[Functional analysis of the thalamocortical pathways in eye movements]

Abstract

Although the roles of the thalamocortical pathways in somatic movements are well documented, their roles in eye movements have only recently been examined. The oculomotor-related areas in the frontal cortex receive inputs from the basal ganglia and the cerebellum via the thalamus. Consistent with this, neurons in the paralaminar part of the ventrolateral (VL), ventroanterior (VA), and mediodorsal (MD) nuclei and those in the intralaminar nuclei exhibit a variety of eye movement-related responses. To date, the thalamocortical pathways are known to play at least 2 roles in eye movements. First, they are involved in the generation of volitional, but not reactive, saccades. Thalamic neurons discharge during anti-saccades, which are known to be impaired in several neurological and psychiatric disorders, such as Parkinson's disease, attention deficit/hyperactivity disorder, and schizophrenia. In addition, neurons in the thalamus also exhibit a gradual increase in firing rate that predicts the timing of self-initiated saccades. Recent inactivation experiments have established the causal roles of these thalamic signals in the generation of volitional saccades. Second, the thalamocortical pathways transmit the efference copy signals for eye movements. During inactivation of the MD thalamus, which relays signals from the superior colliculus to the frontal eye field (FEF), the accuracy of the saccade is reduced in tasks requiring efference copy signals. In addition, inactivation of the same pathways reduces the predictive visual response associated with saccades in neurons in the FEF. Moreover the VL thalamus has been reported to play a role in monitoring smooth pursuit. While the functional analysis of thalamocortical pathways in eye movements is just a beginning, the anatomical data suggest their important roles. Analysis of eye movement control may shed light on the functions of the thalamocortical pathways in general, and may reveal the neural mechanisms of cerebro-cerebellar, cerebro-basal ganglia, and cerebro-thalamic interactions.