Effects of the neurotrophic factors BDNF, NT-3, and FGF2 on dissociated neurons of the cochlear nucleus

Rak, Kristen; Völker, Johannes; Frenz, Silke; Scherzad, Agmal; Schendzielorz, Philipp; Radeloff, Andreas; Jablonka, Sibylle; Hagen, Rudolf; Mlynski, Robert

doi:10.1097/wnr.0000000000000220

Cited by 8 publications

(5 citation statements)

References 21 publications

(19 reference statements)

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“…At present, it is believed that the occurrence of POCD is caused by neuronal necrosis and apoptosis via multiple pathways. Previous animal experiments have indicated that at the onset of POCD, the expression of BDNF is markedly enhanced, which may significantly alleviate ischemic brain injury, inhibit neuronal death, and exert neuroprotective effects (35,36). In the present study, the protein expression levels of BDNF were increased following treatment of isoflurane-treated rats with nobiletin.…”

Section: Discussionsupporting

confidence: 54%

Nobiletin ameliorates isoflurane-induced cognitive impairment via antioxidant, anti-inflammatory and anti-apoptotic effects in aging rats

Zhang

Lü

et al. 2016

Molecular Medicine Reports

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A recent study reported that nobiletin is an active ingredient in Fructus Aurantii immaturus and Pericarpium Citri Reticulatae, which may be capable of preventing ischemic stroke. Therefore, the present study aimed to determine the neuroprotective effects of nobiletin, and to evaluate whether it could ameliorate isoflurane‑induced cognitive impairment via antioxidant, anti‑inflammatory and anti‑apoptotic effects in aging rats. Male Sprague‑Dawley rats (age, 18 months) were used to analyze the neuroprotective effects of nobiletin. Morris water maze test was used to determine cognitive competence. Enzyme‑linked immunosorbent assay and western blot analysis were also used to quantify nuclear factor‑κB, tumor necrosis factor (TNF)‑α, IL‑1β, IL‑6, glutathione, (GSH), GSH‑peroxidase, superoxide dismutase and malondialdehyde concentration and relevant protein expression levels Cognitive competence was increased in isoflurane-treated rats following treatment with nobiletin. In addition, as expected, nobiletin exerted antioxidant, anti-inflammatory and anti‑apoptotic effects on isoflurane‑induced cognitive impairment in aging rats. Treatment with nobiletin induced the activation of phosphorylated (p)‑Akt, p‑cAMP response element binding protein (CREB) and brain‑derived neurotrophic factor (BDNF) protein expression and reduced the levels of B‑cell lymphoma 2‑associated X protein (Bax) in isoflurane‑induced rats. In conclusion, the present study demonstrated that nobiletin may ameliorate isoflurane-induced cognitive impairment through antioxidant, anti‑inflammatory and anti‑apoptotic effects via modulation of Akt, Bax, p‑CREB and BDNF in aging rats. These findings provide support for the molecular mechanisms underlying the effects of nobiletin treatment on isoflurane-induced damage.

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Section: Discussionsupporting

confidence: 54%

Nobiletin ameliorates isoflurane-induced cognitive impairment via antioxidant, anti-inflammatory and anti-apoptotic effects in aging rats

Zhang

Lü

et al. 2016

Molecular Medicine Reports

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“…BDNF expression is absent from all auditory nuclei in the brainstem at birth (Hafidi, 1999), but BDNF and NT-3 positive neurons are widely distributed in the CN beginning in the early post-natal period at about P6 (Hafidi, 1999; Tierney et al, 2001; Wiechers et al, 1999). Further, in vitro studies of the CN, showed an upregulation of BDNF expression in the AVCN and PVCN 3 days after unilateral cochlear ablation in the guinea pig (Suneja et al, 2005), and a study of dissociated neurons of neonatal rat CN (Rak et al, 2014) demonstrated that BDNF stimulated neuronal survival and axonal outgrowth. The results of our current study showing that the total CN volume and spherical cell size were significantly larger on the BDNF-treated side than on the contralateral side, are consistent with these previously reported findings of neurotrophic effects of BDNF in the CN.…”

Section: Discussionmentioning

confidence: 99%

Effects of brain-derived neurotrophic factor (BDNF) on the cochlear nucleus in cats deafened as neonates

2016

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Many previous studies have shown significant neurotrophic effects of intracochlear delivery of BDNF in preventing degeneration of cochlear spiral ganglion (SG) neurons after deafness in rodents and our laboratory has shown similar results in developing cats deafened prior to hearing onset. This study examined the morphology of the cochlear nucleus (CN) in a group of neonatally deafened cats from a previous study in which infusion of BDNF elicited a significant improvement in survival of the SG neurons. Five cats were deafened by systemic injections of neomycin sulfate (60mg/kg, SQ, SID) starting one day after birth, and continuing for 16–18 days until auditory brainstem response (ABR) testing demonstrated profound bilateral hearing loss. The animals were implanted unilaterally at about 1 month of age using custom-designed electrodes with a drug-delivery cannula connected to an osmotic pump. BDNF (94μg/ml; 0.25μl/hr) was delivered for 10 weeks. The animals were euthanized and studied at 14–23 weeks of age. Consistent with the neurotrophic effects of BDNF on SG survival, the total CN volume in these animals was significantly larger on the BDNF-treated side than on the contralateral side. However, total CN volume, both ipsi- and contralateral to the implants in these deafened juvenile animals, was markedly smaller than the CN in normal adult animals, reflecting the severe effects of deafness on the central auditory system during development. Data from the individual major CN subdivisions (DCN, Dorsal Cochlear Nucleus; PVCN, Posteroventral Cochlear Nucleus; AVCN, Anteroventral Cochlear Nucleus) also were analyzed. A significant difference was observed between the BDNF-treated and control sides only in the AVCN. Measurements of the cross-sectional areas of spherical cells showed that cells were significantly larger in the AVCN ipsilateral to the implant than on the contralateral side. Further, the numerical density of spherical cells was significantly lower in the AVCN ipsilateral to the implant than on the contralateral side, consistent with the larger AVCN volume observed with BDNF treatment. Together, findings indicate significant neurotrophic effects of intracochlear BDNF infusion on the developing CN.

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“…They can affect the development of the nervous system in multiple ways, regulate the distribution of neurons, and promote the repair and regeneration of neurons and synapses. Studies have shown that a variety of factors, including BDNF, NT3, CNTF, GDNF, NT4/5, neurturin, artemin, TGF, and FGF[8, [27][28][29], are involved in the development of inner ear tissue and survival of hair cells and SGNs.…”

Section: Expression Of Ntfs In the Auditory Systemmentioning

confidence: 99%

Neuritin restores auditory following cochlear spiral ganglion neuron denervation of gerbils

Gui

Song

Wang

et al. 2023

Preprint

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Spiral ganglion neurons (SGNs) transmit sound signals received by hair cells to the auditory center to produce hearing. The quantity and function are important for maintaining normal hearing function. Limited by the regenerative capacity, SGNs are unable to regenerate spontaneously after injury. Various neurotrophic factors play an important role in the regeneration process. Neuritin, a neurite outgrowth factor, is a neurotrophic factor closely related to neural plasticity. In this study, we used bioinformatics analysis to show that neuritin was negatively correlated with cochlear damage. Then, we aimed to establish a cochlear spiral ganglion-specific sensorineural deafness model in gerbils using ouabain and determine the effects of exogenous neuritin protein in protecting damaged cochlear SGNs and repairing damaged auditory nerve function. The provides a new research strategy and scientific basis for the prevention and treatment of sensorineural deafness caused by the loss of SGNs. We found that neuritin is expressed throughout the development of the gerbil cochlea, primarily in the SGNs and Corti regions. The expression of neuritin was negatively correlated with the sensorineural deafness model. In vitro and in vivo revealed that neuritin significantly maintained the number and arrangement of SGNs and nerve fibers in the damaged cochlea and effectively protected the high-frequency listening function of gerbils.

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Effects of the neurotrophic factors BDNF, NT-3, and FGF2 on dissociated neurons of the cochlear nucleus

Cited by 8 publications

References 21 publications

Nobiletin ameliorates isoflurane-induced cognitive impairment via antioxidant, anti-inflammatory and anti-apoptotic effects in aging rats

Nobiletin ameliorates isoflurane-induced cognitive impairment via antioxidant, anti-inflammatory and anti-apoptotic effects in aging rats

Effects of brain-derived neurotrophic factor (BDNF) on the cochlear nucleus in cats deafened as neonates

Neuritin restores auditory following cochlear spiral ganglion neuron denervation of gerbils

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