Effect of axotomy on perineuronal glial cells in the hypoglossal and dorsal motor vagal nuclei of the cat

Cova, John L.; Aldskogius, Håkan

doi:10.1016/0014-4886(86)90187-1

Cited by 16 publications

(2 citation statements)

References 17 publications

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“…Within the first days after this injury, microglial cells proliferate in the vicinity of the axotomized motoneuron perikarya (for review, see and in central termination areas of peripherally axotomized dorsal root ganglion cells . As a result, there is a marked increase locally in the number of these cells (Cova and Aldskogius, 1986;Cova et al, 1988), a reaction peaking about 1 to 2 weeks postinjury . Concomitantly, astrocytes undergo hypertrophy, as evidenced by the marked increase in immunoreactivity for the major astroglial cell intermediate filament protein, glial fibrillary acidic protein, GFAP (Cheng et al, 1994;Eriksson et al, 1997;Garrison et al, 1991;Gilmore et al, 1990;Hajos et al, 1990;Murray et al, 1990;, and its mRNA (Eriksson et al, 1997).…”

Section: Introductionmentioning

confidence: 97%

Glial cell responses, complement, and clusterin in the central nervous system following dorsal root transection

Liu

Persson

Svensson

et al. 1998

Glia

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Section: Introductionmentioning

confidence: 97%

Glial cell responses, complement, and clusterin in the central nervous system following dorsal root transection

Liu

Persson

Svensson

et al. 1998

Glia

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“…These cellular interactions are likely mediated by many molecules acting as information molecules or signaling molecules under normal and pathological conditions. Peripheral nerve injury models, which often involve lesions from the transection of facial nerves [1,2] or hypoglossal nerves [3,4], have been shown to appropriately model the cellular interactions between neurons and glial cells. Nonetheless, the details and underlying functions of their interactions have not been adequately clarified.…”

Section: Introductionmentioning

confidence: 99%

Events Occurring in the Axotomized Facial Nucleus

Nakajima

Ishijima

2022

Cells

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Transection of the rat facial nerve leads to a variety of alterations not only in motoneurons, but also in glial cells and inhibitory neurons in the ipsilateral facial nucleus. In injured motoneurons, the levels of energy metabolism-related molecules are elevated, while those of neurofunction-related molecules are decreased. In tandem with these motoneuron changes, microglia are activated and start to proliferate around injured motoneurons, and astrocytes become activated for a long period without mitosis. Inhibitory GABAergic neurons reduce the levels of neurofunction-related molecules. These facts indicate that injured motoneurons somehow closely interact with glial cells and inhibitory neurons. At the same time, these events allow us to predict the occurrence of tissue remodeling in the axotomized facial nucleus. This review summarizes the events occurring in the axotomized facial nucleus and the cellular and molecular mechanisms associated with each event.

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Response of endogenous glial cells to motor neuron degeneration induced by toxic ricin

Streit

Kreutzberg

1988

J of Comparative Neurology

356

137

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The injection of toxic lectin from Ricinus communis into the rat facial nerve resulted in suicide transport and rapid degeneration of facial motor neurons. The reaction of glial cells to neuronal death in comparison with nerve crush lesions was studied by using lectin-HRP conjugates derived from Griffonia simplicifolia for the selective staining of microglial cells at both light and electron microscopic levels. In addition, the proliferative activity of microglia was assessed by quantification of 3H-thymidine incorporation. The astrocytic response was evaluated by light microscopic immunocytochemistry for glial fibrillary acidic protein. In the degenerating facial nucleus local microglial cells responded by rapid proliferation and phagocytosis of neuronal debris. After nerve crush, no phagocytes were observed, but microglial proliferation and perineuronal satellitosis were prominent. The astrocytic expression of glial fibrillary acidic protein in response to nerve crush proceeded gradually over a period of several weeks after which it declined, contrasting with accelerated astrocytic hypertrophy and permanent glial scarring after neuronal degeneration. These results show that the expression of glial fibrillary acidic protein by fibrous astrocytes is intensified after lethal neuronal injury compared to sublethal insults. In the absence of any observations indicating participation of hematogenous elements, it is proposed that local microglial cells transform into brain macrophages.

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Effect of axotomy on perineuronal glial cells in the hypoglossal and dorsal motor vagal nuclei of the cat

Cited by 16 publications

References 17 publications

Glial cell responses, complement, and clusterin in the central nervous system following dorsal root transection

Glial cell responses, complement, and clusterin in the central nervous system following dorsal root transection

Events Occurring in the Axotomized Facial Nucleus

Response of endogenous glial cells to motor neuron degeneration induced by toxic ricin

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