Exp Brain Res (1986) 65: 182-188 EXp'erjmentaJ Brain Research © Springer-Verlag 1986 Cortical activity blockade prevents ocular dominance plasticity in the kitten visual cortex* H. O. Reiter!, D. M. Waitzman 2 , and M. P. Stryker 3 Division of lNeurosciences and Departments of 3Physiology and 2Neurology, University of California, San Francisco, CA 94143, USA Summary. Recordings from single units in kitten primary visual cortex show that a reversible blockade of the discharge activities of cortical neurons and geniculocortical afferent terminals by intracortical infusion of the sodium channel blocker tetrodotoxin (TTX) completely prevented the ocular dominance shift that would normally be seen after monocular deprivation. The blockade of cortical plasticity, like the blockade of discharge activity, was reversible, and plasticity was restored following recovery from the effects of TTX. These results extend previous work suggesting involvement of electrical activity at the level of the cortex in the phenomenon of cortical plasticity by demonstrating an absolute requirement for discharge activities in the primary visual cortex. Key words: Visual cortex - Plasticity - TTX - Area 17 - Ocular dominance Introduction Monocular eye occlusion during a critical period in early life leads to a change in the responses of cortical neurons, shifting the predominantly binocular responses toward monocular responses to the eye that had remained open (Wiesel and Hubel 1963). Evidence from a number of sources suggests that the discharge activities of geniculate afferents and cells within the visual cortex are involved in these drama- tic changes. Recent findings that support this notion include observations from three different labora- tories (Cynader and Mitchell 1977; Rauschecker and Singer 1981; Carlson et al. 1986) of orientation- * This work was supported by the NIH (EY02874 and EY00213) and by grants from the March of Dimes Birth Defects Founda- tion and the University of California Academic Senate Offprint requests to: M. P. Stryker (address see above) dependent shifts in the ocular of neurons following monocular exposure to a restricted range of orientations. These studies show that ocular domi- nance shifts are restricted to those populations of cortical neurons that were stimulated with the orien- tations appropriate to drive the cell. Another study supporting the notion that activity at the level of the visual cortex is responsible for plasticity is that by Shaw and Cynader (1984), in which intracortical glutamate infusions raised the spontaneous discharge rates of cortical neurons and drastically attenuated the effects of monocular deprivation. While these findings show that the cortex is involved, they do not answer the question as to whether cortical activity is essential for ocular domi- nance plasticity. We have addressed this question by blocking all discharge activity in a region of visual cortex during a period of monocular deprivation. If the discharge activity of cortical cells or geniculocor- tical afferent terminals is required for plasticity, the area of cortex subjected to activity blockade should show a normal ocular dominance distribution. A reversible activity blockade was produced by intracortical infusion of the sodium channel blocker tetrodotoxin (TTX) during a period of monocular deprivation. We report here that cortical activity blockade completely prevented the ocular domi- nance shift that would normally be seen after such a period of monocular deprivation. Methods In 12 27-32-day-old kittens placed under anesthesia (1.5-2% halothane in 70 : 30 N 2 0-0 2 ) in aseptic conditions, we implanted a sterile 33 ga stainless steel cannula into the right visual cortex (at Horsley-Clarke coordinates posterior 1, lateral 2, depth 2.5 mm from the dural surface). The cannulae were connected through silicon tubing to osmotic minipumps (Alza model 2002) that delivered 0.5 Ill/h of a sterile solution of either 10 IlM TTX