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P. Pereira, J. Gianesini, C. da Silva Barbosa, G.F. Cassol, R. G. Von Borowski, V. F. S. Kahl, S. E. Cappelari and J. N. Picada, “Neurobehavioral and Genotoxic Parameters of Duloxetine in Mice Using the Inhibitory Avoidance Task and Comet Assay As Experimental Models,” Pharmacological Research, Vol. 59, No. 1, 2009, pp. 57-61. doi:10.1016/j.phrs.2008.09.014

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• 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.