scholarly journals Regulation of brain-derived neurotrophic factor-mediated transcription of the immediate early geneArcby intracellular calcium and calmodulin

2009 ◽  
Vol 87 (2) ◽  
pp. 380-392 ◽  
Author(s):  
Fei Zheng ◽  
Yongneng Luo ◽  
Hongbing Wang
Keyword(s):  
Intracellular Calcium ◽  
Neurotrophic Factor ◽  
Brain Derived Neurotrophic Factor ◽  
Immediate Early

scholarly journals Antibody to Varicella-Zoster Virus Immediate-Early Protein 62 Augments Allodynia in Zoster via Brain-Derived Neurotrophic Factor

2009 ◽  
Vol 84 (3) ◽  
pp. 1616-1624 ◽  
Author(s):  
Yuka Hama ◽  
Kimiyasu Shiraki ◽  
Yoshihiro Yoshida ◽  
Atsushi Maruyama ◽  
Makoto Yasuda ◽  
...  
Keyword(s):  
Varicella Zoster Virus ◽  
Nerve Injury ◽  
Neurotrophic Factor ◽  
Mechanical Allodynia ◽  
Brain Derived Neurotrophic Factor ◽  
Cross Reactivity ◽  
Immediate Early ◽  
Morphological Development ◽  
Varicella Zoster ◽  
Early Protein

ABSTRACT Varicella-zoster virus (VZV) expresses immediate-early protein 62 (IE62), and zoster is associated with neuropathic pain. Brain-derived neurotrophic factor (BDNF) is involved in the neuronal mechanism underlying pain hypersensitivity. Zoster is associated with prodrome and the robust production of booster antibody to VZV. We hypothesized that the intrathecal production of antibody to IE62 cross-reacting with BDNF and the nerve injury by skin lesions may augment allodynia in zoster by enhancing BDNF activity. One of three monoclonal antibodies against the 268-556 peptide of IE62 recognized BDNF. Immunological cross-reactivity between IE62 and BDNF and the effects of anti-IE62 monoclonal antibody (anti-IE62 MAb) cross-reactivity with BDNF on BDNF activity in cultured neurons were examined. Anti-IE62 MAb and anti-BDNF MAbs recognized the 414-429 peptide of IE62 and the BDNF dimer. Anti-IE62 MAb significantly augmented BDNF-related transcription in neurons and the morphological development of spinal dorsal horn neurons. Sera from patients recognized IE62 and BDNF and enhanced BDNF activity in neurons. The effect of anti-IE62 antibody on mechanical allodynia was characterized by the threshold of allodynia using von Frey filaments in a spinal nerve injury (SNI) in mice. The administration of anti-IE62 MAb to or immunization with cross-reacting IE62 protein to mice significantly enhanced mechanical allodynia on the side with SNI but not on the uninjured side. Anti-IE62 antibody augmented BDNF activity in neurons and allodynia in mice with SNI. The intrathecal production of anti-IE62 antibody augmenting BDNF activity and peripheral nerve injury by zoster may participate in the pathogenesis of allodynia in zoster.

scholarly journals Induction of the plasticity-associated immediate early gene Arc by stress and hallucinogens: role of brain-derived neurotrophic factor

2012 ◽  
Vol 16 (2) ◽  
pp. 405-415 ◽  
Author(s):  
Madhurima Benekareddy ◽  
Amrita R. Nair ◽  
Brian G. Dias ◽  
Deepika Suri ◽  
Anita E. Autry ◽  
...  
Keyword(s):  
Mrna Expression ◽  
Knockout Mice ◽  
Neurotrophic Factor ◽  
Immobilization Stress ◽  
Immediate Early Gene ◽  
Brain Derived Neurotrophic Factor ◽  
Early Gene ◽  
Immediate Early ◽  
Trophic Factor ◽  
Mrna Levels

Abstract Exposure to stress and hallucinogens in adulthood evokes persistent alterations in neurocircuitry and emotional behaviour. The structural and functional changes induced by stress and hallucinogen exposure are thought to involve transcriptional alterations in specific effector immediate early genes. The immediate early gene, activity regulated cytoskeletal-associated protein (Arc), is important for both activity and experience dependent plasticity. We sought to examine whether trophic factor signalling through brain-derived neurotrophic factor (BDNF) contributes to the neocortical regulation of Arc mRNA in response to distinct stimuli such as immobilization stress and the hallucinogen 2,5-dimethoxy-4-iodoamphetamine (DOI). Acute exposure to either immobilization stress or DOI induced Arc mRNA levels within the neocortex. BDNF infusion into the neocortex led to a robust up-regulation of local Arc transcript expression. Further, baseline Arc mRNA expression in the neocortex was significantly decreased in inducible BDNF knockout mice with an adult-onset, forebrain specific BDNF loss. The induction of Arc mRNA levels in response to both acute immobilization stress or a single administration of DOI was significantly attenuated in the inducible BDNF knockout mice. Taken together, our results implicate trophic factor signalling through BDNF in the regulation of cortical Arc mRNA expression, both under baseline conditions and following stress and hallucinogen exposure. These findings suggest the possibility that the regulation of Arc expression via BDNF provides a molecular substrate for the structural and synaptic plasticity observed following stimuli such as stress and hallucinogens.

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