Fine structural analysis of the cortico‐striatal pathway

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Abstract
Considerable evidence has accumulated indicating that 1 neurotransmitter in the excitatory cortico-striatal tract is glutamate. Lesions of the tract result in reductions in the striatum of glutamate levels and high affinity uptake of glutamate into synaptosomes. Such lesions eliminate the neurotoxicity of the glutamate analog kainic acid when injected into the striatum. The fine structure of the cortico-striatal pathway was studied to provide evidence regarding the morphology of glutamate nerve endings. Seven days after injection of 3H-proline (20-25 .mu.Ci) into the rat frontal cortex, axonally transported label appeared in the striatum with uniform distribution in a single type of nerve ending. The labeled boutons had common round vesicles and made asymmetrical contacts, mostly with dendritic spines. This morphology is typical of excitatory synapses, and similar to that previously shown for cholinergic boutons in the striatum. In 4 animals similarly injected with 3H-proline, kainic acid was administered directly into the striatum to induce degeneration of postsynaptic elements 8-10 h before sacrifice. In areas affected by these injections, grains appear in patches, possibly resulting from glial swelling. Labeled boutons were seen almost 4 times as often in synaptic contact with degenerating dendritic elements as with normal ones. Morphological evidence as to the nature of the probable glutamatergic boutons is provided in the striatum, and the close relationship of such boutons is shown with the neurotoxic effects of kainic acid. This would be anticipated in view of the dependency of kainic acid neurotoxicity on the integrity of the cortico-striatal pathway.