Motor neuronal and glial apoptosis in the adult facial nucleus after intracranial nerve transection

Mattsson, Per; Delfani, Kioumars; Janson, Ann Marie; Svensson, Mikael

doi:10.3171/jns.2006.104.3.411

Cited by 10 publications

(6 citation statements)

References 29 publications

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“…With respect to signals driving the stress-induced secondary hyper-ramification, we have again confirmed that chronic stress, using the repeated restraint paradigm, does not induce any measurable alterations in proteins associated with inflammation or neurodegeneration (Mattsson et al 2006;Graeber et al 2011). This finding, rather than being surprising, is consistent with observations that microglial de-ramification is associated with an increased level of inflammatory signaling within the brain (Wynne et al 2009;Kettenmann et al 2011).…”

Section: Summary and Future Directionssupporting

confidence: 87%

Chronic Stress Induced Remodeling of the Prefrontal Cortex: Structural Re-Organization of Microglia and the Inhibitory Effect of Minocycline

et al. 2012

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Recently, it has been discovered that the working memory deficits induced by exposure to chronic stress can be prevented by treating stressed animals with minocycline, a putative inhibitor of microglial activity. One of the pressing issues that now requires clarification is exactly how exposure to chronic stress modifies microglial morphology, this being a significant issue as microglial morphology is tightly coupled with their function. To examine how chronic stress alters microglial morphology, we digitally reconstructed microglia within the rat medial prefrontal cortex. Our analysis revealed that stress increased the internal complexity of microglia, enhancing ramification (i.e. branching) without altering the overall area occupied by the cell and that this effect was more pronounced in larger cells. We subsequently determined that minocycline treatment largely abolished the pro-ramifying effects of stress. With respect to mechanisms, we could not find any evidence of increased inflammation or neurodegeneration (interleukin-1β, MHC-II, CD68, terminal deoxynucleotidyl transferase dUTP nick end labeling, and activated caspase-3). We did, however, find that chronic stress markedly increased the expression of β1-integrin (CD29), a protein previously implicated in microglial ramification. Together, these findings highlight that increased ramification of microglia may represent an important neurobiological mechanism through which microglia mediate the behavioral effects of chronic psychological stress.

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Section: Summary and Future Directionssupporting

confidence: 87%

Chronic Stress Induced Remodeling of the Prefrontal Cortex: Structural Re-Organization of Microglia and the Inhibitory Effect of Minocycline

et al. 2012

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“…Our preliminary studies showed that facial motor neurons could be adequately stained by the application of 1 -4% FG after 48 h survival time, as suggested by other literature. 18,22,24,25 Injection of FG into the main trunk of the facial nerve, including injections distal to the anastomosis site can, therefore, enable the numbers of motor neurons that project their axons through the anastomosis site to be obtained. Additionally, intrathecal FG injection did not affect facial nerve function, hence the results from the present study confirmed the reliability of the FG retrograde labelling method.…”

Section: Facial Nerve Injury and Regeneration In Ratsmentioning

confidence: 99%

Abnormal Motor Reflexes and Dormant Facial Motor Neurons in Rats with Facial–Facial Anastomosis

et al. 2009

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After facial nerve injury, some post-paralysis sequelae, such as synkinesis, hemispasm and 'crocodile tears' syndrome appear. The psychosocial impact of these sequelae is unavoidable. Despite recent advances and the growing popularity of this field, the pathophysiological mechanisms of facial nerve injury and regeneration are still not well understood. In this report, an abnormal motor reflex coincident with synkinetic facial movement was examined in a rat model using the blink reflex technique. Some dormant facial motor neurons were found which could not innervate through the suture site but remained alive. These results suggest that such dormant neurons might exert roles distinct from those of re-innervated neurons during facial nerve injury and regeneration. Further study is required to elucidate the biomolecular structure and electrophysiological features of such neurons.

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“…Moreover, PACAP deficiency in PACAP knock-out mice leads to a significant delay of axonal regeneration of axotomized facial nerve confirming the role of PACAP in axonal regeneration process (Armstrong et al, 2008). On the other hand, it is possible to speculate that PAC1R downregulation after nerve axotomy may correlate to increased apoptotic death of MNs of facial motor nucleus (Mattsson et al, 2006).…”

Section: Pacap and Alsmentioning

confidence: 58%

Differential Vulnerability of Oculomotor Versus Hypoglossal Nucleus During ALS: Involvement of PACAP

et al. 2020

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Amyotrophic lateral sclerosis (ALS) is a progressive multifactorial disease characterized by the loss of motor neurons (MNs). Not all MNs undergo degeneration: neurons of the oculomotor nucleus, which regulate eye movements, are less vulnerable compared to hypoglossal nucleus MNs. Several molecular studies have been performed to understand the different vulnerability of these MNs. By analyzing postmortem samples from ALS patients to other unrelated decedents, the differential genomic pattern between the two nuclei has been profiled. Among identified genes, adenylate cyclase activating polypeptide 1 (ADCYAP1) gene, encoding for pituitary adenylate cyclaseactivating polypeptide (PACAP), was found significantly up-regulated in the oculomotor versus hypoglossal nucleus suggesting that it could play a trophic effect on MNs in ALS. In the present review, some aspects regarding the different vulnerability of oculomotor and hypoglossal nucleus to degeneration will be summarized. The distribution and potential role of PACAP on these MNs as studied largely in an animal model of ALS compared to controls, will be discussed.

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Motor neuronal and glial apoptosis in the adult facial nucleus after intracranial nerve transection

Abstract: These findings may ultimately lead to new therapeutic strategies in patients suffering from facial nerve palsy due to an intracranial lesion.

Cited by 10 publications

References 29 publications

Chronic Stress Induced Remodeling of the Prefrontal Cortex: Structural Re-Organization of Microglia and the Inhibitory Effect of Minocycline

Chronic Stress Induced Remodeling of the Prefrontal Cortex: Structural Re-Organization of Microglia and the Inhibitory Effect of Minocycline

Abnormal Motor Reflexes and Dormant Facial Motor Neurons in Rats with Facial–Facial Anastomosis

Differential Vulnerability of Oculomotor Versus Hypoglossal Nucleus During ALS: Involvement of PACAP

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