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M. Morelli, A. Pinna, S. Ruii and M. Del Zompo, “Induction of Fos-Like Immunoreactivity in the Central Extended Amygdala by Antidepressant Drugs,” Synapse, Vol. 31, No. 1, 1999, pp. 1-4. doi:10.1002/(SICI)1098-2396(199901)31:1<1::AID-SYN1>3.0.CO;2-S

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.