Brain-derived neurotrophic factor (BDNF) and TrkB in the piglet brainstem after post-natal nicotine and intermittent hypercapnic hypoxia

Tang, Samantha; Machaalani, Rita; Waters, Karen A.

doi:10.1016/j.brainres.2008.07.039

Cited by 22 publications

(15 citation statements)

References 51 publications

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“…Our findings revealed that preferential activation of TrkB in the RVLM sustains central cardiovascular regulation during the pro‐life phase of experimental brain stem death. Because TrkB is the cognate receptor for brain‐derived neurotrophic factor (BDNF) (Liang et al ., 1998; Liu et al ., 2007), our results imply that in addition to its classical neurotrophic effects (Frost, 2001; Tang et al ., 2008), BDNF in the RVLM plays a pro‐life role during experimental brain stem death. The exacerbation of hypotension and antagonism of the increase in power density of LF component of SAP signals or the elevated levels of total Trk, TrkB or pTrkB Y516 in the RVLM during the pro‐life phase induced by K252a or TrkB‐Fc pretreatment further support this notion.…”

Section: Discussionsupporting

confidence: 58%

Amelioration of central cardiovascular regulatory dysfunction by tropomyocin receptor kinase B in a mevinphos intoxication model of brain stem death

Chan

et al. 2011

British Journal of Pharmacology

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BACKGROUND AND PURPOSE Little information exists on the mechanisms that precipitate brain stem death, the legal definition of death in many developed countries. We investigated the role of tropomyocin receptor kinase B (TrkB) and its downstream signalling pathways in the rostral ventrolateral medulla (RVLM) during experimental brain stem death. EXPERIMENTAL APPROACH An experimental model of brain stem death that employed microinjection of the organophosphate insecticide mevinphos bilaterally into the RVLM of Sprague–Dawley rats was used, in conjunction with cardiovascular, pharmacological and biochemical evaluations. KEY RESULTS A significant increase in TrkB protein, phosphorylation of TrkB at Tyr516 (pTrkBY516), Shc at Tyr317 (pShcY317) or ERK at Thr202/Tyr204, or Ras activity in RVLM occurred preferentially during the pro‐life phase of experimental brain stem death. Microinjection bilaterally into RVLM of a specific TrkB inhibitor, K252a, antagonized those increases. Pretreatment with anti‐pShcY317 antiserum, Src homology 3 binding peptide (Grb2/SOS inhibitor), farnesylthioacetic acid (Ras inhibitor), manumycin A (Ras inhibitor) or GW5074 (Raf‐1 inhibitor) blunted the preferential augmentation of Ras activity or ERK phosphorylation in RVLM and blocked the up‐regulated NOS I/protein kinase G (PKG) signalling, the pro‐life cascade that sustains central cardiovascular regulation during experimental brain stem death. CONCLUSIONS AND IMPLICATIONS Activation of TrkB, followed by recruitment of Shc/Grb2/SOS adaptor proteins, leading to activation of Ras/Raf‐1/ERK signalling pathway plays a crucial role in ameliorating central cardiovascular regulatory dysfunction via up‐regulation of NOS I/PKG signalling cascade in the RVLM in brain stem death. These findings provide novel information for developing therapeutic strategies against this fatal eventuality.

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Section: Discussionsupporting

confidence: 58%

Amelioration of central cardiovascular regulatory dysfunction by tropomyocin receptor kinase B in a mevinphos intoxication model of brain stem death

Chan

et al. 2011

British Journal of Pharmacology

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“…Although the mechanisms underlying neuroprotection by nicotine and nicotinic agonists remain poorly understood (Singh et al 2004), neurotrophic factors appear to mediate the long-term effects of nicotine. Nicotine enhances the concentration of several different neurotrophins, including BDNF, nerve growth factor (NGF), and fibroblast growth factor 2 (FGF-2) in the hippocampus, frontal cortex, and striatum of adult rats (Maggio et al 1997(Maggio et al , 1998Kenny et al 2000) and can regulate BDNF expression during development (Tang et al 2008). Chronic nicotine treatment of neonatal rat pups increases the mRNA expression of BDNF, NT-3, FGF-2, and IFG-1 but not NGF during postnatal development (Son and Winzer-Serhan 2009).…”

Section: Discussionmentioning

confidence: 99%

Nicotine dependence and serum BDNF levels in male patients with schizophrenia

et al. 2010

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“…To date, a modest number of studies have examined the effects of nicotine or cigarette smoke exposure, both prenatally and postnatally, on the expression of BDNF within the brain (summarized Table 2). Majority of the studies in Table 2 were conducted in the rat and mouse with the exception of our own study in piglets (Tang et al, 2008). Moreover, the majority focused on the male sex and adult age.…”

Section: Animal Models Of Nicotine and Cigarette Smoke Exposurementioning

confidence: 97%

“…The baseline expression of BDNF has been extensively studied amongst species including the rat pup, (Hafidi et al, 1999), piglet (Pieris et al, 2004, Tang et al, 2008, gerbil (Tierney et al, 2001), adult rat (Hafidi et al, 1999, Kawamoto et al, 1996, Yan et al, 1997, adult monkey (Kawamoto et al, 1999, human infant (Tang et al, 2010, Tang et al, 2011, and human adult (Murer et al, 1999, Tang et al, 2010.…”

Section: Animal Models Of Nicotine and Cigarette Smoke Exposurementioning

confidence: 99%

Brain derived neurotrophic factor (BDNF), its tyrosine kinase receptor B (TrkB) and nicotine

Machaalani

Chen

2018

NeuroToxicology

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Nicotine is the major neurotoxicant in cigarettes that affects many transmitter systems within the brain as well as other factors, including the growth factors. Brain derived neurotrophic factor (BDNF), is the most abundant growth factor in the brain and plays a critical role in early new neuron differentiation, development and synapsis growth, and the survival of fully developed neurons and synaptic activity. Over the past 3 decades, data has emerged on the effects of nicotine and cigarette smoke exposure on the expression of BDNF and its primary specific receptor tyrosine kinase receptor B (TrkB). This review summarizes data regarding the changes in brain BDNF expression after nicotine or cigarette smoke exposure, and discusses their implications considering BDNF's functional roles.

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Brain-derived neurotrophic factor (BDNF) and TrkB in the piglet brainstem after post-natal nicotine and intermittent hypercapnic hypoxia

Cited by 22 publications

References 51 publications

Amelioration of central cardiovascular regulatory dysfunction by tropomyocin receptor kinase B in a mevinphos intoxication model of brain stem death

Amelioration of central cardiovascular regulatory dysfunction by tropomyocin receptor kinase B in a mevinphos intoxication model of brain stem death

Nicotine dependence and serum BDNF levels in male patients with schizophrenia

Brain derived neurotrophic factor (BDNF), its tyrosine kinase receptor B (TrkB) and nicotine

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