The integration of visual information is a critical task that is performed by neurons in the extrastriate cortex of the primate brain. For motion signals, integration is complicated by the geometry of the visual world, which renders some velocity measurements ambiguous and others incorrect. The ambiguity arises because neurons in the early stages of visual processing have small receptive fields, which can only recover the component of motion perpendicular to the orientation of a contour (the aperture problem). Unambiguous motion signals are located at end points and corners, which are referred to as terminators. However, when an object moves behind an occluding surface, motion measurements made at the terminators formed by the intersection of the object and the occluder are generally not consistent with the direction of object motion. To study how cortical neurons integrate these different motion cues, we used variations on the classic "barber pole" stimulus and measured the responses of neurons in the middle temporal area (MT or V5) of extrastriate cortex of alert macaque monkeys. Our results show that MT neurons are more strongly influenced by the unambiguous motion signals generated by terminators than to the ambiguous signals generated by contours. Furthermore, these neurons respond better to terminators that are intrinsic to a moving object than to those that are accidents of occlusion. V1 neurons show similar response patterns to local cues (contours and terminators), but for large stimuli, they do not reflect the global motion direction computed by MT neurons. These observations are consistent with psychophysical findings that show that our perception of moving objects often depends on the motion of terminators.

Following photoreceptor degeneration, ON and OFF retinal ganglion cells (RGCs) in the rd-1/rd-1 mouse receive rhythmic synaptic input that elicits bursts of action potentials at ∼10 Hz. To characterize the properties of this activity, RGCs were targeted for paired recording and morphological classification as either ON alpha, OFF alpha or non-alpha RGCs using two-photon imaging. Identified cell types exhibited rhythmic spike activity. Cross-correlation of spike trains recorded simultaneously from pairs of RGCs revealed that activity was correlated more strongly between alpha RGCs than between alpha and non-alpha cell pairs. Bursts of action potentials in alpha RGC pairs of the same type, i.e. two ON or two OFF cells, were in phase, while bursts in dissimilar alpha cell types, i.e. an ON and an OFF RGC, were 180 degrees out of phase. This result is consistent with RGC activity being driven by an input that provides correlated excitation to ON cells and inhibition to OFF cells. A2 amacrine cells were investigated as a candidate cellular mechanism and found to display 10 Hz oscillations in membrane voltage and current that persisted in the presence of antagonists of fast synaptic transmission and were eliminated by tetrodotoxin. Results support the conclusion that the rhythmic RGC activity originates in a presynaptic network of electrically coupled cells including A2s via a Na+-channel dependent mechanism. Network activity drives out of phase oscillations in ON and OFF cone bipolar cells, entraining similar frequency fluctuations in RGC spike activity over an area of retina that migrates with changes in the spatial locus of the cellular oscillator.

Retinal ganglion cells (RGCs

The amplitude and time course of stimulus evoked second messenger signals carried by intracellular changes in free calcium ([Ca]free) depend on the total influx of Ca2+, the fraction bound to endogenous buffer and the rate of extrusion. Estimates of the values of these three parameters in proximal dendrites of 15 mouse alpha retinal ganglion cells were made using the “added buffer” method and found to vary greatly from one experiment to the next. The variations in the measured parameters were strongly correlated across the sample of cells. This reduced the variability in the amplitude and time course of the dendritic Ca2+ signal and suggests that the expression of Ca2+ channels, binding proteins and extrusion mechanisms is homeostatically coordinated to maintain the amplitude and kinetics of the Ca2+ signal within a physiologically appropriate range.