[1]
Battle, D. E. Diagnostic and Statistical Manual of Mental Disorders (DSM). Codas, 2013, 25(2): 191–192.
[2]
Wang, B., Miao, Z. G., Wan, B., Xu, X. S. Prevention for post-traumatic stress disorder after the COVID-19 epidemic: Lessons from the SARS epidemic. Stress and Brain, 2021, 1(1): 1–10.
[3]
Jacobs, G. A. The development of a national plan for disaster mental health. Professional Psychology: Research and Practice, 1995, 26(6): 543–549.
[4]
Meeres, J., Hariz, M. Deep brain stimulation for post-traumatic stress disorder: A review of the experimental and clinical literature. Stereotactic and Functional Neurosurgery, 2022, 100(3): 143–155.
[5]
Liberzon, I., Sripada, C. S. The functional neuroanatomy of PTSD: A critical review. Progress in Brain Research, 2008, 167: 151–169.
[6]
Davidson, J. R. T., McFarlane, A. C. The extent and impact of mental health problems after disaster. The Journal of Clinical Psychiatry, 2006, 67(Suppl 2): 9–14.
[7]
Raut, S. B., Marathe, P. A., van Eijk, L., Eri, R., Ravindran, M., Benedek, D. M., Ursano, R. J., Canales, J. J., Johnson, L. R. Diverse therapeutic developments for post-traumatic stress disorder (PTSD) indicate common mechanisms of memory modulation. Pharmacology & Therapeutics, 2022, 239: 108195.
[8]
Nabaee, E. Cognitive and hippocampus biochemical changes following sleep deprivation in the adult male rat. Biomedicine & Pharmacotherapy, 2018, 104: 69–76.
[9]
Smith, M. L. The role of the right hippocampus in the recall of spatial location. Neuropsychologia, 1981, 19(6): 781–793.
[10]
Chen, A. C., Etkin, A. Hippocampal network connectivity and activation differentiates post-traumatic stress disorder from generalized anxiety disorder. Neuropsychopharmacology, 2013, 38(10): 1889–1898.
[11]
Levy-Gigi, E., Richter-Levin, G., Kéri, S. The hidden price of repeated traumatic exposure: Different cognitive deficits in different first-responders. Frontiers in Behavioral Neuroscience, 2014, 8: 281.
[12]
Levy-Gigi, E., Szabo, C., Richter-Levin, G., Kéri, S. Reduced hippocampal volume is associated with overgeneralization of negative context in individuals with PTSD. Neuropsychology, 2015, 29(1): 151–161.
[13]
Zhang, D., Wang, X., Wang, B., Garza, J. C., Fang, X., Wang, J., Scherer, P. E., Brenner, R., Zhang, W., Lu, X. Y. Adiponectin regulates contextual fear extinction and intrinsic excitability of dentate gyrus granule neurons through AdipoR2 receptors. Molecular Psychiatry, 2017, 22(7): 1044–1055.
[14]
McHugh, S. B., Fillenz, M., Lowry, J. P., Rawlins, J. N. P., Bannerman, D. M. Brain tissue oxygen amperometry in behaving rats demonstrates functional dissociation of dorsal and ventral hippocampus during spatial processing and anxiety. The European Journal of Neuroscience, 2011, 33(2): 322–337.
[15]
Chowdhury, T. G., Barbarich-Marsteller, N. C., Chan, T. E., Aoki, C. Activity-based anorexia has differential effects on apical dendritic branching in dorsal and ventral hippocampal CA1. Brain Structure and Function, 2014, 219(6): 1935–1945.
[16]
Bannerman, D. M., Rawlins, J. N., McHugh, S. B., Deacon, R. M., Yee, B. K., Bast, T., Zhang, W. N., Pothuizen, H. H., Feldon, J. Regional dissociations within the hippocampus—memory and anxiety. Neuroscience and Biobehavioral Reviews, 2004, 28(3): 273–283.
[17]
Williams, S. A., Gwilt, M., Hock, R., Taylor, C., Loayza, J., Stevenson, C. W., Cassaday, H. J., Bast, T. Hippocampal disinhibition reduces contextual and elemental fear conditioning while sparing the acquisition of latent inhibition. eneuro, 2022, 9(1): ENEURO.0270–21.2021.
[18]
Fanselow, M. S., Dong, H.-W. Are the dorsal and ventral hippocampus functionally distinct structures? Neuron, 2010, 65(1): 7–19.
[19]
Schmidt, M. V., Abraham, W. C., Maroun, M., Stork, O., Richter-Levin, G. Stress-induced metaplasticity: From synapses to behavior. Neuroscience, 2013, 250: 112–120.
[20]
Fa, M. X., Xia, L., Anunu, R., Kehat, O., Kriebel, M., Volkmer, H., Richter-Levin, G. Stress modulation of hippocampal activity—spotlight on the dentate gyrus. Neurobiology of Learning and Memory, 2014, 112: 53–60.
[21]
An, S. M., Wang, J. Y., Zhang, X. L., Duan, Y. H., Xu, Y. Q., Lv, J. Y., Wang, D. S., Zhang, H., Richter-Levin, G., Klavir, O. et al. αCaMKII in the lateral amygdala mediates PTSD-like behaviors and NMDAR-dependent LTD. Neurobiology of Stress, 2021, 15: 100359.
[22]
Kohda, K., Harada, K., Kato, K., Hoshino, A., Motohashi, J., Yamaji, T., Morinobu, S., Matsuoka, N., Kato, N. Glucocorticoid receptor activation is involved in producing abnormal phenotypes of single-prolonged stress rats: A putative post-traumatic stress disorder model. Neuroscience, 2007, 148(1): 22–33.
[23]
Niu, W. Q., Duan, Y. H., Kang, Y., Cao, X. H., Xue, Q. S. Propofol improves learning and memory in post-traumatic stress disorder (PTSD) mice via recovering hippocampus synaptic plasticity. Life Sciences, 2022, 293: 120349.
[24]
Maggio, N., Segal, M. Differential modulation of long-term depression by acute stress in the rat dorsal and ventral hippocampus. The Journal of Neuroscience: the Official Journal of the Society for Neuroscience, 2009, 29(27): 8633–8638.
[25]
Goh, J. J. Role of inhibitory autophosphorylation of calcium/calmodulin-dependent kinase II (αCAMKII) in persistent (>24 h) hippocampal LTP and in LTD facilitated by novel object-place learning and recognition in mice. Behavioural Brain Research, 2015, 285: 79–88.
[26]
Silva, A. J., Stevens, C. F., Tonegawa, S., Wang, Y. Deficient hippocampal long-term potentiation in alpha-calcium-calmodulin kinase II mutant mice. Science, 1992, 257(5067): 201–206.
[27]
Silva, A. J., Paylor, R., Wehner, J. M., Tonegawa, S. Impaired spatial learning in alpha-calcium-calmodulin kinase II mutant mice. Science, 1992, 257(5067): 206–211.
[28]
Ma, J., Duan, Y., Qin, Z., Wang, J., Liu, W., Xu, M., Zhou, S., Cao, X. Overexpression of αCaMKII impairs behavioral flexibility and NMDAR-dependent long-term depression in the medial prefrontal cortex. Neuroscience, 2015, 310: 528–540.
[29]
Chen, D. Y., Bambah-Mukku, D., Pollonini, G., Alberini, C. M. Glucocorticoid receptors recruit the CaMKIIα-BDNF-CREB pathways to mediate memory consolidation. Nature Neuroscience, 2012, 15(12): 1707–1714.
[30]
Wu, Z. M. Genistein alleviates anxiety-like behaviors in post-traumatic stress disorder model through enhancing serotonergic transmission in the amygdala. Psychiatry Research, 2017, 255: 287–291.
[31]
Matsumoto, Y., Morinobu, S., Yamamoto, S., Matsumoto, T., Takei, S., Fujita, Y., Yamawaki, S. Vorinostat ameliorates impaired fear extinction possibly via the hippocampal NMDA-CaMKII pathway in an animal model of posttraumatic stress disorder. Psychopharmacology, 2013, 229(1): 51–62.
[32]
Akirav, I., Sandi, C., Richter-Levin, G. Differential activation of hippocampus and amygdala following spatial learning under stress. The European Journal of Neuroscience, 2001, 14(4): 719–725.
[33]
Ritov, G., Boltyansky, B., Richter-Levin, G. A novel approach to PTSD modeling in rats reveals alternating patterns of limbic activity in different types of stress reaction. Molecular Psychiatry, 2016, 21(5): 630–641.
[34]
Desikan, A., Wills, D. N., Ehlers, C. L. Ontogeny and adolescent alcohol exposure in Wistar rats: Open field conflict, light/dark box and forced swim test. Pharmacology Biochemistry and Behavior, 2014, 122: 279–285.
[35]
Shafia, S., Vafaei, A. A., Samaei, S. A., Bandegi, A. R., Rafiei, A., Valadan, R., Hosseini-Khah, Z., Mohammadkhani, R., Rashidy-Pour, A. Effects of moderate treadmill exercise and fluoxetine on behavioural and cognitive deficits, hypothalamic-pituitary-adrenal axis dysfunction and alternations in hippocampal BDNF and mRNA expression of apoptosis-related proteins in a rat model of post-traumatic stress disorder. Neurobiology of Learning and Memory, 2017, 139: 165–178.
[36]
Burstein, O. Cannabinoids prevent depressive-like symptoms and alterations in BDNF expression in a rat model of PTSD. Progress in Neuro-Psychopharmacology and Biological Psychiatry, 2018, 84: 129–139.
[37]
Diniz, C. R. A. F., da Silva, L. A., Bertacchini, G. L., da Silva-Júnior, A. F., Resstel, L. B. M. Dorsal hippocampal muscarinic cholinergic receptors orchestrate behavioral and autonomic changes induced by contextual fear retrieval. Pharmacology, Biochemistry, and Behavior, 2022, 218: 173425.
[38]
Duan, Y. H., Lv, J. Y., Zhang, Z. H., Chen, Z. Z., Wu, H., Chen, J. N., Chen, Z. D., Yang, J. R., Wang, D. S., Liu, Y. M. et al. Exogenous Aβ1-42 monomers improve synaptic and cognitive function in Alzheimer’s disease model mice. Neuropharmacology, 2022, 209: 109002.
[39]
Lisman, J., Yasuda, R., Raghavachari, S. Mechanisms of CaMKII action in long-term potentiation. Nature Reviews Neuroscience, 2012, 13(3): 169–182.
[40]
Koek, R. J., Schwartz, H. N., Scully, S., Langevin, J. P., Spangler, S., Korotinsky, A., Jou, K., Leuchter, A. Treatment-refractory posttraumatic stress disorder (TRPTSD): A review and framework for the future. Progress in Neuro-Psychopharmacology & Biological Psychiatry, 2016, 70: 170–218.
[41]
Bina, R. W., Langevin, J. P. Closed loop deep brain stimulation for PTSD, addiction, and disorders of affective facial interpretation: Review and discussion of potential biomarkers and stimulation paradigms. Frontiers in Neuroscience, 2018, 12: 300.
[42]
Deschaux, O., Koumar, O. C., Canini, F., Moreau, J. L., Garcia, R. High-frequency stimulation of the hippocampus blocks fear learning sensitization and return of extinguished fear. Neuroscience, 2015, 286: 423–429.
[43]
Cleren, C., Tallarida, I., Guiniec, E. L., Janin, F., Nachon, O., Canini, F., Spennato, G., Moreau, J. L., Garcia, R. Low-frequency stimulation of the ventral hippocampus facilitates extinction of contextual fear. Neurobiol Learn Mem, 2013, 101: 39–45.
[44]
López, J. F. Regulation of Serotonin1A, glucocorticoid, and mineralocorticoid receptor in rat and human hippocampus: Implications for the neurobiology of depression. Biological Psychiatry, 1998, 43(8): 547–573.
[45]
You, W. J., He, Y., Liu, W. Z., Zhu, Y. G., Hu, P., Pan, B. X., Zhang, W. H. Exposure to single prolonged stress fails to induce anxiety-like behavior in mice. Stress and Brain, 2021, 1(2): 145–159.
[46]
Borghans, B., Homberg, J. R. Animal models for posttraumatic stress disorder: An overview of what is used in research. World Journal of Psychiatry, 2015, 5(4): 387–396.
[47]
Zoladz, P. R., Park, C. R., Fleshner, M., Diamond, D. M. Psychosocial predator-based animal model of PTSD produces physiological and behavioral sequelae and a traumatic memory four months following stress onset. Physiology & Behavior, 2015, 147: 183–192.
[48]
Robertson, D. A. F., Beattie, J. E., Reid, I. C., Balfour, D. J. K. Regulation of corticosteroid receptors in the rat brain: The role of serotonin and stress. The European Journal of Neuroscience, 2005, 21(6): 1511–1520.
[49]
Jiang, L. H., Zhang, H., He, Y., Liu, H., Li, S., Chen, R., Han, S., Zhou, Y., Zhang, J., Wan, X. et al. Synapse differentiation-induced gene 1 regulates stress-induced depression through interaction with the AMPA receptor GluA2 subunit of nucleus accumbens in male mice. Neuropharmacology, 2022, 213: 109076.
[50]
Yuan, H., Han, F., Shi, Y. X. Study on the lysosomes and nematolysosomes expression in hippocampal neurons in SPS rats of PTSD. Journal of China Medical University, 2008, 37(4): 433–435. (in Chinese)
[51]
Dalton, G. L., Wang, Y. T., Floresco, S. B., Phillips, A. G. Disruption of AMPA receptor endocytosis impairs the extinction, but not acquisition of learned fear. Neuropsychopharmacology, 2008, 33(10): 2416–2426.
[52]
Lu, W., Isozaki, K., Roche, K. W., Nicoll, R. A. Synaptic targeting of AMPA receptors is regulated by a CaMKII site in the first intracellular loop of GluA1. Proceedings of the National Academy of Sciences of the United States of America, 2010, 107(51): 22266–22271.