BackgroundAlthough the induction of behavioural unconsciousness during sleep and general anaesthesia has been shown to involve overlapping brain mechanisms, sleep involves cyclic fluctuations between different brain states known as active (paradoxical or rapid eye movement: REM) and quiet (slow-wave or non-REM: nREM) stages whereas commonly used general anaesthetics induce a unitary slow-wave brain state.Methodology/Principal FindingsLong-duration, multi-site forebrain field recordings were performed in urethane-anaesthetized rats. A spontaneous and rhythmic alternation of brain state between activated and deactivated electroencephalographic (EEG) patterns was observed. Individual states and their transitions resembled the REM/nREM cycle of natural sleep in their EEG components, evolution, and time frame (∼11 minute period). Other physiological variables such as muscular tone, respiration rate, and cardiac frequency also covaried with forebrain state in a manner identical to sleep. The brain mechanisms of state alternations under urethane also closely overlapped those of natural sleep in their sensitivity to cholinergic pharmacological agents and dependence upon activity in the basal forebrain nuclei that are the major source of forebrain acetylcholine. Lastly, stimulation of brainstem regions thought to pace state alternations in sleep transiently disrupted state alternations under urethane.Conclusions/SignificanceOur results suggest that urethane promotes a condition of behavioural unconsciousness that closely mimics the full spectrum of natural sleep. The use of urethane anaesthesia as a model system will facilitate mechanistic studies into sleep-like brain states and their alternations. In addition, it could also be exploited as a tool for the discovery of new molecular targets that are designed to promote sleep without compromising state alternations.

Our ability to explore our surroundings requires a combination of high-resolution vision and frequent rotations of the visual axis toward objects of interest. Such gaze shifts are themselves a source of powerful retinal stimulation, and so the visual system appears to have evolved mechanisms to maintain perceptual stability during movements of the eyes in space. The mechanisms underlying this perceptual stability can be probed in the laboratory by briefly presenting a stimulus around the time of a saccadic eye movement and asking subjects to report its position. Under such conditions, there is a systematic misperception of the probes toward the saccade end point. This perisaccadic compression of visual space has been the subject of much research, but few studies have attempted to relate it to specific brain mechanisms. Here, we show that the magnitude of perceptual compression for a wide variety of probe stimuli and saccade amplitudes is quantitatively predicted by a simple heuristic model based on the geometry of retinotopic representations in the primate brain. Specifically, we propose that perisaccadic compression is determined by the distance between the probe and saccade end point on a map that has a logarithmic representation of visual space, similar to those found in numerous cortical and subcortical visual structures. Under this assumption, the psychophysical data on perisaccadic compression can be appreciated intuitively by imagining that, around the time of a saccade, the brain confounds nearby oculomotor and sensory signals while attempting to localize the position of objects in visual space.

Amblyopia is characterised by visual deficits in both spatial vision and motion perception. While the spatial deficits are thought to result from deficient processing at both low and higher level stages of visual processing, the deficits in motion perception appear to result primarily from deficits involving higher level processing. Specifically, it has been argued that the motion deficit in amblyopia occurs when local motion information is pooled spatially and that this process is abnormally susceptible to the presence of noise elements in the stimulus. Here we investigated motion direction discrimination for abruptly presented two-frame Gabor stimuli in a group of five strabismic amblyopes and five control observers. Motion direction discrimination for this stimulus is inherently noisy and relies on the signal/noise processing of motion detectors. We varied viewing condition (monocular vs. binocular), stimulus size (5.3-18.5°) and stimulus contrast (high vs. low) in order to assess the effects of binocular summation, spatial summation and contrast on task performance. No differences were found for the high contrast stimuli; however the low contrast stimuli revealed differences between the control and amblyopic groups and between fellow fixing and amblyopic eyes. Control participants exhibited pronounced binocular summation for this task (on average a factor of 3.7), whereas amblyopes showed no such effect. In addition, the spatial summation that occurred for control eyes and the fellow eye of amblyopes was significantly attenuated for the amblyopic eyes relative to fellow eyes. Our results support the hypothesis that pooling of local motion information from amblyopic eyes is abnormal and highly sensitive to noise.

Recent psychophysical work has shown that performance on a direction discrimination task decreases with increasing stimulus size, provided the stimulus is high in contrast. This psychophysical surround suppression has been linked to the inhibitory spatial surrounds that have been observed throughout the primate visual system. In this work we have examined a temporal factor that may also contribute to psychophysical surround suppression. Consistent with previous work, we found that psychophysical surround suppression is strongest when a high-contrast motion stimulus is presented very briefly so that the appearance of the stimulus coincided with its motion. However, when a brief delay was inserted between the stimulus onset and the onset of motion, the counterintuitive effects of stimulus size disappeared. The effect of the motion onset asynchrony (MOA) was strongest when the stationary stimulus immediately preceded the stimulus motion and when stimulus orientation during the MOA was very similar to that during the motion presentation. We conclude that psychophysical surround suppression is partially linked to the temporal structure of the stimulus, more precisely to a masking effect caused by sudden stimulus onsets (and to a smaller degree stimulus offsets).