Journal articles: 'BDNF-TrkB signalling pathways'

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WILLIAMS, Alan G., Andrew C. HARGREAVES, Frank J. GUNN-MOORE, and Jeremy M. TAVARÉ. "Stimulation of neuropeptide Y gene expression by brain-derived neurotrophic factor requires both the phospholipase Cγ and Shc binding sites on its receptor, TrkB." Biochemical Journal 333, no. 3 (August 1, 1998): 505–9. http://dx.doi.org/10.1042/bj3330505.

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In PC12 cells, it has been previously reported that nerve growth factor stimulates neuropeptide Y (NPY) gene expression. In the current study we examined the signalling pathways involved in this effect by transiently expressing in PC12 cells the receptor (TrkB) for the related neurotrophin, brain-derived neurotrophic factor (BDNF). BDNF caused a 3-fold induction of luciferase expression from a transiently co-transfected plasmid possessing the firefly luciferase gene under the control of the NPY promoter. This effect of BDNF was completely blocked by either a Y484F mutation in TrkB (which blocks high-affinity Shc binding to TrkB) or by a Y785F substitution [which blocks the binding, phosphorylation and activation of phospholipase Cγ (PLCγ)]. Activation of the NPY promoter by neurotrophin-3 in PC12 cells overexpressing TrkC was also completely blocked by a naturally occurring kinase insert which prevents the high-affinity binding of Shc and PLCγ. NPY promoter activation by BDNF was blocked by PD98059, suggesting a role for mitogen-activated protein kinase (MAP kinase). Stimulation of NPY gene expression by PMA, but not by BDNF, was blocked by Ro-31-8220, a protein kinase C inhibitor, excluding a role for this serine/threonine protein kinase in the effect of BDNF. In addition, BDNF did not cause an elevation in cytosolic Ca2+ concentration. Taken together, our results suggest that stimulation of the NPY promoter by BDNF requires the simultaneous activation of two distinct pathways; one involves Shc and MAP kinase, and the other appears to be PLCγ-independent but requires an intact tyrosine-785 on TrkB and so may involve an effector of TrkB signalling that remains to be identified.

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Martinez-cengotitabengoa, M., K. Macdowell, S. Alberich, M. Parellada, P. Saiz, R. Rodriguez, E. Berrocoso, M. Bernardo, A. Gonzalez-pinto, and J. C. Leza. "Neutrophin signalling in first-episode psychosis: relationship with treatment response 1 year after the illness onset." European Psychiatry 33, S1 (March 2016): s258. http://dx.doi.org/10.1016/j.eurpsy.2016.01.657.

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IntroductionPro/antiinflammatory imbalance has been found in first-episode psychotic (FEP) patients, even 12 months later. Current research is every time more focused in the need to find biomarkers to understand the underlying pathophysiological mechanisms of this severe illness.ObjectivesTo assess peripherical levels of neurotrophins and their receptors and their correlation with inflammation, clinical symptomatology and response to antipsychotic treatment, over the time.MethodologyNinety-four FEP patients and 80 matched healthy controls were included. Blood samples were taken at baseline to measure BDNF and NGF and their receptor levels (TrkB-full, TrkB-truncated and TrkA) and pro/antiinflammatory parameters (NFkB, COX-2, iNOS, PPARgamma, 15d-PG12). Patients were followed-up during 12 months.ResultsBDNF TrkB-full receptor and NFG TrkA receptor levels increased during the follow-up whereas BDNF TrkB-truncated form receptor decreased. After adjusting for confounding variables, baseline levels of proinflamatory variables were significantly related to TrkB-full/TrkB-truncated ratio (FL/T), suggesting that a higher proinflammatory status is related to a higher FL/T ratio expression. Furthermore, baseline FL/T ratio could have a predictor role of patient's functionality 1 year after the illness onset, depending on whether patient is treated or not with antipsychotic drugs.ConclusionInflammatory processes, neurotrophic pathways and functional status of FEP patients seem to be related which is of great traslational relevance. Specific, the expression of the 2 isoforms of BDNF receptor should be taken into account before starting an antipsychotic drug treatment.Disclosure of interestThe authors have not supplied their declaration of competing interest.

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Ding, Mei-li, Hui Ma, Yi-gang Man, and Hong-yan LV. "Protective effects of a green tea polyphenol, epigallocatechin-3-gallate, against sevoflurane-induced neuronal apoptosis involve regulation of CREB/BDNF/TrkB and PI3K/Akt/mTOR signalling pathways in neonatal mice." Canadian Journal of Physiology and Pharmacology 95, no. 12 (December 2017): 1396–405. http://dx.doi.org/10.1139/cjpp-2016-0333.

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Epigallocatechin-3-gallate (EGCG), a polyphenol in green tea, is an effective antioxidant and possesses neuroprotective effects. Brain-derived neurotrophic factor (BDNF) and cyclic AMP response element-binding protein (CREB) are crucial for neurogenesis and synaptic plasticity. In this study, we aimed to assess the protective effects of EGCG against sevoflurane-induced neurotoxicity in neonatal mice. Distinct groups of C57BL/6 mice were given EGCG (25, 50, or 75 mg/kg body weight) from postnatal day 3 (P3) to P21 and were subjected to sevoflurane (3%; 6 h) exposure on P7. EGCG significantly inhibited sevoflurane-induced neuroapoptosis as determined by Fluoro-Jade B staining and terminal deoxynucleotidyl transferase dUTP nick end labelling (TUNEL). Increased levels of cleaved caspase-3, downregulated Bad and Bax, and significantly enhanced Bcl-2, Bcl-xL, xIAP, c-IAP-1, and survivin expression were observed. EGCG induced activation of the PI3K/Akt pathway as evidenced by increased Akt, phospho-Akt, GSK-3β, phospho-GSK-3β, and mTORc1 levels. Sevoflurane-mediated downregulation of cAMP/CREB and BDNF/TrkB signalling was inhibited by EGCG. Reverse transcription PCR analysis revealed enhanced BDNF and TrkB mRNA levels upon EGCG administration. Improved performance of mice in Morris water maze tests suggested enhanced learning and memory. The study indicates that EGCG was able to effectively inhibit sevoflurane-induced neurodegeneration and improve learning and memory retention of mice via activation of CREB/BDNF/TrkB–PI3K/Akt signalling.

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Zalewska, Teresa, Joanna Jaworska, Joanna Sypecka, and Malgorzata Ziemka-Nalecz. "Impact of a Histone Deacetylase Inhibitor—Trichostatin A on Neurogenesis after Hypoxia-Ischemia in Immature Rats." International Journal of Molecular Sciences 21, no. 11 (May 27, 2020): 3808. http://dx.doi.org/10.3390/ijms21113808.

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Hypoxia-ischemia (HI) in the neonatal brain frequently results in neurologic impairments, including cognitive disability. Unfortunately, there are currently no known treatment options to minimize ischemia-induced neural damage. We previously showed the neuroprotective/neurogenic potential of a histone deacetylase inhibitor (HDACi), sodium butyrate (SB), in a neonatal HI rat pup model. The aim of the present study was to examine the capacity of another HDACi—Trichostatin A (TSA)—to stimulate neurogenesis in the subgranular zone of the hippocampus. We also assessed some of the cellular/molecular processes that could be involved in the action of TSA, including the expression of neurotrophic factors (glial cell line-derived neurotrophic factor (GDNF), nerve growth factor (NGF), and brain-derived neurotrophic factor (BDNF)) as well as the TrkB receptor and its downstream signalling substrate— cAMP response element-binding protein (CREB). Seven-day-old rat pups were subjected to unilateral carotid artery ligation followed by hypoxia for 1 h. TSA was administered directly after the insult (0.2 mg/kg body weight). The study demonstrated that treatment with TSA restored the reduced by hypoxia-ischemia number of immature neurons (neuroblasts, BrdU/DCX-positive) as well as the number of oligodendrocyte progenitors (BrdU/NG2+) in the dentate gyrus of the ipsilateral damaged hemisphere. However, new generated cells did not develop the more mature phenotypes. Moreover, the administration of TSA stimulated the expression of BDNF and increased the activation of the TrkB receptor. These results suggest that BDNF-TrkB signalling pathways may contribute to the effects of TSA after neonatal hypoxic-ischemic injury.

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Perreault, Melissa L., Jace Jones-Tabah, Brian F. O'Dowd, and Susan R. George. "A physiological role for the dopamine D5 receptor as a regulator of BDNF and Akt signalling in rodent prefrontal cortex." International Journal of Neuropsychopharmacology 16, no. 2 (July 25, 2012): 477–83. http://dx.doi.org/10.1017/s1461145712000685.

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Abstract The dopamine D5 receptor (D5R) exhibits a wide distribution in prefrontal cortex (PFC) but its role in this region has not yet been elucidated. In the present study, we identified a novel physiological function for the D5R as a regulator of brain-derived neurotrophic factor (BDNF) and Akt signalling in PFC. Specifically, acute activation of the D5R by the dopamine agonist SKF 83959 enhanced BDNF expression and signalling through its receptor, tropomyosin receptor kinase B (TrkB), in rats and in mice gene-deleted for the D1 receptor but not the D5R. These changes were concomitant with increased expression of GAD67, a protein whose down-regulation has been implicated in the aetiology of schizophrenia. Furthermore, D5R activation increased phosphorylation of Akt at the Ser473 site, consequently decreasing the activity of its substrate GSK-3β. These findings could have wide-reaching implications given evidence showing activation of these pathways in PFC has therapeutic effects in neuropsychiatric disorders such as drug addiction, schizophrenia and depression.

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Tigaret, Cezar M., Tzu-Ching E. Lin, Edward R. Morrell, Lucy Sykes, Anna L. Moon, Michael C. O’Donovan, Michael J. Owen, et al. "Neurotrophin receptor activation rescues cognitive and synaptic abnormalities caused by hemizygosity of the psychiatric risk gene Cacna1c." Molecular Psychiatry 26, no. 6 (February 17, 2021): 1748–60. http://dx.doi.org/10.1038/s41380-020-01001-0.

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AbstractGenetic variation in CACNA1C, which encodes the alpha-1 subunit of CaV1.2 L-type voltage-gated calcium channels, is strongly linked to risk for psychiatric disorders including schizophrenia and bipolar disorder. To translate genetics to neurobiological mechanisms and rational therapeutic targets, we investigated the impact of mutations of one copy of Cacna1c on rat cognitive, synaptic and circuit phenotypes implicated by patient studies. We show that rats hemizygous for Cacna1c harbour marked impairments in learning to disregard non-salient stimuli, a behavioural change previously associated with psychosis. This behavioural deficit is accompanied by dys-coordinated network oscillations during learning, pathway-selective disruption of hippocampal synaptic plasticity, attenuated Ca2+ signalling in dendritic spines and decreased signalling through the Extracellular-signal Regulated Kinase (ERK) pathway. Activation of the ERK pathway by a small-molecule agonist of TrkB/TrkC neurotrophin receptors rescued both behavioural and synaptic plasticity deficits in Cacna1c+/− rats. These results map a route through which genetic variation in CACNA1C can disrupt experience-dependent synaptic signalling and circuit activity, culminating in cognitive alterations associated with psychiatric disorders. Our findings highlight targeted activation of neurotrophin signalling pathways with BDNF mimetic drugs as a genetically informed therapeutic approach for rescuing behavioural abnormalities in psychiatric disorder.

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Chiaramello, S., G. Dalmasso, L. Bezin, D. Marcel, F. Jourdan, P. Peretto, A. Fasolo, and S. De Marchis. "BDNF/ TrkB interaction regulates migration of SVZ precursor cells via PI3-K and MAP-K signalling pathways." European Journal of Neuroscience 26, no. 7 (September 20, 2007): 1780–90. http://dx.doi.org/10.1111/j.1460-9568.2007.05818.x.

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Li, Yi-Zhou, Zi-Yao Wu, Bi-Qi Zhu, Yu-Xiao Wang, Ya-Qi Kan, and Huai-Cai Zeng. "The BDNF–TrkB–CREB Signalling Pathway Is Involved in Bisphenol S-Induced Neurotoxicity in Male Mice by Regulating Methylation." Toxics 10, no. 8 (July 23, 2022): 413. http://dx.doi.org/10.3390/toxics10080413.

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Bisphenol S (BPS), the most common substitute for bisphenol A in manufacturing, is associated with neurotoxicity, but its molecular mechanisms are unclear. Here, we studied the role of the BDNF–TrkB–CREB (brain-derived neurotrophic factor–tropomyosin-related kinase B–CAMP response element-binding protein) signalling pathway in bisphenol S-induced neurotoxicity via methylation regulation in male C57BL/6 mice. The mice were treated with sesame oil or 2, 20 and 200 mg/kg body weight BPS for 28 consecutive days, and the hippocampus was extracted. We recorded the body weight, organ index, and hippocampal pathology and ultrastructure of the mice. The BDNF, TrkB, CREB, phosphorylated (p)-CREB, DNMTs (DNA methyltransferases) levels were determined by qRT-PCR and/or Western blotting. BDNF promoter IV methylation level was detected by bisulfite sequencing PCR. BPS damaged the mouse hippocampus ultrastructure and reduced the number of synapses. Further, it increased the methylation rate of BDNF promoter IV; downregulated BDNF, CREB, p-CREB/CREB and DNMT1 expression; and upregulated DNMT3a and DNMT3b expression. Therefore, we speculate that the BDNF–TrkB–CREB pathway may be involved in BPS-induced neurotoxicity in male mice by regulating methylation.

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Li, Wu, Qing-zhi He, Cheng-qiu Wu, Xiao-yuan Pan, Jing Wang, Yan Tan, Xiao-yun Shan, and Huai-cai Zeng. "PFOS Disturbs BDNF-ERK-CREB Signalling in Association with Increased MicroRNA-22 in SH-SY5Y Cells." BioMed Research International 2015 (2015): 1–10. http://dx.doi.org/10.1155/2015/302653.

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Perfluorooctane sulfonate (PFOS), a ubiquitous environmental pollutant, is neurotoxic to mammalian species. However, the underlying mechanism of its neurotoxicity was unclear. We hypothesized that PFOS suppresses BDNF expression to produce its neurotoxic effects by inhibiting the ERK-CREB pathway. SH-SY5Y human neuroblastoma cells were exposed to various concentrations of PFOS to examine the role of the BDNF-ERK-CREB signalling pathway in PFOS-induced apoptosis and cytotoxicity. Furthermore, to ascertain the mechanism by which PFOS reduces BDNF signalling, we examined the expression levels of miR-16 and miR-22, which potentially regulate BDNF mRNA translation at the posttranscriptional level. Results indicated that PFOS significantly decreased cell viability and induced apoptosis in SH-SY5Y cells. In addition, BDNF and pERK protein levels decreased after PFOS treatment; however, pCREB protein levels were significantly elevated in PFOS treated groups. TrkB protein expression increased in the 10 μM and 50 μM PFOS groups and significantly decreased in the 100 μM PFOS group. Our results demonstrated that PFOS exposure decreased miR-16 expression and increased miR-22 expression, which may represent a possible mechanism by which PFOS decreases BDNF protein levels. PFOS may inhibit BDNF-ERK-CREB signalling by increasing miR-22 levels, which may, in part, explain the mechanism of PFOS neurotoxicity.

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Gibon, Julien, Jean-Christophe Deloulme, Tiphaine Chevallier, Elodie Ladevèze, Djoher Nora Abrous, and Alexandre Bouron. "The antidepressant hyperforin increases the phosphorylation of CREB and the expression of TrkB in a tissue-specific manner." International Journal of Neuropsychopharmacology 16, no. 1 (February 1, 2013): 189–98. http://dx.doi.org/10.1017/s146114571100188x.

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Abstract Hyperforin is one of the main bioactive compounds that underlie the antidepressant actions of the medicinal plant Hypericum perforatum (St. John's wort). However, the effects of a chronic hyperforin treatment on brain cells remains to be fully addressed. The following study was undertaken to further advance our understanding of the biological effects of this plant extract on neurons. Special attention was given to its impact on the brain-derived neurotrophic factor (BDNF) receptor TrkB and on adult hippocampal neurogenesis since they appear central to the mechanisms of action of antidepressants. The consequences of a chronic hyperforin treatment were investigated on cortical neurons in culture and on the brain of adult mice treated for 4 wk with a daily injection (i.p.) of hyperforin (4 mg/kg). Its effects on the expression of the cyclic adenosine monophosphate response element-binding protein (CREB), phospho-CREB (p-CREB), TrkB and phospho-TrkB (p-TrkB) were analysed by Western blot experiments and its impact on adult hippocampal neurogenesis was also investigated. Hyperforin stimulated the expression of TRPC6 channels and TrkB via SKF-96365-sensitive channels controlling a downstream signalling cascade involving Ca2+, protein kinase A, CREB and p-CREB. In vivo, hyperforin augmented the expression of TrkB in the cortex but not in the hippocampus where hippocampal neurogenesis remained unchanged. In conclusion, this plant extract acts on the cortical BDNF/TrkB pathway leaving adult hippocampal neurogenesis unaffected. This study provides new insights on the neuronal responses controlled by hyperforin. We propose that the cortex is an important brain structure targeted by hyperforin.

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Ferrini, Francesco, and Yves De Koninck. "Microglia Control Neuronal Network Excitability via BDNF Signalling." Neural Plasticity 2013 (2013): 1–11. http://dx.doi.org/10.1155/2013/429815.

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Microglia-neuron interactions play a crucial role in several neurological disorders characterized by altered neural network excitability, such as epilepsy and neuropathic pain. While a series of potential messengers have been postulated as substrates of the communication between microglia and neurons, including cytokines, purines, prostaglandins, and nitric oxide, the specific links between messengers, microglia, neuronal networks, and diseases have remained elusive. Brain-derived neurotrophic factor (BDNF) released by microglia emerges as an exception in this riddle. Here, we review the current knowledge on the role played by microglial BDNF in controlling neuronal excitability by causing disinhibition. The efforts made by different laboratories during the last decade have collectively provided a robust mechanistic paradigm which elucidates the mechanisms involved in the synthesis and release of BDNF from microglia, the downstream TrkB-mediated signals in neurons, and the biophysical mechanism by which disinhibition occurs, via the downregulation of the K+-Cl−cotransporter KCC2, dysrupting Cl−homeostasis, and hence the strength ofGABAA- and glycine receptor-mediated inhibition. The resulting altered network activity appears to explain several features of the associated pathologies. Targeting the molecular players involved in this canonical signaling pathway may lead to novel therapeutic approach for ameliorating a wide array of neural dysfunctions.

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Li, Yuehua, Manhon Chung, Rehanguli Aimaier, Chengjiang Wei, Wei Wang, Lingling Ge, Beiyao Zhu, et al. "Knockdown of NCOR2 Inhibits Cell Proliferation via BDNF/TrkB/ERK in NF1-Derived MPNSTs." Cancers 14, no. 23 (November 24, 2022): 5798. http://dx.doi.org/10.3390/cancers14235798.

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(1) Background: malignant peripheral nerve sheath tumours (MPNSTs) are aggressive Schwann cell-derived sarcomas with dismal prognoses. Previous studies have shown that nuclear receptor corepressor 2 (NCOR2) plays a vital role in neurodevelopment and in various tumours. However, the impact of NCOR2 on the progression of MPNST remains unclear. (2) Methods: by GEO database, MPNST tissue microarray, and NF1-related tumour tissues and cell lines were used to explore NCOR2 expression level in the MPNSTs. The role and mechanism of NCOR2 in NF1-derived MPNSTs were explored by experiments in vivo and in vitro and by transcriptome high-throughput sequencing. (3) Results: NCOR2 expression is significantly elevated in NF1-derived MPNSTs and is associated with patient 10-year survival time. Knockdown of NCOR2 suppressed NF1-derived MPNST cell proliferation by blocking the cell cycle in the G0/G1 phase. Moreover, decreased NCOR2 expression could down-regulate MAPK signal activity through the BDNF/TrkB pathway. (4) Conclusions: our findings demonstrated that NCOR2 expression is significantly elevated in NF1-derived MPNSTs. NCOR2 knockdown can inhibit NF1-derived MPNST cell proliferation by weakened BDNF/TrkB/ERK signalling. Targeting NF1-derived MPNSTs with TrkB inhibitors, or in combination with ERK inhibitors, may be a novel therapeutic strategy for clinical trials.

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Annamneedi, Anil, Miguel del Angel, Eckart D. Gundelfinger, Oliver Stork, and Gürsel Çalışkan. "The Presynaptic Scaffold Protein Bassoon in Forebrain Excitatory Neurons Mediates Hippocampal Circuit Maturation: Potential Involvement of TrkB Signalling." International Journal of Molecular Sciences 22, no. 15 (July 26, 2021): 7944. http://dx.doi.org/10.3390/ijms22157944.

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A presynaptic active zone organizer protein Bassoon orchestrates numerous important functions at the presynaptic active zone. We previously showed that the absence of Bassoon exclusively in forebrain glutamatergic presynapses (BsnEmx1cKO) in mice leads to developmental disturbances in dentate gyrus (DG) affecting synaptic excitability, morphology, neurogenesis and related behaviour during adulthood. Here, we demonstrate that hyperexcitability of the medial perforant path-to-DG (MPP-DG) pathway in BsnEmx1cKO mice emerges during adolescence and is sustained during adulthood. We further provide evidence for a potential involvement of tropomyosin-related kinase B (TrkB), the high-affinity receptor for brain-derived neurotrophic factor (BDNF), mediated signalling. We detect elevated TrkB protein levels in the dorsal DG of adult mice (~3–5 months-old) but not in adolescent (~4–5 weeks-old) mice. Electrophysiological analysis reveals increased field-excitatory-postsynaptic-potentials (fEPSPs) in the DG of the adult, but not in adolescent BsnEmx1cKO mice. In line with an increased TrkB expression during adulthood in BsnEmx1cKO, blockade of TrkB normalizes the increased synaptic excitability in the DG during adulthood, while no such effect was observed in adolescence. Accordingly, neurogenesis, which has previously been found to be increased in adult BsnEmx1cKO mice, was unaffected at adolescent age. Our results suggest that Bassoon plays a crucial role in the TrkB-dependent postnatal maturation of the hippocampus.

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Cui, Xiaoyan, Zhenqiang Fu, Menghan Wang, Xiaofei Nan, and Boai Zhang. "Pitavastatin treatment induces neuroprotection through the BDNF-TrkB signalling pathway in cultured cerebral neurons after oxygen-glucose deprivation." Neurological Research 40, no. 5 (March 16, 2018): 391–97. http://dx.doi.org/10.1080/01616412.2018.1447318.

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Yoon, Eun-Jung, Yunseo Choi, and Dongsun Park. "Improvement of Cognitive Function in Ovariectomized Rats by Human Neural Stem Cells Overexpressing Choline Acetyltransferase via Secretion of NGF and BDNF." International Journal of Molecular Sciences 23, no. 10 (May 16, 2022): 5560. http://dx.doi.org/10.3390/ijms23105560.

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Menopause is associated with memory deficits attributed to reduced serum estrogen levels. We evaluated whether an increase in brain-derived neurotrophic factor (BDNF) and nerve-growth factor (NGF) levels, through transplantation of choline acetyltransferase (ChAT)-overexpressing neural stem cells (F3.ChAT), improved learning and memory in ovariectomized rats. PD13 mouse neuronal primary culture cells were treated with estradiol or co-cultured with F3.ChAT cells; choline transporter1 (CHT1), ChAT, and vesicular acetylcholine transporter (VAChT) expression was evaluated using real-time PCR. The relationship between estrogen receptors (ERs) and neurotrophin family members was analyzed using immunohistochemistry. After the transplantation of F3.ChAT cells into OVx rats, we evaluated the memory, ACh level, and the expression of ER, neurotrophin family proteins, and cholinergic system. Estradiol upregulated CHT1, ChAT, and VAChT expression in ER; they were co-localized with BDNF, NGF, and TrkB. Co-culture with F3.ChAT upregulated CHT1, ChAT, and VAChT by activating the neurotrophin signalling pathway. Transplantation of F3.ChAT cells in OVX animals increased the ACh level in the CSF and improved memory deficit. In addition, it increased the expression of ERs, neurotrophin signaling, and the cholinergic system in the brains of OVX animals. Therefore, the estradiol deficiency induced memory loss by the down-regulation of the neurotrophin family and F3.ChAT could ameliorate the cognitive impairment owing to the loss or reduction of estradiol.

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Zhong, Liang, Foquan Luo, Weilu Zhao, Yunlin Feng, Liuqin Wu, Jiamei Lin, Tianyin Liu, Shengqiang Wang, Xuexue You, and Wei Zhang. "Propofol exposure during late stages of pregnancy impairs learning and memory in rat offspring via the BDNF ‐TrkB signalling pathway." Journal of Cellular and Molecular Medicine 20, no. 10 (June 14, 2016): 1920–31. http://dx.doi.org/10.1111/jcmm.12884.

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Ying, Xinwang, Qingfeng Xie, Xiaolan Yu, Shengcun Li, Qiaoyun Wu, Xiaolong Chen, Jingjing Yue, Kecheng Zhou, Wenzhan Tu, and Songhe Jiang. "Water treadmill training protects the integrity of the blood-spinal cord barrier following SCI via the BDNF/TrkB-CREB signalling pathway." Neurochemistry International 143 (February 2021): 104945. http://dx.doi.org/10.1016/j.neuint.2020.104945.

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Ahmed, Marwa A., and Esam O. Kamel. "Involvement of H 2 S, NO and BDNF‐TrkB signalling pathway in the protective effects of simvastatin against pentylenetetrazole‐induced kindling and cognitive impairments in mice." Basic & Clinical Pharmacology & Toxicology 127, no. 6 (July 28, 2020): 461–76. http://dx.doi.org/10.1111/bcpt.13457.

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Banerjee, Madhuparna, and Rekha R. Shenoy. "Emphasizing roles of BDNF promoters and inducers in Alzheimer's disease for improving impaired cognition and memory." Journal of Basic and Clinical Physiology and Pharmacology, November 8, 2021. http://dx.doi.org/10.1515/jbcpp-2021-0182.

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Abstract Brain-derived neurotrophic factor (BDNF) is a crucial neurotrophic factor adding to neurons’ development and endurance. The amount of BDNF present in the brain determines susceptibility to various neurodegenerative diseases. In Alzheimer’s disease (AD), often it is seen that low levels of BDNF are present, which primarily contributes to cognition deficit by regulating long-term potentiation (LTP) and synaptic plasticity. Molecular mechanisms underlying the synthesis, storage and release of BDNF are widely studied. New molecules are found, which contribute to the signal transduction pathway. Two important receptors of BDNF are TrkB and p75NTR. When BDNF binds to the TrkB receptor, it activates three main signalling pathways-phospholipase C, MAPK/ERK, PI3/AKT. BDNF holds an imperative part in LTP and dendritic development, which are essential for memory formation. BDNF supports synaptic integrity by influencing LTP and LTD. This action is conducted by modulating the glutamate receptors; AMPA and NMDA. This review paper discusses the aforesaid points along with inducers of BDNF. Drugs and herbals promote neuroprotection by increasing the hippocampus’ BDNF level in various disease-induced animal models for neurodegeneration. Advancement in finding pertinent molecules contributing to the BDNF signalling pathway has been discussed, along with the areas that require further research and study.

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Kawamura, Namiko, Goro Katsuura, Nobuko Yamada-Goto, Riho Nakama, Yuki Kambe, Atsuro Miyata, Tomoyuki Furuyashiki, Shuh Narumiya, Yoshihiro Ogawa, and Akio Inui. "Brain fractalkine-CX3CR1 signalling is anti-obesity system as anorexigenic and anti-inflammatory actions in diet-induced obese mice." Scientific Reports 12, no. 1 (July 23, 2022). http://dx.doi.org/10.1038/s41598-022-16944-3.

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AbstractFractalkine is one of the CX3C chemokine family, and it is widely expressed in the brain including the hypothalamus. In the brain, fractalkine is expressed in neurons and binds to a CX3C chemokine receptor 1 (CX3CR1) in microglia. The hypothalamus regulates energy homeostasis of which dysregulation is associated with obesity. Therefore, we examined whether fractalkine-CX3CR1 signalling involved in regulating food intake and hypothalamic inflammation associated with obesity pathogenesis. In the present study, fractalkine significantly reduced food intake induced by several experimental stimuli and significantly increased brain-derived neurotrophic factor (BDNF) mRNA expression in the hypothalamus. Moreover, tyrosine receptor kinase B (TrkB) antagonist impaired fractalkine-induced anorexigenic actions. In addition, compared with wild-type mice, CX3CR1-deficient mice showed a significant increase in food intake and a significant decrease in BDNF mRNA expression in the hypothalamus. Mice fed a high-fat diet (HFD) for 16 weeks showed hypothalamic inflammation and reduced fractalkine mRNA expression in the hypothalamus. Intracerebroventricular administration of fractalkine significantly suppressed HFD-induced hypothalamic inflammation in mice. HFD intake for 4 weeks caused hypothalamic inflammation in CX3CR1-deficient mice, but not in wild-type mice. These findings suggest that fractalkine-CX3CR1 signalling induces anorexigenic actions via activation of the BDNF-TrkB pathway and suppresses HFD-induced hypothalamic inflammation in mice.

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Chong, Pit Shan, Chi Him Poon, Jaydeep Roy, Ka Chun Tsui, Sze Yuen Lew, Michael Weng Lok Phang, Rachael Julia Yuenyinn Tan, et al. "Neurogenesis-dependent antidepressant-like activity of Hericium erinaceus in an animal model of depression." Chinese Medicine 16, no. 1 (December 2021). http://dx.doi.org/10.1186/s13020-021-00546-8.

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Abstract Background Depression is a severe neuropsychiatric disorder that affects more than 264 million people worldwide. The efficacy of conventional antidepressants are barely adequate and many have side effects. Hericium erinaceus (HE) is a medicinal mushroom that has been reported to have therapeutic potential for treating depression. Methods Animals subjected to chronic restraint stress were given 4 weeks HE treatment. Animals were then screened for anxiety and depressive-like behaviours. Gene and protein assays, as well as histological analysis were performed to probe the role of neurogenesis in mediating the therapeutic effect of HE. Temozolomide was administered to validate the neurogenesis-dependent mechanism of HE. Results The results showed that 4 weeks of HE treatment ameliorated depressive-like behaviours in mice subjected to 14 days of restraint stress. Further molecular assays demonstrated the 4-week HE treatment elevated the expression of several neurogenesis-related genes and proteins, including doublecortin, nestin, synaptophysin, brain-derived neurotrophic factor (BDNF), tropomyosin receptor kinase B (TrkB), phosphorylated extracellular signal-regulated kinase, and phosphorylated cAMP response element-binding protein (pCREB). Increased bromodeoxyuridine-positive cells were also observed in the dentate gyrus of the hippocampus, indicating enhanced neurogenesis. Neurogenesis blocker temozolomide completely abolished the antidepressant-like effects of HE, confirming a neurogenesis-dependent mechanism. Moreover, HE induced anti-neuroinflammatory effects through reducing astrocyte activation in the hippocampus, which was also abolished with temozolomide administration. Conclusion HE exerts antidepressant effects by promoting neurogenesis and reducing neuroinflammation through enhancing the BDNF-TrkB-CREB signalling pathway.

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Journal articles on the topic 'BDNF-TrkB signalling pathways'

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