this situation, the tracking eye movement induces motion of the background images on the retina (reafference) that competes with the motion of the target's retinal image, potentially disrupting the tracking of the target. Previous work on humans reported that brief perturbations of the background in the opposite direction to pursuit were much less disruptive than perturbations in the same direction as pursuit. Furthermore, if the background moved together with the pursuit target—so as to effectively eliminate the reafference—then the effects of a subsequent background perturbation showed less dependence on direction. This suggested that the direction selectivity to background perturbations during pursuit against a stationary background was due, at least in part, to the prior motion of the background secondary to the pursuit. We now report similar findings in monkeys, and in addition, have investigated the effect of moving the background while the animal was fixating a stationary target. In this situation, the ocular tracking responses to subsequent brief perturbations of the moving background were weaker when the perturbations were in the same direction as the prior background motion than when in the opposite direction. This suggests that the selective insensitivity to the reafferent visual input associated with pursuit across a stationary background is, at least in part, independent of pursuit per se and attributable to a progressive reduction in the sensitivity to sustained background motion.

Congenital nystagmus (CN) is an aperiodic oscillatory eye movement disorder. Horizontal rectus tenotomy with simple re-attachment has been proposed as a therapy for CN. This therapy might affect vision and/or eye movements. Another paper deals with improvements in visual acuity. This and the companion paper examine changes in eye movements. In this study, we examined the effect of tenotomy on nystagmus waveforms using wavelet spectral analysis. No common effect was found across the patients on the wavelet spectra of the CN beat, suggesting that tenotomy surgery has no effect, or only a quite small effect, on the waveform structure of CN.