Control of Visual Cortex Ocular Dominance Shift

Daniels, Jerry

Abstract

We propose new experiments to understand factors which control ocular dominance plasticity of neurons in developing kitten visual cortex. The study has three parts: (1) A new method of depleting norepinephrine (NE) from kitten CNS will be used to provide a definitive test of the controversial notion that the presence of catecholamines (CA) is required for plasticity. (2) Firing rates of neurons in the locus coeruleus (LC) will be altered pharmacologically, in kittens with monocular deprivation (MD), to investigate LC's role in gating plasticity. (3) Because LC's firing (and its release of NE) is much less during sleep, we will determine whether ocular dominance can be shifted if kittens receive monocular experience only during episodes of sleep. In Preliminary Results, we show that a technique well established with rodents for depleting CA's (immediate post-birth i.p. injection of 6 hydroxydopamine--600HDA--) works effectively well in kittens. We further show, however, that kittens with such permanently reduced (by 90%) levels of NE still exhibit a normal ocular dominance shift after one week of MD, i.e., plasticity is unimpaired. In the first phase of this project we propose to extend these results in two ways (a) combine immediate post-birth depletion with later minipump implant of 6-OHDA to test for non-specific effects of direct 6-OHDA application and (b) apply NE itself, or selective agonists, to test whether post-synaptic NE receptors become supersensitive and therefore compensate for lower levels of NE. In the second phase we will take advantage of selectively acting drugs, clonidine and piperoxane, to lower and rise LC neuron firing rates. If LC-released NE is responsible for ocular dominance plasticity, then these drugs should prevent or accelerate, respectively, the ocular dominance shift after MD. For the third phase, we describe a number of novel experimental precautions which will allow us to give kittens monocular experience only during normal sleep and, therefore, allow us to test whether sleep (and the correlated LC firing reductions) and ocular dominance plasticity are incompatible.