Changes in nuclear envelope invaginations in axotomized immature and mature hamster facial motoneurons

Jones, Kathryn J.; LaVelle, Arthur

doi:10.1016/0165-3806(85)90212-3

Cited by 26 publications

(13 citation statements)

References 17 publications

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“…Mice were anesthetized with 3% halothane for all surgical procedures. Using aseptic techniques, the right facial nerve of each animal was exposed at its exit from the stylomastoid foramen and completely transected (Serpe et al ., 1999; Jones and LaVelle, 1985). The distal nerve stump was resected and pushed away from the proximal nerve stump, thereby, preventing reconnection of the facial nerve.…”

Section: Methodsmentioning

confidence: 99%

IL-10 within the CNS is necessary for CD4+ T cells to mediate neuroprotection

Xin¹,

Wainwright²,

Mesnard³

et al. 2011

Brain, Behavior, and Immunity

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We have previously shown that immunodeficient mice exhibit significant facial motoneuron (FMN) loss compared to wild-type (WT) mice after a facial nerve axotomy. Interleukin-10 (IL-10) is known as a regulatory cytokine that plays an important role in maintaining the anti-inflammatory environment within the central nervous system (CNS). IL-10 is produced by a number of different cells, including Th2 cells, and may exert an anti-apoptotic action on neurons directly. In the present study, the role of IL-10 in mediating neuroprotection following a facial nerve axotomy model in Rag2- and IL-10-deficient mice was investigated. Results indicate that IL-10 is neuroprotective, but only in the presence of CD4+ T cells that are not the requisite source of IL-10. In addition, using real-time PCR analysis of laser microdissected brainstem sections, results show that IL-10 mRNA is constitutively expressed in the facial nucleus and that a transient, significant reduction of IL-10 mRNA occurs following axotomy under immunodeficient conditions. Dual labeling immunofluorescence data show, unexpectedly, that the IL-10 receptor (IL-10R) is constitutively expressed by facial motoneurons, but is selectively induced in astrocytes within the facial nucleus after axotomy. Thus, a non-CD4+ T cell source of IL-10 is necessary for modulating both glial and neuronal events that mediate neuroprotection of injured motoneurons, but only with the cooperation of CD4+ T cells, providing an avenue of novel investigation into therapeutic approaches to prevent or reverse motoneuron diseases, such as amyotrophic lateral sclerosis (ALS).

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Section: Methodsmentioning

confidence: 99%

IL-10 within the CNS is necessary for CD4+ T cells to mediate neuroprotection

Xin¹,

Wainwright²,

Mesnard³

et al. 2011

Brain, Behavior, and Immunity

Self Cite

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“…The mice were anesthetized with 3% isoflurane prior to and during all surgical procedures. Using aseptic techniques, the right facial nerve was exposed at its exit from the stylomastoid foramen and completely transected (Jones and LaVelle, 1985; Serpe et al, 1999). The proximal and distal facial nerve stumps were manually pushed away from each other in order to prevent reconnection.…”

Section: Methodsmentioning

confidence: 99%

Differential gene expression in the axotomized facial motor nucleus of presymptomatic SOD1 mice

Mesnard

Sanders

Jones

2011

J of Comparative Neurology

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Previously, we compared molecular profiles of one population of wild-type (WT) mouse facial motoneurons (FMNs) surviving with FMNs undergoing significant cell death after axotomy. Regardless of their ultimate fate, injured FMNs respond with a vigorous pro-survival/regenerative molecular response. In contrast, the neuropil surrounding the two different injured FMN populations contained distinct molecular differences that support a causative role for glial and/or immune-derived molecules in directing contrasting responses of the same cell types to the same injury. In the current investigation, we utilized the facial nerve axotomy model and a presymptomatic amyotrophic lateral sclerosis (ALS) mouse (SOD1) model to experimentally mimic the axonal die-back process observed in ALS pathogenesis without the confounding variable of disease onset. Pre-symptomatic SOD1 mice had a significant decrease in FMN survival compared with WT, which suggests an increased susceptibility to axotomy. Laser microdissection was used to accurately collect uninjured and axotomized facial motor nuclei of WT and presymptomatic SOD1 mice for mRNA expression pattern analyses of pro-survival/pro-regeneration genes, neuropil-specific genes, and genes involved in or responsive to the interaction of FMNs and non-neuronal cells. Axotomized pre-symptomatic SOD1 FMNs displayed a dynamic pro-survival/regenerative response to axotomy, similar to WT, despite increased cell death. However, significant differences were revealed when the axotomy-induced gene expression response of presymptomatic SOD1 neuropil was compared with WT. We propose that the increased susceptibility of presymptomatic SOD1 FMNs to axotomy-induced cell death and, by extrapolation, disease progression, is not intrinsic to the motoneuron, but rather involves a dysregulated response by non-neuronal cells in the surrounding neuropil.

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“…Testosterone is neuroprotective after facial nerve axotomy on P7 Previous work using the developing hamster facial nerve injury paradigm has established that significant cell death occurs as a result of injury during the first postnatal week LaVelle, 1958, 1984;Jones and LaVelle, 1985, 1986, 1987Clark et al, 1992Clark et al, , 1993. Based on that work and the results of the AR immunocytochemistry time-course study presented above, P7 was chosen as the best age to test the ability of gonadal steroids to rescue injured developing FMNs from axotomy-induced cell death.…”

Section: Ars First Appear In Developing Hamster Fmns By P2 In Males Amentioning

confidence: 99%

Gonadal Steroid Attenuation of Developing Hamster Facial Motoneuron Loss by Axotomy: Equal Efficacy of Testosterone, Dihydrotestosterone, and 17-β Estradiol

Huppenbauer¹,

Tanzer²,

DonCarlos³

et al. 2005

J. Neurosci.

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In the hamster facial nerve injury paradigm, we have established that androgens enhance both functional recovery from facial nerve paralysis and the rate of regeneration in the adult, through intrinsic effects on the nerve cell body response to injury and via an androgen receptor (AR)-mediated mechanism. Whether these therapeutic effects of gonadal steroids encompass neuroprotection from axotomyinduced cell death is the focus of the present study. Virtually 100% of adult hamster facial motoneurons (FMNs) survive axotomy at the stylomastoid foramen (SMF), whereas, before postnatal day 15 (P15), developing FMNs undergo substantial axotomy-induced cell death. The first part of the present study focuses on determining when ARs are first expressed in developing hamster FMNs. Using AR immunocytochemistry, it was found that males express ARs by P2 and females by P4, which is the earliest demonstration of AR expression in mammalian motoneurons reported thus far in the literature. The second half examines the neuroprotective effects of testosterone propionate, 17-␤ estradiol, and dihydrotestosterone on FMNs of P7 hamsters after facial nerve transection at the SMF. The results demonstrate that androgens and estrogens are equally able to rescue ϳ20% of FMNs from axotomy-induced cell death, with the effects permanent. This study is the first to investigate the effects of both androgens and estrogens on axotomy-induced cell death in one system and, with our previously published work, to validate the hamster FMN injury paradigm as a model of choice in the investigation of both neurotherapeutic and neuroprotective actions of gonadal steroids.

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Changes in nuclear envelope invaginations in axotomized immature and mature hamster facial motoneurons

Cited by 26 publications

References 17 publications

IL-10 within the CNS is necessary for CD4+ T cells to mediate neuroprotection

IL-10 within the CNS is necessary for CD4+ T cells to mediate neuroprotection

Differential gene expression in the axotomized facial motor nucleus of presymptomatic SOD1 mice

Gonadal Steroid Attenuation of Developing Hamster Facial Motoneuron Loss by Axotomy: Equal Efficacy of Testosterone, Dihydrotestosterone, and 17-β Estradiol

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