Journal of Neuroscience, Vol 6, 266-273, Copyright © 1986 by Society for Neuroscience
Doses of 6-hydroxydopamine sufficient to deplete norepinephrine are not sufficient to decrease plasticity in the visual cortex
P Trombley, EE Allen, J Soyke, CD Blaha, RF Lane and B Gordon
These experiments were designed to test Kasamatsu and Pettigrew's (1979,
1983, and see below) hypothesis that plasticity in the visual cortex
requires cortical norepinephrine (NE). Kittens were treated with various
doses of intraventricular 6-hydroxydopamine (6-OHDA) or vehicle solution.
Cortical NE content was measured with high-performance liquid
chromatography with electrochemical detection. We sutured the right eyes of
some kittens approximately 6 weeks of age for 1 week and recorded from the
left visual cortex of these kittens at the end of the week of suture. We
measured the ability of the deprived eye to drive cortical cells in animals
that received either 0.2 or 4.8 mg of 6-OHDA, and also in control animals
that received only vehicle solution. We concluded that a particular dose of
6-OHDA decreased plasticity if it increased (relative to controls) the
ability of the deprived eye to drive cortical cells. Doses of 6-OHDA as
small as 0.2 mg were sufficient to produce approximately maximal depletion
of NE but did not decrease cortical plasticity. Doses of 4.8 mg or more did
decrease cortical plasticity, although not as much as was reported by
Kasamatsu and Pettigrew. We conclude that 6-OHDA can alter cortical
plasticity but the decrease in plasticity does not result from NE
depletion.