Our choice is influenced by choices we made in the past, but the mechanism responsible for the choice bias remains elusive. Here we show that the history-dependent choice bias can be explained by an autonomous learning rule whereby an estimate of the likelihood of a choice to be made is updated in each trial by comparing between the actual and expected choices. We found that in perceptual decision making without performance feedback, a decision on an ambiguous stimulus is repeated on the subsequent trial more often than a decision on a salient stimulus. This inertia of decision was not accounted for by biases in motor response, sensory processing, or attention. The posterior cingulate cortex and frontal eye field represent choice prediction error and choice estimate in the learning algorithm, respectively. Interactions between the two regions during the intertrial interval are associated with decision inertia on a subsequent trial.

A plane lying in depth is vividly perceived by viewing a random-dot stereogram (RDS) with a slight binocular disparity. Perception of a plane-in-depth is lost by reversing the contrast of dots seen by one of the eyes to generate an anticorrelated RDS. From a computational perspective, the visual system cannot find a globally consistent solution for matching the left and right eye images of an anticorrelated RDS. The neural representation of a global match should therefore be insensitive to binocular disparity in an anticorrelated RDS. Most neurons in the striate cortex (V1) respond to binocular disparity in anticorrelated RDSs, suggesting that further cortical processing in extrastriate areas is necessary to fully account for the matching computation. We examined neural responses to dynamic RDSs, both normal (correlated) and anticorrelated, in area V4 of the monkey visual cortex. More than half of the V4 cells were sensitive to the horizontal disparity embedded in a correlated RDS. Most of them greatly attenuated their selectivity for disparity when the RDS was anticorrelated. This attenuation was apparent from the response onset, and the degree of attenuation did not correlate with neuronal response latencies. Unlike the disparity tuning of V1 neurons to anticorrelated RDSs, that of V4 neurons was not an inversion of tuning to normal RDSs. Our results suggest that responses to false matches between contrast-reversed dots in the left and right eye images elicited in V1 are substantially reduced by the stage of V4.

Stereoscopic vision is characterized by greater visual acuity when a background feature serves as a reference. When a reference is present, the perceived depth of an object is predominantly dependent on this reference. Neural representations of stereoscopic depth are expected to have a relative frame of reference. The conversion of absolute disparity encoded in area V1 to relative disparity begins in area V2, although the information encoded in this area appears to be insufficient for stereopsis. This study examines whether relative disparity is encoded in a higher cortical area. We recorded the responses of V4 neurons from macaque monkeys to various combinations of the absolute disparities of two features: the center patch and surrounding annulus of a dynamic random-dot stereogram. We analyzed the effects of the disparity of the surrounding annulus on the tuning for the disparity of the center patch; the tuning curves of relative-disparity-selective neurons for disparities of the center patch should shift with changes in the disparity of the surrounding annulus. Most V4 tuning curves exhibited significant shifts. The magnitudes of the shifts were larger than those reported for V2 neurons and smaller than that expected for an ideal relative-disparity-selective cell. No correlation was found between the shift magnitude and the degree of size suppression, suggesting that the two phenomena are not the result of a common mechanism. Our results suggest that the coding of relative disparity advances as information flows along the cortical pathway that includes areas V2 and V4.

Stereo processing begins in the striate cortex and involves several extrastriate visual areas. We quantitatively analyzed the disparity-tuning characteristics of neurons in area V4 of awake, fixating monkeys. Approximately half of the analyzed V4 cells were tuned for horizontal binocular disparities embedded in dynamic random-dot stereograms (RDSs). Their response preferences were strongly biased for crossed disparities. To characterize the disparity-tuning profile, we fitted a Gabor function to the disparity-tuning data. The distribution of V4 cells showed a single dense cluster in a joint parameter space of the center and the phase parameters of the fitted Gabor function; most V4 neurons were maximally sensitive to fine stereoscopic depth increments near zero disparity. Comparing single-cell responses with background multiunit responses at the same sites showed that disparity-sensitive cells were clustered within V4 and that nearby cells possessed similar preferred disparities. Consistent with a recent report by Hegdé and Van Essen, the disparity tuning for an RDS drastically differed from that for a solid-figure stereogram (SFS). Disparity-tuning curves were generally broader for SFSs than for RDSs, and there was no correlation between the fitted Gabor functions' amplitudes, widths, or peaks for the two types of stereograms. The differences were partially attributable to shifts in the monocular images of an SFS. Our results suggest that the representation of stereoscopic depth in V4 is suited for detecting fine structural features protruding from a background. The representation is not generic and differs when the stimulus is broad-band noise or a solid figure.

The hippocampal mossy fiber (MF)-CA3 synapse exhibits NMDA receptor-independent long-term potentiation (LTP), which is expressed by presynaptic mechanisms leading to persistent enhancement of transmitter release. Recent studies have identified several molecules that may play an important role in MF-LTP. These include Rab3A, RIM1alpha, kainate autoreceptor, and hyperpolarization-activated cation channel (I(h)). However, the precise cellular expression mechanism remains to be determined because some studies noticed essential roles of release machinery molecules, whereas others suggested modulation of the ionotropic processes affecting Ca2+ entry into the presynaptic terminals. Using fluorescence recordings of presynaptic Ca2+ in hippocampal slices, here we demonstrated that MF-LTP is not accompanied by an increase in presynaptic Ca2+ influx during an action potential. Whole-cell recordings from CA3 neurons revealed long-lasting increases in mean frequency, but not mean amplitude, of miniature EPSCs after the high-frequency stimulation of MFs. These data indicate that the presynaptic expression mechanisms responsible for enhanced transmitter release during MF-LTP involve persistent modification of presynaptic molecular targets residing downstream of Ca2+ entry.