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M. Iwata, Y. Shirayama, H. Ishida and R. Kawahara, “Hippocampal Synapsin 1, Growth-Associated Protein-43, and Microtuble-Associated Protein-2 Immunoreactivity in Learned Helplessness Rats and Antidepressant-Treated rats,” Neuroscience, Vol. 141, No. 3, 2006, pp. 1301-1313. doi:10.1016/j.neuroscience.2006.04.060

has been cited by the following article:

• TITLE: Neural Activation by Milnacipran and Memory Extinction

  AUTHORS: Hisahito Ishida, Masaaki Iwata, Yukihiko Shirayama, Katsumasa Muneoka

  KEYWORDS: Milnacipran; Passive Avoidance Task; Prefrontal Cortex; Nucleus Accumbens; Hippocampus; Septum

  JOURNAL NAME: Journal of Behavioral and Brain Science, Vol.2 No.2, May 30, 2012

  ABSTRACT: Background: Among neurotransmitter influencing memory formation, the noradrenergic system has been recognized as an important system. Memory formation involves various regions including the prefrontal cortex, hippocampus, amygdala and septum. Method: We investigated the effects of milnacipran on passive avoidance task and evaluated Fos counting in the prefrontal cortex, hippocampus, septum, amygdala and nucleus accumbens. Results: The milnacipran-treated rats (20 mg/kg, 4 days) showed a significant decrease in the number of Fos-immunoreactive cells in the infralimbic portion of prefrontal cortex, the shell portion of nucleus accumbens and the CA1 region of hippocampus, but a significant increase in the Fos counts in the lateral septum with no changes in the Fos counts in the striatum and amygdala. The milnacipran-treated rats showed amelioration in memory extinction (although not statistically significant), but not in memory acquisition and consolidation in the passive avoidance test. Conclusion: The differential activation of the brain regions might be possible sites for ameliorating memory extinction as well as antidepressant effects.