RAPID COMMUNICATION Deficits in Smooth-Pursuit Eye Movements After Muscimol Inactivation Within the Primate’s Frontal Eye Field

Shi, Dexiu, Harriet R. Friedman, and Charles J. Bruce. Deficits aminobutyric acid (GABA) agonist. The data presented here in smooth-pursuit eye movements after muscimol inactivation show that muscimol deactivation in FEFsem profoundly imwithin the primate’s frontal eye field. J. Neurophysiol. 80: 458– pairs SP eye movements. These reversible deficits in visually 464, 1998. To evaluate smooth-pursuit (SP) function in the primate guided pursuit are similar in many aspects to the chronic SP frontal eye field (FEF), microinjections of muscimol, a g-aminodeficits caused by large aspiration lesions targeting the entire butyric acid (GABA) agonist, were used to reversibly deactivate FEF (Keating 1991, 1993; Keating et al. 1996; Lynch 1987; physiologically characterized sites in FEF. SP was severely imMacAvoy et al. 1991). The severity of pursuit deficits obpaired by deactivation at sites in the FEF’s smooth eye movement tained from these discrete inactivations by muscimol injecregion (FEFsem) located in the fundus and posterior bank of the tion indicates that, even though FEFsem is smaller than its macaque monkey’s arcuate sulcus. These SP deficits were apparent immediately after the muscimol injection and persisted for several saccadic counterpart (FEFsac), the integrity of FEFsem is hours but recovered by the next day. SP was most drastically and critical for achieving high-gain SP that matches visual target consistently impaired for directions similar to the injected site’s velocity. Parts of these data were published earlier in abstract elicited smooth eye movement direction or to the optimal SP direcform (Shi et al. 1997). tion for its neuronal responses. Targets moving in these directions,