Structural alteration and possible growth of afferents after kainate lesion in the adult rat thalamus

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Abstract
Afferents to the thalamic ventrobasal complex (VB) originating from the spinal cord, the dorsal column nuclei, and the somatosensory cortex were anterogradely labeled by WGA‐HRP 30 days after an injection of kainic acid (KA), which produced a complete unilateral neuronal loss in the VB, the opposite side being used as a control. At the light microscopic level, there was no obvious rerouting of spinal afferents away from the lesioned areas towards unlesioned parts of VB. There was an apparent decrease in the number of lemniscal afferents to the lesioned side, which may indicate a progressive retrograde degeneration. At higher magnification, all three afferent systems studied demonstrated morphological changes, predominantly manifested by terminal swellings that reached up to 25 μm in diameter. Control experiments suggested that these morphological alterations were related neither to a direct action of the excitotoxin nor to the absence of a different afferent system but to the loss of neuronal postsynaptic targets. At the electron microscopic level, the normal ultrastructural features of VB were not observed after a KA lesion. No neuronal somata, dendrites, or normal presynaptic elements were observed. Neural elements, some of which were labeled from the somatosensory cortex or the dorsal column nuclei, were essentially of two types: varicosities and unmyelinated axonal profiles. Varicosities could be separated into two broad classes: (1) The majority were large structures derived from large, sometimes myelinated, axons and containing a wealth of organelles. Since they were not completely surrounded by glial elements, we have denoted them unensheathed varicosities. Among the organelles, the most obvious features were vesicles and tubules of smooth endoplasmic reticulum, microtubules, mitochondria, and various lysosome‐like inclusions. These unensheathed varicosities gave rise to large, mound‐like protrusions containing large vacuoles and thin long protrusions either filled with neurofilaments or resembling unmyelinated axonal profiles. (2) Others were completely surrounded by a glial sheet and were therefore called ensheathed varicosities. These ensheathed varicosities presented several characteristics typical of degenerating profiles, including neurofilamentous proliferation and morphological alterations of the mitochondria. Unmyelinated axonal profiles occupied a substantial territory in the lesioned area. They were most often grouped in bundles sometimes wrapped by glial processes. The proliferation of unmyelinated fibers and the appearance of axonal varicosities are compared to the regeneration phenomena described in the literature after a lesion in the central nervous system. The hypothesis that the varicosities are growth‐cone‐like structures in the adult CNS is discussed.