Lawrence E. Mays

Movement fields of saccade-related burst neurons in the monkey superior colliculus

The presaccadic burst of superior colliculus (SC) neurons was examined in detail to determine whether or not information concerning the vector components (amplitude and direction) of a saccade is contained within the burst. Results indicate that the pattern of spike activity originating from a single saccade-related burst neuron in the SC does not encode saccade direction or amplitude. Identical discharges may precede a wide range of saccades. Neither the magnitude, configuration nor timing of the discharge are related in any unique way to the duration of the saccade alone or the amplitude of the saccade alone. Furthermore, it is unlikely that information concerning saccade amplitude or direction is encoded by different types of signals originating from different SC neurons. For different neurons, there is no consistent relationship between the parameters of the burst and the optimal saccade amplitude or direction. It is suggested that the discharge of saccade-related burst neurons of the SC serves as a trigger input to pontine circuitry generating the required saccadic burst signals. Information concerning saccade direction and amplitude is not contained within the trigger signal, but must be extracted from the spatial distribution of SC activity.

Neuronal circuitry controlling the near response.

Experiments in primates have contributed greatly to our understanding of the neural mechanisms involved in the eye movements required to view objects at different distances. Early work focused on the circuitry for generating horizontal vergence eye movements alone. However, vergence eye movements are associated with lens accommodation and are usually accompanied by saccadic eye movements, so more recent work has been directed at understanding the interactions between vergence and accommodation, and between vergence and saccades. A new model explains the neural basis for interactions between vergence and accommodation by a neural network in which pre-motor elements are shared by these two systems. The effects of saccades on vergence eye movements appear to be the result of shared pre-motor circuits as well. Current evidence suggests that pontine omnipause neurons, known to be crucial for the generation of saccades, play an important role in the vergence pre-motor circuitry.

A Neural Mechanism Subserving Saccade-Vergence Interactions

Abstract When a saccade occurs during a vergence movement, the amplitudes of the saccades in the two eyes may be markedly unequal (Ono, Nakamizo & Steinbach, 1978; Kenyon, Ciuffreda & Stark, 1980). This results in a large increase in vergence velocity, regardless of the direction of the saccade or vergence movement. The observation of unequal saccades in the two eyes has led to speculation that humans retain circuitry which allows relatively independent control of the movements of the two eyes (Enright, 1984). This hypothesis is notable because, if it were correct, it would require an extensive revision of our basic models of oculomotor control systems. We report experiments which suggest an alternative hypothesis: saccadic facilitation of vergence results from the interruption of inhibition of vergence burst neurons by pontine omnipause neurons, which are involved in initiating saccades.

Serotonergic modulation of eye blinks in cat and monkey

Serotonergic modulation of spontaneous and reflexive blinking was studied in four cats and one monkey. In cats, facial nucleus injections of the type-2 serotonin receptor (5-HT2) antagonist ketanserin tended to increase the latency of the first (R1) and second (R2) components of the blink reflex to supraorbital nerve stimulation. Injections of serotonin tended to increase and of ketanserin, to decrease the duration and amplitude of R2. Serotonin also produced unilateral blepharospasm and hemifacial spasm. In the monkey, the 5-HT2 agonist 2,5-dimethoxy-4-iodoamphetamine increased spontaneous blink frequency while ketanserin decreased both peak blink velocity and spontaneous blink frequency. These findings in cat and monkey indicate that serotonergic innervation of the facial nucleus has a behaviorally important role in modulation of spontaneous and reflexive blinks and suggest that dysfunction of serotonergic systems could be important to the pathophysiology of some cases of blepharospasm.

Role of the Monkey Superior Colliculus in the Spatial Localization of Saccade Targets

It has long been recognized that information about the position of the eyes in the orbit plays an important role in the perception of visual direction. With the eyes, head, and body stationary, there is a one-to-one correspondence between the direction of a visual stimulus and the location of its image on the retina. However, since the eyes do not remain stationary, the perception of visual direction must be based upon a combination of information about the location of the retinal image and the position of the eyes in the orbit (Helmholtz, 1866; Hoist & Mittelstaedt, 1950; Matin, 1972; Shebilske, 1977; Skavenski, 1976).

Properties of Saccade-Related Unit Activity In the Monkey Superior Colliculus

The foveation hypothesis of SCHILLER and KOERNER (1) maintains that the superior colliculus (SC) is part of a neural system which acquires visual targets for foveal viewing. The SC is thought to be involved in coding the location of an object relative to the fovea and in eliciting saccadic movements which produce foveal acquisition of the object. A major line of evidence offered in support of this hypothesis is the finding that neurons in the intermediate and deeper layers of the SC discharge maximally prior to eye movements with a particular direction and amplitude (1–9). These neurons have a movement field — that is, the neurons discharge prior to a range of movements of similar directions and amplitudes. However, the temporal relationship between the spike discharge and saccade onset has not been examined carefully. Furthermore, it has been suggested that the discharge of SC neurons reflects an attentional mechanism rather than a command to initiate a particular saccade (10,11).