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The octopus cell area (OCA) of the posteroventral cochlear nucleus was studied electron microscopically in kittens. The adult OCA, a region of morphologically homogeneous neurons receiving heterotypic synapses from the cochlea, was used to define the mature state. The OCA reaches cytological maturity at three weeks postnatally, after progression through four stages, defined on the basis of octopus cell cytology (including relative numbers of somatic and dendritic filopodia and spines) and the frequency, ultrastructure and location of previously defined synaptic terminals. Octopus cell size was also studied in rapid Golgi impregnations. The OCA from birth through three postnatal days (stage 1) showed small neurons, few identifiable synaptic types, small, mostly unmyelinated axons, mitotic cells and undifferentiated glia. Between the fourth and seventh postnatal days (stage 2) distinct type 1 and type 2 endings appeared and dendrites thickened, expanded peripherally and developed mature spines. During stage 3 (8-19 days) loss of filopodia, increased somatic spicules, larger somas and clearer differentiation of type 1 and type 2 synapses occurred. After three postnatal weeks (stage 4) the OCA contained morphologically mature octopus cell somas, all three synaptic types ending upon somas and thick basal dendrites, and fascicles of myelinated fibers. Although cytologically mature, the OCA at this stage (about 20-35 days) is substantially smaller than the adult OCA. This smaller size will facilitate further study of OCA synaptic organization.

Relatively discrete unilateral lesions were made in the lateral portion of the substantia nigra of eight cats and in the medial substantia nigra of two. After a 10-day survival period the animals were killed, brains were stored in buffered 10% formalin, and frozen sections were stained for degenerating axons and terminals, or by Weil and cresyl violet methods. Electordes passed through the midial suprasylvian gyrus, pulvinar and/or posterolateral thalamic nucleus and the medial geniculate body. The stria terminalis and hippocampus were undamaged. Degeneration from the lesion followed two paths. One projected through the reticular nucleus into the internal capsule and then ventrolaterally below the putamen to enter the lateral and central amygdaloid nuclei, with degenerated terminals. The second path ran dorsolaterally in the internal capsule to enter the external capsule where some of the fibers spread into the lateral amygdaloid nucleus. It appears that some of the terminals in the lateral amygdaloid nucleus are from the external capsule. Perhaps these connections link the extrapyramidal system to the amygdaloid body.