As a first step in analyzing the influence of various afferent projections on the development of the hamster lateral posterior nucleus, its normal organization was studied using both light and electron microscopic techniques. Rostrolateral, rostromedial, and caudal subdivisions were identified. The rostrolateral subdivision receives dense projections from the ipsilateral superior colliculus and posterior neocortex, as well as sparser, more restricted projections from the contralateral colliculus and retina. The ipsilateral colliculus is by far the major source of medium‐sized (M)terminals with round vesicles. These terminals synapse around the shafts of large central dendrites to form distinctive synaptic clusters. The contralateral colliculus and retina contribute a few M‐terminals to the clusters. In contrast, axons from the posterior neocortex form very large (RL‐)terminals with round vesicles from the posterior neocortex form very large (RL)terminals with round vesicles which synapse onto numerous appendages of a single proximal dendrite, are surrounded by glial lamellae, and rarely participate in the clusters. Axons from all four sources also form small (RS)terminals with round vesicles which synapse on the shafts of small dendrites. Finally, F‐terminals with flat or pleomorphic vesicles form symmetric synaptic contacts both within and outside the clusters. The only identified projection to the rostromedial subdivision is from the ipsilateral posterior neocortex, which contributes RL‐ and RS‐ terminals. F‐terminals are also found, but neither M‐terminals nor synaptic clusters are present. The caudal subdivision also receives RL‐ and RS‐terminals from the ipsilateral posterior neocortex. Small inputs from the ipsilateral and contralateral colliculi are present, but their axons form only RS‐terminals. No M‐terminals or synaptic clusters are found. These results indicate that a large neonatal superior colliculus lesion would eliminate the vast majority of the M‐terminals in the synaptic clusters of the ipsilateral lateral posterior nucleus. In subsequent studies (Crain and Hall, '80 a, b, c), we will examine how the remaining inputs from the retina, contralateral superior colliculus, and posterior neocortex contribute to the synaptic organization when it develops after such a lesion.
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