Induction of kf-1 after repeated electroconvulsive treatment and chronic antidepressant treatment in rat frontal cortex and hippocampus

Abstract

It has been proposed that signaling pathways involved in adaptive neural plasticity are long-term targets for the action of electroconvulsive treatment (ECT), which is widely used in the treatment of drug-resistant depression. We have previously performed EST analysis to identify some molecular machinery responsible for antidepressant effect. One of the cDNA fragments identified as antidepressant related genes/ESTs was identified as kf-1 which has a RING-H2 finger motif at the carboxy-terminus. In the present study, we have demonstrated the induction of kf-1 in rat frontal cortex and hippocampus not only after chronic antidepressant treatment, but also after a single and repeated ECT. RING finger proteins are proposed to play some important roles in the ubiquitin-proteasome system. In conclusion, the current investigation has identified kf-1 as a novel molecular target for antidepressants and ECT.

ROCK inhibition produces anxiety-related behaviors in mice

“…Using a differential cloning strategy, we previously analyzed gene expression in rat frontal cortex after acute treatment with antidepressants (Yamada et al 2000Nishioka et al 2003;Takahashi et al 2005). We found decreased expression of several Rho/ROCK pathway components in the frontal cortex of rats 24 h after a single administration of several different antidepressants (selective 5-HT reuptake inhibitors, 5-HT/norepinephrine reuptake inhibitors, and tricyclic antidepressants) when compared to the expression in the frontal cortex of control rats.…”

“…Recently, the kind of regulation of dendritic and axonal morphology that occurs during development has also been proposed to be involved in the expression of pharmacological actions induced by anxiolytics and antidepressants (Magarinos et al 1999;Ouimet 2000, 2001;Hajszan et al 2005). In addition, we found the decreased expression of several Rho/ROCK pathway components in the frontal cortex of rats 24 h after a single administration of several different antidepressants [selective serotonin (5-HT) reuptake inhibitors, 5-HT/norepinephrine reuptake inhibitors, and tricyclic antidepressants] when compared to the gene expression in rat frontal cortex after acute treatment with antidepressants using a differential cloning strategy (Yamada et al 2000Nishioka et al 2003;Takahashi et al 2005). Very little is known, however, about the role of the Rho/ ROCK pathway in emotional behaviors.…”

Repetitive transcranial magnetic stimulation induces kf-1 expression in the rat brain

“…The expression of kf-1 (ADRG34) in ADRG microarray was 2.39 times increased in rTMS group when compared to controls. While, the expression of kf-1 in ADRG microarray was 2.17 times in antidepressant treatment group (Yamada et al, 2000) and 1.97 times in ECT group (Nishioka et al, 2003). Photograph of the gel demonstrated that the total RNA samples used in this study contained intact and similar levels of 28S and 18S ribosomal RNA bands as determined by denaturing gel electrophoresis.…”

“…These proteins activate or repress genes that encode specific proteins by binding to DNA regulatory elements, and they may be involved in critical steps that mediate treatmentinduced neural plasticity. Interestingly, we recently demonstrated the induction of kf-1 in rat frontal cortex and hippocampus after chronic antidepressant treatment and repeated ECT (Yamada et al, 2000, Nishioka et al, 2003. Therefore, in the present study, to identify a novel candidate target molecule of rTMS, we have examined the expression of kf-1 after rTMS in the rat brain, and compared the effects to those of chronic antidepressant treatment and repeated ECT.…”

KF-1 Ubiquitin Ligase: Anxiety Suppressor Model

“…1). kf-1 gene expression is up-regulated in the frontal cortex and hippocampus of rats after anti-depressant treatments such as chronic administration of serotonin selective re-uptake inhibitor (SSRI) [21], electroconvulsive therapy [22], and repetitive transcranial magnetic stimulation [23]. These observations suggest that the elevated kf-1 transcription is associated with some physiological responses to the antidepressant pathway but not merely with chemical reactions to SSRIs.…”