Fibrillary astrocytes proliferate in response to brain injury

Latov, Norman; Nilaver, Gajanan; Zimmerman, Earl A.; Johnson, William G.; Silverman, Ann‐Judith; Defendini, Richard; Côté, Lucien J.

doi:10.1016/0012-1606(79)90127-1

Cited by 379 publications

(83 citation statements)

References 19 publications

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“…2 A). As described for endogenous GFAP and for transgenic reporter expressions (Latov et al, 1979;Mathewson and Berry, 1985;Salhia et al, 2000;Nolte et al, 2001), large numbers of astrocytes located around the wound lesion (100 -500 m) exhibited strong GFP expression in GFAP/GFP transgenic slices, in both the cell bodies and processes ( Fig. 2 B, C).…”

Section: Methodssupporting

confidence: 56%

“…2 B, C). Moreover, astrocytes in the hemisphere ipsilateral to the wound showed the typical hypertrophy described for stab injury-induced reactive astrogliosis (Latov et al, 1979;Mathewson and Berry, 1985; Salhia et al, 2000;Nolte et al, 2001). Thus, although resting astrocytes in the contralateral cortex were ϳ4 m in size and showed extremely thin processes (Fig.…”

Section: Methodsmentioning

confidence: 74%

“…Lesioned mice were used 2 d later. Reactive astrocytes were recognized by the increased GFP fluorescence signal and their typical hypertrophied morphology (Latov et al, 1979;Mathewson and Berry, 1985;Salhia et al, 2000;Nolte et al, 2001).…”

Section: Methodsmentioning

confidence: 99%

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Neuronal Activity Regulates Correlated Network Properties of Spontaneous Calcium Transients in AstrocytesIn Situ

et al. 2002

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Spontaneous neuronal activity is essential to neural development. Until recently, neurons were believed to be the only excitable cells to display spontaneous activity. However, cultured astrocytes and, more recently, astrocytes in situ are now known to exhibit spontaneous Ca 2ϩ transients. Here we used Ca 2ϩ imaging of astrocytes from transgenic mice for the simultaneous monitoring of [Ca 2ϩ ] i changes in large numbers of astrocytes. We found that spontaneous activity is a common property of most brain astrocytes that is lost in response to a lesion. These spontaneous [Ca 2ϩ ] i oscillations require extracellular and intracellular Ca 2ϩ . Moreover, network analysis revealed that most astrocytes formed correlated networks of dozens of these cells, which were synchronous with both astrocytes and neurons. We found that decreasing spontaneous [Ca 2ϩ ] i transients in neurons by TTX does not alter the number of active astrocytes, although it impairs their synchronous network activity. Conversely, bicuculline-induced epileptic patterns of [Ca 2ϩ ] i transients in neurons cause an increase in the number of active astrocytes and in their network synchrony. Furthermore, activation of non-NMDA and NMDA ionotropic glutamate receptors is required to correlate astrocytic networks. These results show that spontaneous activity in astrocytes and neurons is patterned into correlated neuronal/astrocytic networks in which neuronal activity regulates the network properties of astrocytes. This network activity may be essential for neural development and synaptic plasticity.

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Section: Methodssupporting

confidence: 56%

Section: Methodsmentioning

confidence: 74%

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Neuronal Activity Regulates Correlated Network Properties of Spontaneous Calcium Transients in AstrocytesIn Situ

et al. 2002

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“…Although IB4 is a common marker of nonpeptidergic afferents, the galactose recognized by the IB4 lectin also is expressed on microglia (Streit and Kreutzberg, 1987) and these microglia contribute to the dense IB4 expression we observed after rhizotomy. Additionally, the GFAP-and IB4-positive fiber-like processes we detected in the dorsal horn are most likely the long processes of fibrous astrocytes, i.e., fibers that contribute to gliotic scar formation in injured brain tissue (Hájos and Kálmán, 1989;Hantaz-Ambroise et al, 1994;Latov et al, 1979). Furthermore, the IB4-positive fibrous astrocytes are also present in control mice and other uninjured mouse models such as wild-type and reeler mice (see Fig.…”

Section: What Is the Source Of The Aberrant Ib4 Immunoreactivity?mentioning

confidence: 79%

L1 cell adhesion molecule is not required for small-diameter primary afferent sprouting after deafferentation

Runyan

Roy²,

Zhong³

et al. 2007

Neuroscience

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L1 is a cell adhesion molecule associated with axonal outgrowth and fasciculation during spinal cord development and may reiterate its developmental role in adults following injury; L1 is upregulated on certain sprouting and regenerating axons in adults, but it is unclear if L1 expression is necessary for, or contributes to, regrowth of axons. This study asks if L1 is required for small-diameter primary afferents to sprout by conducting unilateral dorsal rhizotomies (6 segments; T10-L2) on both wildtype and L1 mutant mice. First we determined that L1 co-localizes substantially with the peptidergic (calcitonin gene-related peptide; CGRP) but minimally with the nonpeptidergic (isolectin B4; IB4) primary afferents in intact wild-type and L1 mutant mice. However, we encountered a complication using IB4 to identify primary afferents post-rhizotomy; we detected extensive abnormal IB4 expression in the dorsal horn and dorsal columns. Much of this aberrant IB4 labeling is associated with fibrous astrocytes and microglia. Five days after dorsal rhizotomy a large decrease in peptidergic and nonpeptidergic afferents is evident on the deafferented side in both wild-type and L1 mutants. Three months after surgery the peptidergic primary afferents sprouted into the center of the denervated dorsal horn in both wild-type and mutant mice, and quantitative analyses confirmed a sprouting density of similar magnitude in both genotypes. In contrast, we did not detect sprouting in the nonpeptidergic primary afferents in either genotype. These results suggest that the absence of L1 neither diminishes nor enhances sprouting of peptidergic small-diameter primary afferent axons following a dorsal rhizotomy. Keywordscell adhesion molecule; denervated; IB4; CGRP; nociceptors; rhizotomy The cell adhesion molecule L1 (L1 CAM) is an axonal glycoprotein and a member of the immunoglobulin superfamily (Kamiguchi et al., 1997). L1 plays a role in axonal outgrowth, fasciculation, and guidance during spinal cord development (Stallcup et al., 1985;Jessell, 1988;Stoeckli and Landmesser, 1995;Orlino et al., 2000;Tran and Phelps, 2000;Akopians et al., 2003) through homophilic and various heterophilic binding partners such as integrins (αVβ3 and α5β1) and the fibroblast growth factor receptor (Kamiguchi and Lemmon, 1997 Publisher's Disclaimer: This is a PDF file of an unedited manuscript that has been accepted for publication. As a service to our customers we are providing this early version of the manuscript. The manuscript will undergo copyediting, typesetting, and review of the resulting proof before it is published in its final citable form. Please note that during the production process errors may be discovered which could affect the content, and all legal disclaimers that apply to the journal pertain. Lemmon, 1997;Castellani et al., 2000). NIH Public AccessMutations in X-linked L1 in humans cause major developmental errors and result in a group of symptoms that include corpus callosum hypoplasia, spastic paraplegia and hydrocephalus (Fran...

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“…[44,54,55]). GFAP levels increase in response to CNS injuries such as toxins, stab wounds, pharmaceutical insults, transplantation and disease (see Latov et al [33]; reviewed in Ref. [15]).…”

Section: Discussionmentioning

confidence: 99%

Region-specific astrogliosis in brains of mice heterozygous for mutations in the neurofibromatosis type 1 (Nf1) tumor suppressor

et al. 1999

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Brains from human neurofibromatosis type 1 (NF1) patients show increased expression of glial fibrillary acidic protein (GFAP), consistent with activation of astrocytes (M.L. Nordlund, T.A. Rizvi, C.I. Brannan, N. Ratner, Neurofibromin expression and astrogliosis in neurofibromatosis (type 1) brains, J. Neuropathol. Exp. Neurology 54 (1995) 588-600). We analyzed brains from transgenic mice in which the Nf1 gene was targeted by homologous recombination. We show here that, in all heterozygous mice analyzed, there are increased numbers of astrocytes expressing high levels of GFAP in medial regions of the periaqueductal gray and in the nucleus accumbens. More subtle, but significant, changes in the number of GFAP positive astrocytes were observed in the hippocampus in 60% of mutant mice analyzed. Astrocytes with elevated GFAP were present at 1 month, 2 months, 6 months and 12 months after birth. Most brain regions, including the cerebellum, basal ganglia, cerebral cortex, hypothalamus, thalamus, cortical amygdaloid area, and white matter tracts did not show any gliotic changes. No evidence of degenerating neurons was found using de Olmos' cupric silver stain. We conclude that Nf1/nf1 mice provide a model to study astrogliosis associated with neurofibromatosis type 1.

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Fibrillary astrocytes proliferate in response to brain injury

Cited by 379 publications

References 19 publications

Neuronal Activity Regulates Correlated Network Properties of Spontaneous Calcium Transients in AstrocytesIn Situ

Neuronal Activity Regulates Correlated Network Properties of Spontaneous Calcium Transients in AstrocytesIn Situ

L1 cell adhesion molecule is not required for small-diameter primary afferent sprouting after deafferentation

Region-specific astrogliosis in brains of mice heterozygous for mutations in the neurofibromatosis type 1 (Nf1) tumor suppressor

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