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Motion signals in the visual field can cause strong biases in the perceived positions of stationary objects. Local motion signal within an object induces a shift in the perceived object position in the direction of motion, whereas adaptation to motion stimuli causes a perceptual shift in the opposite direction. The neural mechanisms underlying these illusions are poorly understood. Here we report two novel receptive field (RF) properties in cat primary visual cortex that may account for these motion-position illusions. First, motion signal in a stationary test stimulus causes a displacement of the RF in the direction opposite to motion. Second, motion adaptation induces a shift of the RF in the direction of adaptation. Comparison with human psychophysical measurements under similar conditions indicates that these RF properties can primarily account for the motion-position illusions. Importantly, both RF properties indicate a spatial asymmetry in the synaptic connections from direction-selective cells, and this circuit feature can be predicted by spike-timing-dependent synaptic plasticity, a widespread phenomenon in the nervous system. Thus, motion-induced perceptual mislocalization may be mediated by asymmetric cortical circuits, as a natural consequence of experience-dependent synaptic modification during circuit development.

The purpose of the present study was to find out what particular stimulus features, in addition to the direction and velocity of motion, specifically activate neurons in the nucleus lentiformis mesencephali (nLM) in pigeons. Visual responses of 60 nLM cells to a variety of computer-generated stimuli were extracellularly recorded and quantitatively analyzed. Ten recording sites were histologically verified to be localized within nLM with cobalt sulfide markings. It was shown that the pigeon nLM cells were specifically sensitive to the leading edge moving at the optimal velocity in the preferred direction through their excitatory receptive fields (ERFs). Generally speaking, nLM cells preferred black edges to white ones. However, this preference cannot be explained by OFF-responses to a light spot. The edge sharpness was also an essential factor influencing the responsive strength, with blurred edges producing little or no visual responses at all. These neurons vigorously responded to black edge orientated perpendicular to, and moved in, the preferred direction; the magnitude of visual responses was reduced with changing orientation. The spatial summation occurred in all neurons tested, characterized by the finding that neuronal firings increased as the leading edge was lengthened until saturation was reached. On the other hand, it appeared that nLM neurons could not detect any differences in the shape and area of stimuli with an identical edge. These data suggested that feature extraction characteristics of nLM neurons may be specialized for detecting optokinetic stimuli, but not for realizing pattern recognition. This seems to be at least one of the reasons why large-field gratings or random-dot patterns have been used to study visual responses of accessory optic neurons and optokinetic nystagmus, because many high-contrast edges in these stimuli can activate a neuron to periodically discharge, or groups of neurons to simultaneously fire to elicit optokinetic reflex.

The grave interferences in the calculus of bounded capacities(BoCa) can be regarded as programming errors and could be disastrous. In order to avoid the problems and to control the movement of resources, some BoCa primitives are modified. A new calculus, the safe bounded capacities (Safe BoCa) is proposed that modifies two capacities and adds three new capabilities and two new co-capabilities. The reduction semantics is modified accordingly. A type system for the safe BoCa is given to control the mobility of ambients and the number of threads, and to guarantee that the intended capacity bounds are statically preserved throughout computation.

We propose the concept of simple perturbation of fuzzy sets, we estimate the upper and lower bounds of output error affected by perturbation parameters of input in many fuzzy reasoning schemes. Additionally, we illustrate that some fuzzy reasoning schemes are short of stability.

Plasticity in the nervous system is essential for information processing and storage. At the synaptic level, various forms of activity-dependent plasticity have been characterized, and their cellular mechanisms have been investigated intensely. At the circuitry level, sensory stimuli are known to play crucial roles in shaping the structures of neuronal circuits both during development and in adult life. At the functional level, perceptual performance of the animal can be strongly influenced by prior sensory experience. In spite of the extensive investigations at each level, however, the relationship between activity-dependent neural modifications at different levels remains to be firmly established. In this chapter, we will review a set of recent studies on spike timing-dependent plasticity in the visual cortex, the results of which support a causal link between experience-induced cortical modifications at different levels.

The circuitry and function of mammalian visual cortex are shaped by patterns of visual stimuli, a plasticity likely mediated by synaptic modifications. In the adult cat, asynchronous visual stimuli in two adjacent retinal regions controlled the relative spike timing of two groups of cortical neurons with high precision. This asynchronous pairing induced rapid modifications of intracortical connections and shifts in receptive fields. These changes depended on the temporal order and interval between visual stimuli in a manner consistent with spike timing–dependent synaptic plasticity. Parallel to the cortical modifications found in the cat, such asynchronous visual stimuli also induced shifts in human spatial perception.

In the motion-extrapolation hypothesis, the visual system can extrapolate the instantaneous position of a moving object from its past trajectory. The existence of such a mechanism in human vision has been intensely debated. Here, we show compelling perceptual extrapolation of both first- and second-order moving stimuli, the magnitude of which depends on blurring of the visual target. The spatiotemporal characteristics of the extrapolation can be quantitatively accounted for by a simple model based on temporally biphasic neuronal response, a property widely observed among sensory neurons. Thus, motion-induced perceptual extrapolation exists in human vision, and spatial blurring is an important factor in the interaction between motion and perceptual localization.

Centrifugal modulation of visual responsiveness of tectal cells by the isthmo-optic nucleus (ION) through the retina was studied in homing pigeons. Visual activity evoked by computer-generated stimuli was reduced by an average of 59% in tectal cells whose receptive fields (RFs) either overlapped with, or were close to, those of isthmo-optic cells whose activity was blocked by the injection of lidocaine through micropipettes. Activity usually recovered to 87% of pre-drug controls in 8-17 min (average 12.3 min) after stopping lidocaine injections. Those tectal cells whose RFs were far from those of ION cells did not show clear-cut changes in their visual responsiveness to isthmo-optic lidocaine application. The spatial relationship between receptive fields of tectal and isthmo-optic cells, saline controls, as well as the specificity, reproducibility and reversibility of effects of ION-injected lidocaine on tectal activity, show that this chemical action is pharmacological, not toxicological. Neuronal circuitry underlying centrifugal modulation of tectal activity by isthmo-optic cells is discussed.