Modulation by Dopamine of Rat Corticostriatal Input

Abstract

Publisher Summary Ultrastructural studies have shown that dopamine synapses are localized to the necks of dendritic spines on striatal neurons. The researchers have examined the rat neostriatum in the electron microscope to investigate whether the increase in enkephalin that follows dopamine destruction, resulted from sprouting of enkephalin-containing terminal onto the spine neck sites vacated by dopamine. Enkephalin-immunoreactive synaptic boutons have been 50% larger after dopamine denervation, but they did not contact spines more frequently than in the control striatum. Detailed spine counting revealed that the number of dendritic spines on the output cells of the striatum, from which the dopamine has been removed by a 6-hydroxydopamine injection, is reduced. In a recent study using “unbiased” stereological methods to count the number of asymmetric synapses the total number of asymmetric synapses in the striatum on the lesioned side has been reduced by about 18% that is similar to the reduction in spine density at equivalent times after the lesion. The synapses that disappear after dopamine depletion might be the most vulnerable of a system of corticostriatal synapses maintained somehow by dopamine. Thus, taking the morphological and physiological experiments together suggests that long term potentiation (LTP) induced by dopamine has morphological consequences. It could be potentiated synapses survive and in the absence of dopamine, nonpotentiated synapses are eliminated. Testing these ideas will require more detail about how potentiation happens and some pharmacological tools with which to interfere with various stages of it.