Neurofilament expression in the rat brain after cerebral infarction: effect of age

Schroeder, Eike; Vogelgesang, Silke; Popa‐Wagner, Aurel; Kessler, C.

doi:10.1016/s0197-4580(02)00063-5

Cited by 24 publications

(22 citation statements)

References 25 publications

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“…This result indicates that the accumulation of NF-200 in the mitral cell axons co-occurs with the degradation of the NF network induced by ischemia. This finding is supported by a study which found that the number of NF-200 immunostained axons was clearly increased in the penumbral region after focal cerebral ischemia in the rat [24]. These workers suggested that NF proteins are involved in response of the brain to focal ischemia, an interpretation consistent with reports that at an advanced age, trauma or damage by free oxygen radicals can lead to a degradation of the NF network, disrupting axonal and dendritic transport, and resulting in the accumulation of NFs [10,35].…”

Section: Discussionsupporting

confidence: 62%

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Transient ischemia-induced changes of neurofilament 200 kDa immunoreactivity and protein content in the main olfactory bulb in gerbils

Hwang¹,

Koh²,

Lee³

et al. 2005

Journal of the Neurological Sciences

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Section: Discussionsupporting

confidence: 62%

“…Brain injury leads to neuronal degeneration with loss of synaptic connectivity [24]. In response, compensatory axonal sprouting in the surviving deafferented neurons leads to the establishment of new synaptic contacts with other neurons [25,26].…”

Section: Discussionmentioning

confidence: 99%

Transient ischemia-induced changes of neurofilament 200 kDa immunoreactivity and protein content in the main olfactory bulb in gerbils

Hwang¹,

Koh²,

Lee³

et al. 2005

Journal of the Neurological Sciences

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“…Although we did not perform dose-response or antagonist studies to provide definitive demonstration that the effects are mediated through ␤ 2 ARs within the developing brain, the fact that the pattern of alterations mirrors the regional and temporal distribution of the receptors, incorporates the known consequences of ␤AR overstimulation on cell replication and cell death, and parallels the effects of terbutaline on cell signaling all point to a receptor-mediated origin (Joseph et al, 1983;Lorton et al, 1988;Erdtsieck-Ernste et al, 1991;Teerlink et al, 1994;Hodges-Savola et al, 1996;Communal et al, 1998;Shizukuda et al, 1998;Gu et al, 2000;Yan et al, 2000;Singh et al, 2001;Slotkin et al, 2001Slotkin et al, , 2003Garofolo et al, 2003). Using neuroprotein biomarkers for astroglia (GFAP) and proximal neuronal projections (NF68), we obtained patterns that are typical of neuronal damage and reactive gliosis: initial increases in GFAP that eventually resolve and are replaced by elevated NF68, which is associated with reactive sprouting in response to injury (O'Callaghan, 1988;Schroeder et al, 2003). There are two important features of the alterations in neuroproteins.…”

Section: Discussionmentioning

confidence: 91%

Terbutaline Is a Developmental Neurotoxicant: Effects on Neuroproteins and Morphology in Cerebellum, Hippocampus, and Somatosensory Cortex

Rhodes

Seidler²,

Abdel-Rahman³

et al. 2003

J Pharmacol Exp Ther

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␤ 2 -Adrenoceptor agonists, especially terbutaline, are widely used to arrest preterm labor, but they also cross the placenta to stimulate fetal ␤-adrenoceptors that control neural cell differentiation. We evaluated the effects of terbutaline administration in neonatal rats, a stage of neurodevelopment corresponding to human fetal development. Terbutaline administered on postnatal days PN2 to 5 elicited neurochemical changes indicative of neuronal injury and reactive gliosis: immediate increases in glial fibrillary acidic protein and subsequent induction of the 68-kDa neurofilament protein. Quantitative morphological evaluations carried out on PN30 indicated structural abnormalities in the cerebellum, hippocampus, and somatosensory cortex. In the cerebellum, PN2 to 5 terbutaline treatment reduced the number of Purkinje cells and elicited thinning of the granular and molecular layers. The hippocampal CA3 region also displayed thinning, along with marked gliosis, effects that were restricted to females. In the somatosensory cortex, terbutaline evoked a reduction in the proportion of pyramidal cells and an increase in smaller, nonpyramidal cells; again, females were affected more than males. Although abnormalities were obtained with later terbutaline treatment (PN11 to 14), in general the effects were smaller than those seen with PN2 to 5 exposure. Our results indicate that terbutaline is a neurotoxicant that elicits biochemical alterations and structural damage in the immature brain during a critical period. These effects point to a causal relationship between fetal terbutaline exposure and the higher incidence of cognitive and neuropsychiatric disorders reported for the offspring of women receiving terbutaline therapy for preterm labor.

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“…Declining levels of oestrogen with age may also underlie the larger infarct volume observed in middle-aged and older female rats [16]. With respect to age, disparity in stroke outcomes has been associated with age-related down-regulation of several proteins including NKCC (Na + –K + –Cl − co-transporter) [33], BDNF (brain-derived neurotrophic factor), bFGF (basic fibroblast growth factor) [34] and neuron-specific intermediate filaments, NFs (neurofilaments) [35]. In clinical studies, NO was shown to be reduced in serum of aged stroke patients compared with younger patients, whereas IL-6 (interleukin-6) was elevated in aged patients with a poor outcome [36].…”

Section: Discussionmentioning

confidence: 99%

Circulating miRNA profiles provide a biomarker for severity of stroke outcomes associated with age and sex in a rat model

et al. 2014

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Small non-coding RNA [miRNA (microRNA)] found in the circulation have been used successfully as biomarkers and mechanistic targets for chronic and acute disease. The present study investigated the impact of age and sex on miRNA expression following ischaemic stroke in an animal model. Adult (6 month) and middle-aged (11–12 months) female and male rats were subject to MCAo (middle cerebral artery occlusion) using ET-1 (endothelin-1). Circulating miRNAs were analysed in blood samples at 2 and 5 days post-stroke, and brain miRNAs were analysed at 5 days post-stroke. Although stroke-associated infarction was observed in all groups, infarct volume and sensory-motor deficits were significantly reduced in adult females compared with middle-aged females, adult males or middle-aged males. At 2 days post-stroke, 21 circulating miRNAs were differentially regulated and PCA (principal component analysis) confirmed that most of the variance was due to age. At 5 days post-stroke, 78 circulating miRNAs exhibited significantly different regulation, and most of the variance was associated with sex. A small cohort (five) of miRNAs, miR-15a, miR-19b, miR-32 miR-136 and miR-199a-3p, were found to be highly expressed exclusively in adult females compared with middle-aged females, adult males and middle-aged males. Predicted gene targets for these five miRNAs analysed for KEGG (Kyoto Encyclopedia of Genes and Genomes) pathways revealed that the top ten KEGG pathways were related to growth factor signalling, cell structure and PI3K (phosphoinositide 3-kinase)/Akt and mTOR (mammalian target of rapamycin) signalling. Overall, the pattern of circulating miRNA expression suggests an early influence of age in stroke pathology, with a later emergence of sex as a factor for stroke severity.

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Neurofilament expression in the rat brain after cerebral infarction: effect of age

Cited by 24 publications

References 25 publications

Transient ischemia-induced changes of neurofilament 200 kDa immunoreactivity and protein content in the main olfactory bulb in gerbils

Transient ischemia-induced changes of neurofilament 200 kDa immunoreactivity and protein content in the main olfactory bulb in gerbils

Terbutaline Is a Developmental Neurotoxicant: Effects on Neuroproteins and Morphology in Cerebellum, Hippocampus, and Somatosensory Cortex

Circulating miRNA profiles provide a biomarker for severity of stroke outcomes associated with age and sex in a rat model

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