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Can lithium enhance the extent of axon regeneration and neurological recovery following peripheral nerve trauma?

ABSTRACT: The clinical "gold standard" technique for attempting to restore function to nerves with a gap is to bridge the gap with sensory autografts. However, autografts induce good to excellent recovery only across short nerve gaps, in young patients, and when repairs are performed a short time post nerve trauma. Even under the best of conditions, < 50% of patients recover good recovery. Although many alternative techniques have been tested, none is as effective as autografts. Therefore, alternative techniques are required that increase the percentage of patients who recover function and the extent of their recovery. This paper examines the actions of lithium, and how it appears to trigger all the cellular and molecular events required to promote axon regeneration, and how both in animal models and clinically, lithium administration enhances both the extent of axon regeneration and neurological recovery. The paper proposes more extensive clinical testing of lithium for its ability and reliability to increase the extent of axon regeneration and functional recovery.

SUBMITTER: Kuffler DP

PROVIDER: S-EPMC8552832 | biostudies-literature | 2022 May

REPOSITORIES: biostudies-literature

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Can lithium enhance the extent of axon regeneration and neurological recovery following peripheral nerve trauma?

Kuffler Damien P DP

Neural regeneration research 20220501 5

The clinical "gold standard" technique for attempting to restore function to nerves with a gap is to bridge the gap with sensory autografts. However, autografts induce good to excellent recovery only across short nerve gaps, in young patients, and when repairs are performed a short time post nerve trauma. Even under the best of conditions, < 50% of patients recover good recovery. Although many alternative techniques have been tested, none is as effective as autografts. Therefore, alternative tec ...[more]

PMID: 34558506

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Project description:INTRODUCTION:Neonatal hypoxia-ischemic brain damage (HIBD) can lead to serious neuron damage and dysfunction, causing a significant worldwide health problem. bFGF as a protective reagent promotes neuron repair under hypoxia/ischemia (HI). However, how bFGF and downstream molecules were regulated in HI remains elusive. METHODS:We established an in vitro HI model by culturing primary cortical neurons and treated with oxygen-glucose deprivation (OGD). We suppressed the expression of bFGF by using siRNA (small interfering RNA) interference to detect the neuronal morphological changes by immunofluorescence staining. To determine the potential mechanisms regulated by bFGF, the change of downstream molecular including IL-1? was examined in bFGF knockdown condition. IL-1? knockout (KO) rats were generated using CRISPR/Cas9-mediated technologies. We used an accepted rat model of HI, to assess the effect of IL-1? deletion on disease outcomes and carried out analysis on the behavior, histological, cellular, and molecular level. RESULTS:We identified that OGD can induce endogenous expression of bFGF. Both OGD and knockdown of bFGF resulted in reduction of neuron numbers, enlarged cell body and shortened axon length. We found molecules closely related to bFGF, such as interleukin-1? (IL-1?). IL-1? was up-regulated after bFGF interference under OGD conditions, suggesting complex signaling between bFGF and OGD-mediated pathways. We found HI resulted in up-regulation of IL-1? mRNA in cortex and hippocampus. IL-1? KO rats markedly attenuated the impairment of long-term learning and memory induced by HI. Meanwhile, IL-1?-/- (KO, homozygous) group showed better neurite growth and less apoptosis in OGD model. Furthermore, serine/threonine protein kinase (AKT1) mRNA and protein expression was significantly up-regulated in IL-1? KO rats. CONCLUSIONS:We showed that IL-1?-mediated axon regeneration underlie the mechanism of bFGF for the treatment of HIBD in neonatal rats. Results from this study would provide insights and molecular basis for future therapeutics in treating HIBD.

Dataset Information

Can lithium enhance the extent of axon regeneration and neurological recovery following peripheral nerve trauma?

Publications

Can lithium enhance the extent of axon regeneration and neurological recovery following peripheral nerve trauma?

Similar Datasets

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