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

Abstract

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.

Cotinine and 6-Hydroxy-L-Nicotine Reverses Memory Deficits and Reduces Oxidative Stress in Aβ25-35-Induced Rat Model of Alzheimer’s Disease

“…Brain-derived neurotrophic factor (BDNF) is the most widely distributed neurotrophin in the CNS and is important for cellular growth, development, survival and synaptic activity [ 107 , 108 ]. All these actions are mediated by the selective binding of BDNF to the tyrosine kinase receptor B (TrkB) [ 108 ]. A reduced BDNF signaling through TrkB leads to spatial memory deficits [ 107 , 109 ].…”

Co‐administration of ethanol and nicotine heightens sensitivity to ethanol reward within the nucleus accumbens (NAc) shell and increasing NAc shell BDNF is sufficient to enhance ethanol reward in naïve Wistar rats

“…BDNF is part of the neurotrophin family and via binding with tropomyosin receptor kinase B (TrkB) promotes neuronal development, modulates synaptic function, and regulates synaptic plasticity (Park and Poo ; Nakahata and Yasuda ). A number of studies have examined BDNF in response to acute exposure, seeking, dependence, and relapse to EtOH or NIC (Logrip et al ; Machaalani and Chen ). However, preclinical research has demonstrated a relationship between BDNF expression and drug‐related changes in the brain that is dependent upon a variety of factors including duration of exposure, drug dose, and ROI (Lu et al ; Logrip et al ; Vargas‐Perez et al ; Bobadilla et al ; Haun et al ).…”

Neuroprotective Effects of Nicotine on Hippocampal Long-Term Potentiation in Brain Disorders

“…Among the neuronal growth factors affected by nicotine is BDNF, which plays a principal role in the expression and support of synaptic plasticity including LTP (Figurov et al, 1996;Ying et al, 2002). BDNF is the most abundant neuronal growth factor in the brain (Webster et al, 2002;reviewed in Cunha et al, 2010;Machaalani and Chen, 2018). BDNF produces its positive effects on neuronal development, growth and synaptic plasticity through activation of tyrosine kinase receptor B (Fayard et al, 2005), which eventually leads to involvement of cAMP-response-element-binding protein (CREB) to regulate genes expression involved in the expression and support of LTP (Ernfors and Bramham, 2003).…”

“…Most studies have provided strong evidence showing that exposure to nicotine leads to increased brain BDNF levels (Zhang et al, 2010;Suriyaprom et al, 2013;Jamal et al, 2015;Neves et al, 2017; for review, see Machaalani and Chen, 2018). The expression of BDNF and its tyrosine kinase receptor B receptor are linked to a7nAChRs where evidence shows BDNF and nAChRs mutually influencing each other (Freedman et al, 1993;.…”