Regular ArticleBDNF Restores the Expression of Jun and Fos Inducible Transcription Factors in the Rat Brain Following Repetitive Electroconvulsive Seizures
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Cited by (24)
Electroconvulsive seizures activate anorexigenic signals in the ventromedial nuclei of the hypothalamus
2013, NeuropharmacologyCitation Excerpt :The dissected VMH and the residual brain sections from a typical microdissection are shown in Fig. 2. To confirm the gene expression changes induced by ECS in the dissected VMH samples, we examined the expression of the fos and jun families of immediate-early genes, which are induced rapidly but transiently in the brain in response to various stimuli, including ECS (Hsieh et al., 1998). A single ECS treatment robustly induced the expression of Fos (c-Fos; t(6) = 4.412, p < 0.01), Fosb (FosB; t(6) = 4.95, p < 0.01), and Jun (c-Jun; t(6) = 4.41, p < 0.01) in the VMH 2 h after stimulation (Fig. 3A–C).
Actions of two GABA<inf>A</inf> receptor benzodiazepine-site ligands that are mediated via non-γ2-dependent modulation
2011, European Journal of PharmacologyCitation Excerpt :The amount of freezing from both conditioning and testing days was collected by an infrared video camera and automatically analyzed with Video Freeze Version 2.1.0.0 software (MedAssociates). Electroconvulsive shock induces robust c-Fos expression in the granule cell layer of the dentate gyrus (Hsieh et al., 1998; Kim et al., 1994). In order to study the inhibitory actions of zolpidem in vivo, WT and γ2I77 mice were given a short electroshock 15 min after saline or zolpidem (30 mg/kg, i.p.) administration.
Chapter X c-Jun, JNK and p38: visualization of neuronal stress responses
2002, Handbook of Chemical NeuroanatomyJun, Fos and Krox in the hippocampus after noxious stimulation: Simultaneous-input-dependent expression and nuclear speckling
2001, Brain ResearchCitation Excerpt :It can also be transported to terminals [11], and upon release both stimulate and inhibit other hippocampal neurons [6]; e.g. by enhancing transmitter release [40], by enhancing AMPA- and GABA-mediated currents, and by inhibiting their responses to GABA [80], and by lasting phosphorylation of their trk [41,59] and NMDA receptors [79] which induces ITF expression. However, the mutual modulation of BDNF and c-Fos is not simple because, although infusion of BDNF into the hippocampus restores the expression of c-Fos after its down-regulation by repeated electroconvulsive seizures, BDNF alone appears not to induce c-Fos in the hippocampus [30]. Brief stimulation can cause persisting changes in the composition and functioning of AMPA and NMDA receptors [42], which again will affect ITF expressions.