Woodward W R, Meshul C K, Coull B M
Department of Neurology, Oregon Health Sciences University, Portland 97201.
Brain Res. 1989 Aug 7;494(1):42-54. doi: 10.1016/0006-8993(89)90142-x.
After a kainic acid lesion in the dorsal lateral geniculate nucleus of rat, retrograde axonal transport of fluorescent dyes is blocked in corticogeniculate but not in retinogeniculate neurons. This inhibition, however, can be reversed by electrical stimulation in the subcortical white matter (Woodward and Coull, Brain Research 454 (1988) 106-115). These observations suggest that retrograde axonal transport in corticogeniculate neurons is impulse-dependent and that neuronal activity in this pathway is reduced as a consequence of the lesions. To test this we examined retrograde transport of horseradish peroxidase (HRP) and cytochrome oxidase activity in the cortex of lesioned animals. Unilateral kainic acid lesions in the geniculate inhibit the retrograde transport of HRP, but this inhibition is reversed by electrical stimulation of white matter. Moreover, histochemical staining for cytochrome oxidase activity is less intense over visual cortex on the lesioned side, implying that cortical activity in intrinsic and efferent pathways is reduced as a consequence of removal of geniculate afferents. Inasmuch as the retrograde transport of HRP is dependent upon impulse activity in neurons and is thought to be mediated by synaptic vesicle recycling, these results suggest that terminals of corticogeniculate fibers survive the kainic acid lesions in the geniculate and are capable of releasing synaptic vesicles. Ultrastructural examination of lesioned geniculates strongly supports this conclusion and reveals the presence of axon terminal profiles which are filled with small round synaptic vesicles and have membrane specializations reminiscent of synaptic contacts. These terminal profiles are presumed to be of retinal and cortical origin.
