10 [84] X. Qi, W. Lin, J. Li, Y. Pan, and W. Wang, “The depressive- like behaviors are correlated with decreased phosphorylation of mitogen-activated protein kinases in rat brain following chronic forced swim stress,” Behavioural Brain Research, vol. 175, no. 2, pp. 233–240, 2006. [85] X. Qi, W. Lin, J. Li et al., “Fluoxetine increases the activity of the ERK-CREB signal system and alleviates the depressive- like behavior in rats exposed to chronic forced swim stress,” Neurobiology of Disease, vol. 31, no. 2, pp. 278–285, 2008. [86] A. Trentani, S. D. Kuipers, G. J. Ter Horst, and J. A. Den Boer, “Selective chronic stress-induced in vivo ERK1/2 hyperphosphorylation in medial prefrontocortical dendrites: implications for stress-related cortical pathology?” European Journal of Neuroscience, vol. 15, no. 10, pp. 1681–1691, 2002. [87] S. D. Kuipers, A. Trentani, J. A. Den Boer, and G. J. Ter Horst, “Molecular correlates of impaired prefrontal plasticity in response to chronic stress,” Journal of Neurochemistry, vol. 85, no. 5, pp. 1312–1323, 2003. [88] H.-T. Wang, F. Han, J.-L. Gao, and Y.-X. Shi, “Increased phosphorylation of extracellular signal-regulated kinase in the medial prefrontal cortex of the single-prolonged stress rats,” Cellular and Molecular Neurobiology, vol. 30, pp. 437–444, 2010. [89] B. Budziszewska, M. Szymanska, M. Leskiewicz et al., “The decrease in JNK- and p38-MAP kinase activity is accompanied by the enhancement of PP2A phosphatase level in the brain of prenatally stressed rats,” Journal of Physiology and Pharmacology, vol. 61, no. 2, pp. 207–215, 2010. [90] P. Zhong, W. Liu, Z. Gu, and Z. Yan, “Serotonin facilitates long-term depression induction in prefrontal cortex via p38 MAPK/Rab5-mediated enhancement of AMPA receptor internalization,” Journal of Physiology, vol. 586, no. 18, pp. 4465–4479, 2008. [91] M. Rubinstein, J. S. Mogil, M. Japo´ n, E. C. Chan, R. G. Allen, and M. J. Low, “Absence of opioid stress-induced analgesia in mice lacking β-endorphin by site-directed mutagenesis,” Proceedings of the National Academy of Sciences of the United States of America, vol. 93, no. 9, pp. 3995–4000, 1996. [92] K. Sasaguri, M. Kikuchi, N. Hori, N. Yuyama, M. Onozuka, and S. Sato, “Suppression of stress immobilization-induced phosphorylation of ERK 1/2 by biting in the rat hypothalamic paraventricular nucleus,” Neuroscience Letters, vol. 383, no. 1- 2, pp. 160–164, 2005. [93] D. C. Turk, “Cognitive-behavioral approach to the treatment of chronic pain patients,” Regional Anesthesia and Pain Medicine, vol. 28, no. 6, pp. 573–579, 2003. [94] T. Mizushima, K. Obata, H. Katsura et al., “Intensity- dependent activation of extracellular signal-regulated protein kinase 5 in sensory neurons contributes to pain hypersensitiv- ity,” Journal of Pharmacology and Experimental Therapeutics, vol. 321, no. 1, pp. 28–34, 2007. [95] K. Obata, H. Katsura, T. Mizushima et al., “Roles of extra- cellular signal-regulated protein kinases 5 in spinal microglia and primary sensory neurons for neuropathic pain,” Journal of Neurochemistry, vol. 102, no. 5, pp. 1569–1584, 2007. [96] C. Xiao, L. Zhang, Q.-P. Cheng, and L.-C. Zhang, “The activa- tion of extracellular signal-regulated protein kinase 5 in spinal cord and dorsal root ganglia contributes to inﬂammatory pain,” Brain Research, vol. 1215, pp. 76–86, 2008. [97] H. Qi, F. Mailliet, M. Spedding et al., “Antidepressants reverse the attenuation of the neurotrophic MEK/MAPK cascade in frontal cortex by elevated platform stress; reversal of eﬀects on LTP is associated with GluA1 phosphorylation,” Neuropharmacology, vol. 56, no. 1, pp. 37–46, 2009. Journal of Signal Transduction [98] S. Kamakura, T. Moriguchi, and E. Nishida, “Activation of the protein kinase ERK5/BMK1 by receptor tyrosine kinases. Identiﬁcation and characterization of a signaling pathway to the nucleus,” Journal of Biological Chemistry, vol. 274, no. 37, pp. 26563–26571, 1999.