Synaptic rearrangement in the ventrobasal complex of the mouse following partial cortical deafferentation

Donoghue, J.P.; Wells, Joseph

doi:10.1016/0006-8993(77)90629-1

Cited by 13 publications

(1 citation statement)

References 8 publications

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“…Following axonal injury of motoneurons in the brain stem or spinal cord, microglia are responsible for the synaptic stripping of excitatory afferents from the somata of axotomized neurons [4,15]. It is noteworthy that relay neurons in the thalamus do not exhibit synaptic stripping following cortical trauma [3,7,20]. Based on the present data, this difference could be due to the fact that microglia are devoted to the phagocytosis of degenerating corticothalamic axons.…”

Section: Discussionmentioning

confidence: 58%

Microglial and astrocytic reactions prior to onset of thalamic cell death after traumatic lesion of the rat sensorimotor cortex

et al. 2000

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The temporospatial relationship between microglial and astrocytic reactions and delayed thalamic cell death was examined 1-7 days following a traumatic cold lesion of the rat sensorimotor cortex using immunocytochemistry in combination with terminal deoxynucleotidyltransferase-mediated biotinylated dUTP nick end labeling (TUNEL) of nuclear DNA fragmentation. No or only occasional TUNEL-positive cells were found in the thalamic relay nuclei up to 3 days after trauma. After 7 days, on the other hand, a considerable number of TUNEL-positive cells were seen in the ventrobasal, the ventrolateral and posterior thalamic nuclei. Already 3 days after trauma, i.e., before cell injury was detectable, many protoplasmic astrocytes, which were reactive for glial fibrillary acidic protein, and ramified microglia, which were positive for complement receptor type 3b (CR3b) but negative for major histocompatibility complex (MHC) class II antigen, were noticed in the thalamus. The number of labeled astro- and microglia further increased after 7 days, when DNA fragmentation became evident. At this time, the morphology of microglia shifted towards bushy and rod-like cells, and microglia became also reactive for MHC class II antigen. Clusters of CR3b- and MHC class II-positive microglia were found in the ventrobasal thalamus. The present findings demonstrate that trauma-induced microglial and astrocytic reactions appear in the thalamus prior the onset of cell damage.

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Section: Discussionmentioning

confidence: 58%

Microglial and astrocytic reactions prior to onset of thalamic cell death after traumatic lesion of the rat sensorimotor cortex

et al. 2000

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The structural organization of the ventral posterolateral nucleus in the rat

McAlliser

Wells

1981

J of Comparative Neurology

132

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The structural plan of the ventral posterolateral nucleus (VLP) in the rat was analyzed by using a variety of techniques to study the pattern of distribution of the ascending afferent fibers and the synaptology of the neuropil within this somatosensory relay nucleus. Golgi stains, Fink-Heimer methods, HRP labeling methods, and electron microscopy were all used in the analysis. The neurons in VPL are aligned in rostrocaudal and dorsoventral rows that are roughly parallel to the curvature of the external medullary lamina (EML) and curve partially around the rostral pole of the ventral posteromedial nucleus (VPM). Golgi-impregnated sections reveal that the dendritic trees of the VPL neurons conform in general to the laminar pattern of VPL. Thick proximal dendrites extend about 25 mu m from the cell bodies. Most proximal dendrites are aligned with the laminae of VPL but the distal dendrites spread over many laminae within VPL. The inputs from the dorsal column nuclei (DCN) end only on proximal dendrites as large, round-vesicle terminals. About 20--25% of the small round-vesicle terminals originate in the cerebral cortex and synapse only on the distal dendrites. The third type of synapse contains many flattened vesicles and is of unknown origin. No serial synapses or vesicle-containing dendrites were observed. Input from the spinal cord projects to two segregated zones which are transitional between the ventral lateral nucleus (VL) and VPL rostrally and between the posterior thalamic complex (PO) and VPL caudally. Each transition zone contains neurons characteristic of both VPL and the adjacent region. Ascending afferent projections were demonstrated by the antegrade transport of HRP following injections into the ventral mesencephalon and by Fink-Heimer stains of degeneration resulting from small lesions of the DCN. Both methods indicate that large-caliber axons course parallel to each other and give off collaterals that diverge to widespread areas of the VPL. The widespread terminal fields that result do not conform to the laminar pattern of the nucleus. Small punctate lesions of DCN result in sparse degeneration that is also widespread in VPL. Structures which appear to be clusters of terminal arborizations of the ascending afferent input were also observed in VPL. These results suggest that somatotopy and modality separation in VPL may be determined either by intrinsic and/or corticothalamic morphological relationships and not by precise topographical ordering of sensory input.

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Morphological alterations in subcortical vibrissal relays following vibrissal follicle destruction at birth in the mouse

Hámori

Savy

Madarász

et al. 1986

J of Comparative Neurology

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Morphological modifications of two subcortical vibrissal relays were analyzed, following destruction of vibrissal follicles in newborn mice. The volume of the nucleus interpolaris (NI) of the trigeminal nuclear complex in the brainstem decreased by 33%, while the number of its neuronal perikarya decreased only moderately. Vibrissal deafferentation caused no shrinkage of the ventrobasal complex (VB). In the damaged medial vibrissal part of VB (VBm), however, neuronal density was higher than normal, indicating the prevention or retardation of physiologically programmed cell death in the afferentation deprived thalamic somatosensory relay station. It is suggested that the difference in neuron density produced by deafferentation is related to the states of maturation at birth of the two subcortical vibrissal relays. Following vibrissal deafferentation the basic organization of the synaptic neuropil appeared to be similar to the control. Quantitative electron microscopic (EM) analysis revealed, however, an increased number of axon terminals with ovoid synaptic vesicles in both deafferented relay stations. The increased density of gamma-aminobutyric acid (GABA)-immunostained boutons observed in the VBm following vibrissal deprivation suggested a compensatory increase most probably of the inhibitory axon endings. Quantitative EM analysis also provided evidence that many or most of the specific afferent terminals in the damaged VBm were not identical with but were substitutes for the original "vibrissal" specific afferents. Forty percent of all "specific" afferents were shown to be modified corticothalamic terminals. The modification and the resemblence of some cortical endings to specific afferents demonstrated the morphogenetic plasticity of synaptogenesis in these terminals during development as well as the importance and inductive potential of the postsynaptic target in the differentiation of presynaptic axon terminals.

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Synaptic rearrangement in the ventrobasal complex of the mouse following partial cortical deafferentation

Cited by 13 publications

References 8 publications

Microglial and astrocytic reactions prior to onset of thalamic cell death after traumatic lesion of the rat sensorimotor cortex

Microglial and astrocytic reactions prior to onset of thalamic cell death after traumatic lesion of the rat sensorimotor cortex

The structural organization of the ventral posterolateral nucleus in the rat

Morphological alterations in subcortical vibrissal relays following vibrissal follicle destruction at birth in the mouse

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