Two types of Lugaro cells were identified in the cat cerebellar cortex using sections impregnated with silver nitrate by the Golgi-Kopsch method; these cells were fusiform and triangular and their bodies were located at different levels in the granular layer. Their processes were directed horizontally, vertically, or obliquely to the axis of the leaf; axons never left the cerebellar cortex. These cells should therefore be regarded as interneurons. The processes of Lugaro cells were very extended, with the result that these cells formed numerous axosomatic and axodendritic contacts with all cerebellar cortical neurons and fibers. The structural and topographical characteristics of Lugaro cells and the features of their contacts with other cells in the cerebellar cortex, taken together with data on their neurotransmitter contents, show that they function as inhibitory interneurons.
The cerebellar cortex contains five types of cell: stellate and basket cells in a molecular layer, Purkinje cells (piriform cells) in the piriform neuron layer, and granular cells and Golgi cells (large stellate neurons) in the granular layer [6]. All these neurons are identified in terms of their locations, sizes, and morphological characteristics. In addition to this large class of neuronal elements, there is a less numerous group of neurons in the cerebellar cortex. These cells are spindleshaped, spherical, or polygonal, and were first described by Golgi [5]. Subsequently, Lugaro [7, 8] and Ram6n y Cajal [3] described them in more detail. These cellular elements of the cerebellar cortex are known in the literature as Lugaro cells [6]. Further studies on these cells have been carried out in monkeys [4] and rats [1, 10, 11].The aim of the present study was to investigate these neurons in the cat cerebellar cortex and compare the results obtained with data from other animal species. MATERIALS AND METHODSStudies were carried out on adult cats aged 2-3 months and 2-week-old kittens. Under Nembutal (55 mg/kg) anesthesia, adult animals underwent intracardiac perfusion with 3.5% calcium bichromate in 10% neutral formalin; kittens were sacrificed under ether anesthesia. After material was processed by the method of Golgi-Kopsch, serial sections 100-200 #m thick were cut in the horizontal, sagittal, and frontal plains. Neurons were drawn with an RA--4 drawing apparatus, and microphotographs were taken using an MBI-6 microscope. RESULTS AND DISCUSSION
Projections of the central cerebellar nuclei to the intralaminar thalamic nuclei were studied in cats with the use of light and electron microscopy. Almost all intralaminar nuclei were shown to obtain cerebello-thaiamic projections. The entire complex of the central cerebellar nuclei serves as a source of such projections; yet, involvement of different nuclei is dissimilar. Destruction of the central and, especially, caudal regions of the fastigial nucleus evoked in the intralaminar thalamic nuclei degenerative changes in the nerve fibers (from swelling and development of varicosities up to total fragmentation). Pathological phenomena could be noticed in the most caudal regions of the above thalamic nuclear group, including the medial dorsal nucleus. Projections of the cerebellar interpositus nucleus were directedtoward nearly the same regions of the intralaminar nuclei; degeneration was more intensive (covered the centrurn medianum) when posterior regions of the interpositus nucleus were destroyed. Destruction of the lateral cerebellar nucleus evoked a similar pattern of pathological changes, but degeneration was also observed in some structures of the ventral and anterior nuclear groups of the thalamus. Electron microscopic examination showed that degeneration of dark and light types developed in the fiber preterminals and terminals. It can be concluded that the central cerebellar nuclei project not only to the ventral complex of the thatamic nuclei, but also to the anterior, medial, and intralaminar nuclear groups {roslral and caudal portions).
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Prior unilateral transection of the bulbar pyramid facilitated recovery of operant reflexes and compensatory processes occurring after removal of the ipsilateral sensorimotor cortex in rats. This increase in corticofugal plasticity was absent when only the sensorimotor cortex was removed. This phenomenon is explained by switching of descending influences to the corticorubrospinal system via the following loop: corticobulbar projection--red nucleus--lower olive--cerebellum--thalamus--cortex. A general property of this phenomenon is that prior lesioning of the peripheral part of the descending spinal projection acquires anticipatory signal value for mobilizing the compensatory abilities of the brain with the aim of recovering from the deficit of the central branch of the system.
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