Events Occurring in the Axotomized Facial Nucleus

Nakajima, Kazuyuki; Ishijima, Takashi

doi:10.3390/cells11132068

Cited by 6 publications

(4 citation statements)

References 289 publications

(337 reference statements)

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“…A peripheral nerve axotomy model was found to be appropriate for analyzing the proliferation of microglia. For example, axotomy of the rat facial nerve does not cause the infiltration of blood-derived cells in the ipsilateral facial nucleus [ 50 , 51 , 52 ], enabling us to examine the response of microglia alone in the parenchyma ( Figure 1 A). That being said, we need to take care when mice are used for this purpose.…”

Section: The Proliferative Feature Of Microgliamentioning

confidence: 99%

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Mechanisms of Microglia Proliferation in a Rat Model of Facial Nerve Anatomy

Ishijima

Nakajima

2023

Biology

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Although microglia exist as a minor glial cell type in the normal state of the brain, they increase in number in response to various disorders and insults. However, it remains unclear whether microglia proliferate in the affected area, and the mechanism of the proliferation has long attracted the attention of researchers. We analyzed microglial mitosis using a facial nerve transection model in which the blood–brain barrier is left unimpaired when the nerves are axotomized. Our results showed that the levels of macrophage colony-stimulating factor (M-CSF), cFms (the receptor for M-CSF), cyclin A/D, and proliferating cell nuclear antigen (PCNA) were increased in microglia in the axotomized facial nucleus (axotFN). In vitro experiments revealed that M-CSF induced cFms, cyclin A/D, and PCNA in microglia, suggesting that microglia proliferate in response to M-CSF in vivo. In addition, M-CSF caused the activation of c-Jun N-terminal kinase (JNK) and p38, and the specific inhibitors of JNK and p38 arrested the microglial mitosis. JNK and p38 were shown to play roles in the induction of cyclins/PCNA and cFms, respectively. cFms was suggested to be induced through a signaling cascade of p38-mitogen- and stress-activated kinase-1 (MSK1)-cAMP-responsive element binding protein (CREB) and/or p38-activating transcription factor 2 (ATF2). Microglia proliferating in the axotFN are anticipated to serve as neuroprotective cells by supplying neurotrophic factors and/or scavenging excite toxins and reactive oxygen radicals.

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Section: The Proliferative Feature Of Microgliamentioning

confidence: 99%

“…On the other hand, the microglial cell number in the contFN did not change at any time. Since blood cells hardly infiltrate to parenchyma in rat injury models [ 50 , 51 , 52 ], the increase in microglial cells in the axotFN is ascribed primarily to the proliferation of microglia themselves.…”

Section: Rat Facial Nerve Transection Modelmentioning

confidence: 99%

Mechanisms of Microglia Proliferation in a Rat Model of Facial Nerve Anatomy

Ishijima

Nakajima

2023

Biology

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“…These cellular responses are speculated to be mediated by specific signaling pathways following facial nerve transection. Moreover, glial activity and proliferation have been reported to be closely related to motor neuron survival, repair, and regeneration [ 9 , 10 ].…”

Section: Introductionmentioning

confidence: 99%

Role of Facial Nerve Reconstruction With Anastomosis and Polyglycolic Acid Tube in Accelerating Functional Recovery After Axotomy in the Rat Facial Nucleus

Noda,

Koshu,

Takaso

et al. 2024

Cureus

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Facial nerve injuries stem from trauma or tumor surgery, triggering neurodegeneration and neuronal cell death in the facial nucleus, consequently inducing irreversible nerve paralysis. Following facial nerve transection, glial cells are activated and undergo proliferation, facilitating motor neuron survival, repair, and regeneration. Clinical approaches, including nerve anastomosis and hypoglossal nerve grafting, require delicate microscopic techniques. Recent advancements involve nerve reconstruction using polyglycolic acid (PGA) tubes, which yield nerve function improvement. However, the central pathophysiological effects of these procedures remain unclear. Therefore, using PGA tubes, we evaluated neurodegeneration and microglial inflammatory response in rats after facial nerve transection. Facial nerve functions were evaluated using vibrissae and blink reflex scores. In the end-to-end anastomosis and PGA tube reconstruction groups, a partial improvement in facial motor function was observed, with increased nerve fiber survival in the former. Approximately 90% of neurons survived in both groups, wherein gliosis exhibited increased microglial activation compared to that in the transection group. These results indicate that PGA tube-assisted nerve reconstruction post-facial nerve transection, although inferior to end-to-end anastomosis, improved certain functions and prevented neuronal cell death. Furthermore, the prolonged inflammatory response in the facial nerve nucleus underscored the correlation between neuronal function and survival and microglia.

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“…Therefore, by synthesizing and transmitting acetylcholine, cholinergic neurons play a crucial role in regulating the activity of motor neurons involved in muscle contraction. Cholinergic neurotransmitters in the facial nucleus of the CNS are downregulated after axotomy, disrupting signaling processes between nerves and muscles [8]. Axotomy impairs nerve cell functions involved in muscle movement, hindering proper synthesis and the secretion of acetylcholine.…”

Section: Introductionmentioning

confidence: 99%

Expression of ChAT, Iba-1, and nNOS in the Central Nervous System following Facial Nerve Injury

Lee,

Yoo,

Kim

et al. 2024

Antioxidants

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Facial nerve injury can cause significant functional impairment, impacting both the peripheral and central nervous systems. The present study evaluated changes in facial motor function, numbers of cholinergic neurons and microglia, and nNOS levels in the facial nucleus of the central nervous system (CNS) following peripheral facial nerve injury. Facial nerve function, as determined by eyeblink and whisker-movement reflexes, was evaluated at baseline and 1, 2, 3, 4, 8, and 12 weeks after inducing facial nerve injury through compression or axotomy. The expression of choline acetyltransferase (ChAT), ionized calcium-binding adaptor molecule 1 (Iba-1), and neuronal nitric oxide synthase (nNOS) in the facial nucleus of the CNS was analyzed 2, 4, and 12 weeks after peripheral facial nerve injury. Compression-induced facial nerve injury was found to lead to temporary facial motor impairment, whereas axotomy resulted in persistent impairment. Moreover, both compression and axotomy reduced ChAT expression and increased Iba-1 and nNOS expression in the facial nucleus, indicating upregulation of an inflammatory response and neurodegeneration. These results indicate that, compared with compression-induced injury, axotomy-induced facial nerve injury results in greater facial motor dysfunction and more persistent microglial and nitric oxide activation in the facial nucleus of the CNS.

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Events Occurring in the Axotomized Facial Nucleus

Cited by 6 publications

References 289 publications

Mechanisms of Microglia Proliferation in a Rat Model of Facial Nerve Anatomy

Mechanisms of Microglia Proliferation in a Rat Model of Facial Nerve Anatomy

Role of Facial Nerve Reconstruction With Anastomosis and Polyglycolic Acid Tube in Accelerating Functional Recovery After Axotomy in the Rat Facial Nucleus

Expression of ChAT, Iba-1, and nNOS in the Central Nervous System following Facial Nerve Injury

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