When looking between targets located in three-dimensional space, information about relative depth is sent from the visual cortex to the motor control centers in the brainstem, which are responsible for generating appropriate motor commands to move the eyes. Surprisingly, how the neurons in the brainstem use the depth information supplied by the visual cortex to precisely aim each eye on a visual target remains highly controversial. This review will consider the results of recent studies that have focused on determining how individual neurons contribute to realigning gaze when we look between objects located at different depths. In particular, the results of new experiments provide compelling evidence that the majority of saccadic neurons dynamically encode the movement of an individual eye, and show that the time-varying discharge of the saccadic neuron population encodes the drive required to account for vergence facilitation during disconjugate saccades. Notably, these results suggest that an additional input (i.e. from a separate vergence subsystem) is not required to shape the activity of motoneurons during disconjugate saccades. Furthermore, whereas motoneurons drive both fast and slow vergence movements, saccadic neurons discharge only during fast vergence movements, emphasizing the existence of distinct premotor pathways for controlling fast vs. slow vergence. Taken together, these recent findings contradict the traditional view that the brain is circuited with independent pathways for conjugate and vergence control, and thus provide an important new insight into how the brain controls three-dimensional gaze shifts.

Van Horn MR, Sylvestre PA, Cullen, KE. The brain stem saccadic burst generator encodes gaze in three-dimensional space. J Neurophysiol 99: 2602-2616, 2008. First published March 12, 2008 doi:10.1152/jn.01379.2007. When we look between objects located at different depths the horizontal movement of each eye is different from that of the other, yet temporally synchronized. Traditionally, a vergence-specific neuronal subsystem, independent from other oculomotor subsystems, has been thought to generate all eye movements in depth. However, recent studies have challenged this view by unmasking interactions between vergence and saccadic eye movements during disconjugate saccades. Here, we combined experimental and modeling approaches to address whether the premotor command to generate disconjugate saccades originates exclusively in "vergence centers." We found that the brain stem burst generator, which is commonly assumed to drive only the conjugate component of eye movements, carries substantial vergence-related information during disconjugate saccades. Notably, facilitated vergence velocities during disconjugate saccades were synchronized with the burst onset of excitatory and inhibitory brain stem saccadic burst neurons (SBNs). Furthermore, the time-varying discharge properties of the majority of SBNs (Ͼ70%) preferentially encoded the dynamics of an individual eye during disconjugate saccades. When these experimental results were implemented into a computer-based simulation, to further evaluate the contribution of the saccadic burst generator in generating disconjugate saccades, we found that it carries all the vergence drive that is necessary to shape the activity of the abducens motoneurons to which it projects. Taken together, our results provide evidence that the premotor commands from the brain stem saccadic circuitry, to the target motoneurons, are sufficient to ensure the accurate control shifts of gaze in three dimensions. I N T R O D U C T I O NPrecisely coordinating the movements of our eyes is critical for achieving an accurate visual perception in a three-dimensional world. In particular, unequal yet tightly controlled rotations of the eyes must be programmed whenever the point of fixation is shifted between objects located at different depths. The difference between the rotations of the eyes is referred to as a vergence eye movement. Traditionally saccadic and vergence eye movements are considered as two distinct subclasses of eye movements generated by largely distinct neuronal circuitries. However, numerous studies have provided results that argue against this view. Vergence velocities are greater than what would be predicted by a linear summation of a conjugate saccade with a saccade-free vergence movement, while conjugate velocities are decreased

The development of new techniques to study glial cells has revealed that they are active participants in the development of functional neuronal circuits. Calcium imaging studies demonstrate that glial cells actively sense and respond to neuronal activity. Glial cells can produce and release neurotransmitter-like molecules, referred to as gliotransmitters, that can in turn influence the activity of neurons and other glia. One putative gliotransmitter, D-serine is believed to be an endogenous co-agonist for synaptic N-methyl-D-aspartate receptors (NMDARs), modulating synaptic transmission and plasticity mediated by this receptor. The observation that D-serine levels in the mammalian brain increase during early development, suggests a possible role for this gliotransmitter in normal brain development and circuit refinement. In this review we will examine the data that D-serine and its associated enzyme serine racemase are developmentally regulated. We will consider the evidence that D-serine is actively released by glial cells and examine the studies that have implicated D-serine as a critical player involved in regulating NMDAR-mediated synaptic transmission and neuronal migration during development. Furthermore, we will consider how dysregulation of D-serine may play an important role in the etiology of neurological and psychiatric diseases.

No abstract

The rostral superior colliculus (rSC) encodes position errors for multiple types of eye movements, including microsaccades, small saccades, smooth pursuit, and fixation. Here we address whether the rSC contributes to the development of neural signals that are suitable for controlling vergence eye movements. We use both single-unit recording and microstimulation techniques in monkey to answer this question. We found that vergence eye movements can be evoked using microstimulation in the rSC. Moreover, among the previously described neurons in rSC, we recorded a novel population of neurons that either increased (i.e., convergence neurons) or decreased (i.e., divergence neurons) their activity during vergence eye movements. In particular, these neurons dynamically encoded changes in vergence angle during vergence tracking, fixation in 3D space and the slow binocular realignment that occurs after disconjugate saccades, but were completely unresponsive during conjugate or the rapid component of disconjugate saccades (i.e., fast vergence) and conjugate smooth pursuit. Together, our microstimulation and single-neuron results suggest that the SC plays a role in the generation of signals required to precisely align the eyes toward targets in 3D space. We propose that accurate maintenance of 3D eye position, critical for the perception of stereopsis, may be mediated via the rSC.