TrkB receptor antagonism inhibits stab injury induced proliferative response in adult zebrafish (Danio rerio) brain

Anand, Surendra Kumar; Mondal, Amal Chandra

doi:10.1016/j.neulet.2018.02.040

Cited by 18 publications

(18 citation statements)

References 29 publications

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“…Inducing an injury in the mid‐dorsal region of the right telencephalic hemisphere in zebrafish causes a dramatic increase in the proliferation of neural progenitors. However, if the injured zebrafish is treated with TrkB antagonist ANA‐12, the proliferation fails to increase and remains comparable to the baseline level (Anand & Mondal, ). In case of an experimentally induced injury in the dorsolateral telencephalon of zebrafish brain, BDNF mRNA level increases considerably after 1 day, followed by a progressive decline at 4, 7, and 15 days (Cacialli, D'Angelo, et al, ).…”

Section: Bdnf In Adult Neurogenesismentioning

confidence: 99%

Neuroanatomical distribution and functions of brain‐derived neurotrophic factor in zebrafish (Danio rerio) brain

Anand

Mondal

2019

J of Neuroscience Research

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Brain‐derived neurotrophic factor (BDNF) is an extensively studied protein that is evolutionarily conserved and widely distributed in the brain of vertebrates. It acts via its cognate receptors TrkB and p75NTR and plays a central role in the developmental neurogenesis, neuronal survival, proliferation, differentiation, synaptic plasticity, learning and memory, adult hippocampal neurogenesis, and brain regeneration. BDNF has also been implicated in a plethora of neurological disorders. Hence, understanding the processes that are controlled by BDNF and their regulating mechanisms is important. Although, BDNF has been thoroughly studied in the mammalian models, contradictory effects of its functions have been reported on several occasions. These contradictory effects may be attributed to the sheer complexity of the mammalian brain. The study of BDNF and its associated functions in a simpler vertebrate model may provide some clarity about the effects of BDNF on the neurophysiology of the brain. Keeping that in mind, this review aims at summarizing the current knowledge about the distribution of BDNF and its associated functions in the zebrafish brain. The main focus of the review is to give a comparative overview of BDNF distribution and function in zebrafish and mammals with respect to distinct life stages. We have also reviewed the regulation of bdnf gene in zebrafish and discussed its role in developmental and adult neurogenesis.

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Section: Bdnf In Adult Neurogenesismentioning

confidence: 99%

Neuroanatomical distribution and functions of brain‐derived neurotrophic factor in zebrafish (Danio rerio) brain

Anand

Mondal

2019

J of Neuroscience Research

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“…In fish, pro and mature BDNF proteins exist [ 38 , 41 , 42 , 43 , 44 , 139 ], and in homogenates’ brains of Turquoise killifish, both forms are present [ 78 ]. In adult zebrafish, the presence of the TrkB protein was generally reported in the brain [ 140 ] and in the cerebellum [ 97 ], and treatment with the selective TrkB antagonist, ANA-12, after stab injury reduced the proliferation activity in the adult zebrafish brain [ 141 ]. In addition, in the brain of the adult Turquoise killifish, the TrkB protein was identified in neurons of different regions of the forebrain and in radial glial cells lining the mesencephalic and rhombencephalic ventricles [ 142 ].…”

Section: Bdnf and Adult Neurogenesis Neuroregeneration In Vertebrmentioning

confidence: 99%

BDNF, Brain, and Regeneration: Insights from Zebrafish

Lucini

D’Angelo

Cacialli

et al. 2018

IJMS

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Zebrafish (Danio rerio) is a teleost fish widely accepted as a model organism for neuroscientific studies. The adults show common basic vertebrate brain structures, together with similar key neuroanatomical and neurochemical pathways of relevance to human diseases. However, the brain of adult zebrafish possesses, differently from mammals, intense neurogenic activity, which can be correlated with high regenerative properties. Brain derived neurotrophic factor (BDNF), a member of the neurotrophin family, has multiple roles in the brain, due also to the existence of several biologically active isoforms, that interact with different types of receptors. BDNF is well conserved in the vertebrate evolution, with the primary amino acid sequences of zebrafish and human BDNF being 91% identical. Here, we review the available literature regarding BDNF in the vertebrate brain and the potential involvement of BDNF in telencephalic regeneration after injury, with particular emphasis to the zebrafish. Finally, we highlight the potential of the zebrafish brain as a valuable model to add new insights on future BDNF studies.

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“…Therefore, suppression of microglia activation could have a beneficial effect after GMH. TrkB is the high affinity receptor for several neurotrophins, such as BDNF, NT-4 and NT-3 (Khan and Smith 2015, Anand and Mondal 2018, Esmaeili, Pakravan et al 2018. Its expression level is relatively high in the brain tissues.…”

Section: Introductionmentioning

confidence: 99%

NT-4 attenuates neuroinflammation via TrkB/PI3K/FoxO1 pathway after germinal matrix hemorrhage in neonatal rats

Wang

Zhang

Ding

et al. 2020

Preprint

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Background: Neuroinflammation plays an important role in pathogenesis of germinal matrix hemorrhage (GMH). Neurotrophin-4 (NT-4) is a member of the neurotrophin family, and it interacts with the tyrosine kinase B (TrkB) receptor. It has been studied that NT-4 has neuroprotective effects following cerebral ischemia. We aimed to investigate the neuroprotective function of NT-4 and it’s high affinity receptor TrkB as well as its downstream mediator phosphatidylinositol-3-kinases (PI3K)/protein kinase B (Akt)/Forkhead box protein O1 (FoxO1) following GMH in neonatal rats, with a specific focus on inflammation. Methods: GMH was induced by intraparenchymal injection of bacterial collagenase (0.3U) in P7 rat pups. A total of 163 seven-day-old pups were used in this study. The recombinant human NT-4 was administered intranasally at 1 hour after the collagenase injection. The selective TrkB antagonist ANA-12, selective PI3K inhibitor LY294002 and FoxO1 activating CRISPR were administered intracerebroventricularly at 24 hours prior to NT-4 treatment to investigate the potential mechanism. Short-and-long-term neurobehavior assessments, immunofluorescence staining, Nissl’s staining and Western blot were performed. Results ： The expression of p-TrkB increased after GMH with a peak at day3. The TrkB receptor was expressed by neurons, microglia, and astrocytes. The administration of rh-NT-4 increased phosphorylation of TrkB, expression of PI3K, phosphorylation of Akt and decreased FoxO1, IL-1beta and IL-6 levels. Selective inhibition of TrkB/PI3K/Akt signaling in microglia increased the expression levels of FoxO1 and pro-inflammatory cytokines. The use of FoxO1 activation CRISPR increased the expression of IL-6, suggesting that FoxO1 might potentially induce pro-inflammatory factors. These results demonstrated that PI3K/Akt/FoxO1 may be the downstream pathway of TrkB phosphorylation. The rat pups treated with rh-NT-4 performed better than untreated animals both in short-and-long-term behavior test. Conclusion： These data showed that rh-NT-4 can reduce the expression of pro-inflammatory cytokines, improve neurological function, attenuate neuroinflammation and post-hemorrhagic hydrocephalus after GMH by promoting TrkB/PI3K/Akt/FoxO1 pathway. These results indicated that rh-NT-4 could be a promising therapeutic target to ameliorate neuroinflammation and hydrocephalus after GMH or other similar brain injuries.

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TrkB receptor antagonism inhibits stab injury induced proliferative response in adult zebrafish (Danio rerio) brain

Cited by 18 publications

References 29 publications

Neuroanatomical distribution and functions of brain‐derived neurotrophic factor in zebrafish (Danio rerio) brain

Neuroanatomical distribution and functions of brain‐derived neurotrophic factor in zebrafish (Danio rerio) brain

BDNF, Brain, and Regeneration: Insights from Zebrafish

NT-4 attenuates neuroinflammation via TrkB/PI3K/FoxO1 pathway after germinal matrix hemorrhage in neonatal rats

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