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9. Edaravone ameliorates depressive and anxiety-like behaviors via Sirt1/Nrf2/HO-1/Gpx4 pathway

Author

Dang, R, Wang, M, Li, X, Wang, H, Liu, L, Wu, Q, Zhao, J, Ji, P, Zhong, L, Licinio, J, Xie, P, Dang, R, Wang, M, Li, X, Wang, H, Liu, L, Wu, Q, Zhao, J, Ji, P, Zhong, L, Licinio, J, and Xie, P

Abstract

BACKGROUND: The inflammation and oxidative stress (OS) have been considered crucial components of the pathogenesis of depression. Edaravone (EDA), a free radical scavenger, processes strong biological activities including antioxidant, anti-inflammatory and neuroprotective properties. However, its role and potential molecular mechanisms in depression remain unclear. The present study aimed to investigate the antidepressant activity of EDA and its underlying mechanisms. METHODS: A chronic social defeat stress (CSDS) depression model was performed to explore whether EDA could produce antidepressant effects. Behaviors tests were carried out to examine depressive, anxiety-like and cognitive behaviors including social interaction (SI) test, sucrose preference test (SPT), open field test (OFT), elevated plus maze (EPM), novel object recognition (NOR), tail suspension test (TST) and forced swim test (FST). Hippocampal and medial prefrontal cortex (mPFC) tissues were collected for Nissl staining, immunofluorescence, targeted energy metabolomics analysis, enzyme-linked immunosorbent assay (ELISA), measurement of MDA, SOD, GSH, GSH-PX, T-AOC and transmission electron microscopy (TEM). Western blotting (WB) and quantitative real-time polymerase chain reaction (qRT-PCR) detected the Sirt1/Nrf2/HO-1/Gpx4 signaling pathway. EX527, a Sirt1 inhibitor and ML385, a Nrf2 inhibitor were injected intraperitoneally 30 min before EDA injection daily. Knockdown experiments were performed to determine the effects of Gpx4 on CSDS mice with EDA treatment by an adeno-associated virus (AAV) vector containing miRNAi (Gpx4)-EGFP infusion. RESULTS: The administrated of EDA dramatically ameliorated CSDS-induced depressive and anxiety-like behaviors. In addition, EDA notably attenuated neuronal loss, microglial activation, astrocyte dysfunction, oxidative stress damage, energy metabolism and pro-inflammatory cytokines activation in the hippocampus (Hip) and mPFC of CSDS-induced mice. Further examinat

Published
2022

26. Chromaffin cells: the peripheral brain

Author

Bornstein, S R, Ehrhart-Bornstein, M, Androutsellis-Theotokis, A, Eisenhofer, G, Vukicevic, V, Licinio, J, Wong, M L, Calissano, P, Nisticò, G, Preziosi, P, and Levi-Montalcini, R

Published
2012
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32. Offensive behavior, striatal glutamate metabolites, and limbic–hypothalamic–pituitary–adrenal responses to stress in chronic anxiety

Author

Ullmann, E. Chrousos, G. Perry, S.W. Wong, M.-L. Licinio, J. Bornstein, S.R. Tseilikman, O. Komelkova, M. Lapshin, M.S. Vasilyeva, M. Zavjalov, E. Shevelev, O. Khotskin, N. Koncevaya, G. Khotskina, A.S. Moshkin, M. Cherkasova, O. Sarapultsev, A. Ibragimov, R. Kritsky, I. Fegert, J.M. Tseilikman, V. Yehuda, R.

Abstract

Variations in anxiety-related behavior are associated with individual allostatic set-points in chronically stressed rats. Actively offensive rats with the externalizing indicators of sniffling and climbing the stimulus and material tearing during 10 days of predator scent stress had reduced plasma corticosterone, increased striatal glutamate metabolites, and increased adrenal 11-dehydrocorticosterone content compared to passively defensive rats with the internalizing indicators of freezing and grooming, as well as to controls without any behavioral changes. These findings suggest that rats that display active offensive activity in response to stress develop anxiety associated with decreased allostatic set-points and increased resistance to stress. © 2020 by the authors. Licensee MDPI, Basel, Switzerland.

Published
2020

34. Erratum: A Neuroethics Framework for the Australian Brain Initiative (Neuron (2019) 101(3) (365–369), (S0896627319300054), (10.1016/j.neuron.2019.01.004))

Author

Carter, A, Richards, LJ, Apthorp, D, Azghadi, MR, Badcock, DR, Balleine, B, Bekkers, JM, Berk, M, Bourne, JA, Bradley, AP, Breakspear, M, Brichta, A, Carter, O, Castles, A, Chakli, K, Cohen-Woods, S, Conn, SJ, Cornish, J, Cornish, K, de Zubicaray, G, Egan, GF, Enticott, PG, Fitzgibbon, BM, Forlini, C, Fornito, A, Griffiths, L, Gullifer, J, Hall, W, Halliday, G, Hannan, AJ, Harrer, S, Harvey, A, Hatherly, C, Hickie, IB, Kennett, J, Kiernan, M, Kilpatrick, T, Kiral-Kornek, I, Korgaonkar, MS, Lawrence, AJ, Leventer, R, Levy, N, Licinio, J, Lovell, N, Mackellar, G, Malcolm, L, Mason, A, Mattingley, JB, Medland, SE, Michie, PT, Nithianantharajah, J, Parker, J, Payne, JM, Poole-Warren, L, Sah, P, Sarnyai, Z, Schofield, PR, Shimoni, O, Shum, DHK, Silk, T, Slee, M, Smith, AE, Soulis, T, Sriram, S, Stuart, GJ, Tapson, J, Thompson, MB, van Schaik, A, Vincent, NA, Vissel, B, Waters, A, Carter, A, Richards, LJ, Apthorp, D, Azghadi, MR, Badcock, DR, Balleine, B, Bekkers, JM, Berk, M, Bourne, JA, Bradley, AP, Breakspear, M, Brichta, A, Carter, O, Castles, A, Chakli, K, Cohen-Woods, S, Conn, SJ, Cornish, J, Cornish, K, de Zubicaray, G, Egan, GF, Enticott, PG, Fitzgibbon, BM, Forlini, C, Fornito, A, Griffiths, L, Gullifer, J, Hall, W, Halliday, G, Hannan, AJ, Harrer, S, Harvey, A, Hatherly, C, Hickie, IB, Kennett, J, Kiernan, M, Kilpatrick, T, Kiral-Kornek, I, Korgaonkar, MS, Lawrence, AJ, Leventer, R, Levy, N, Licinio, J, Lovell, N, Mackellar, G, Malcolm, L, Mason, A, Mattingley, JB, Medland, SE, Michie, PT, Nithianantharajah, J, Parker, J, Payne, JM, Poole-Warren, L, Sah, P, Sarnyai, Z, Schofield, PR, Shimoni, O, Shum, DHK, Silk, T, Slee, M, Smith, AE, Soulis, T, Sriram, S, Stuart, GJ, Tapson, J, Thompson, MB, van Schaik, A, Vincent, NA, Vissel, B, and Waters, A

Abstract

(Neuron 101, 365–369; February 6, 2019) In the original publication of this NeuroView, the member list for the Australian Brain Alliance was omitted. This has now been corrected online. Neuron apologizes for the error.

Published
2020

35. Correction : A Neuroethics Framework for the Australian Brain Initiative (Neuron (2019) 101(3) (365–369), (S0896627319300054), (10.1016/j.neuron.2019.01.004))

Author

Carter, Adrian, Richards, Linda J., Apthorp, D, Azghadi, MR, Badcock, DR, Balleine, B, Bekkers, JM, Berk, Michael, Bourne, JA, Bradley, AP, Breakspear, M, Brichta, A, Carter, O, Castles, A, Chakli, K, Cohen-Woods, S, Conn, SJ, Cornish, J, Cornish, K, de Zubicaray, G, Egan, GF, Enticott, Peter, Fitzgibbon, BM, Forlini, Cynthia, Fornito, A, Griffiths, L, Gullifer, J, Hall, W, Halliday, G, Hannan, AJ, Harrer, S, Harvey, A, Hatherly, C, Hickie, IB, Kennett, J, Kiernan, M, Kilpatrick, T, Kiral-Kornek, I, Korgaonkar, MS, Lawrence, Andrew J, Leventer, R, Levy, N, Licinio, J, Lovell, N, Mackellar, G, Malcolm, L, Mason, A, Mattingley, JB, Medland, SE, Michie, PT, Nithianantharajah, J, Parker, J, Payne, JM, Poole-Warren, L, Sah, P, Sarnyai, Z, Schofield, PR, Shimoni, O, Shum, DHK, Silk, Timothy, Slee, M, Smith, AE, Soulis, T, Sriram, S, Stuart, GJ, Tapson, J, Thompson, MB, van Schaik, A, Vincent, NA, Vissel, B, Waters, A, Carter, Adrian, Richards, Linda J., Apthorp, D, Azghadi, MR, Badcock, DR, Balleine, B, Bekkers, JM, Berk, Michael, Bourne, JA, Bradley, AP, Breakspear, M, Brichta, A, Carter, O, Castles, A, Chakli, K, Cohen-Woods, S, Conn, SJ, Cornish, J, Cornish, K, de Zubicaray, G, Egan, GF, Enticott, Peter, Fitzgibbon, BM, Forlini, Cynthia, Fornito, A, Griffiths, L, Gullifer, J, Hall, W, Halliday, G, Hannan, AJ, Harrer, S, Harvey, A, Hatherly, C, Hickie, IB, Kennett, J, Kiernan, M, Kilpatrick, T, Kiral-Kornek, I, Korgaonkar, MS, Lawrence, Andrew J, Leventer, R, Levy, N, Licinio, J, Lovell, N, Mackellar, G, Malcolm, L, Mason, A, Mattingley, JB, Medland, SE, Michie, PT, Nithianantharajah, J, Parker, J, Payne, JM, Poole-Warren, L, Sah, P, Sarnyai, Z, Schofield, PR, Shimoni, O, Shum, DHK, Silk, Timothy, Slee, M, Smith, AE, Soulis, T, Sriram, S, Stuart, GJ, Tapson, J, Thompson, MB, van Schaik, A, Vincent, NA, Vissel, B, and Waters, A

Published
2020

36. Offensive behavior, striatal glutamate metabolites, and limbic–hypothalamic–pituitary–adrenal responses to stress in chronic anxiety

Author

Ullmann, E., Chrousos, G., Perry, S. W., Wong, M. -L., Licinio, J., Bornstein, S. R., Tseilikman, O., Komelkova, M., Lapshin, M. S., Vasilyeva, M., Zavjalov, E., Shevelev, O., Khotskin, N., Koncevaya, G., Khotskina, A. S., Moshkin, M., Cherkasova, O., Sarapultsev, A., Ibragimov, R., Kritsky, I., Fegert, J. M., Tseilikman, V., Yehuda, R., Ullmann, E., Chrousos, G., Perry, S. W., Wong, M. -L., Licinio, J., Bornstein, S. R., Tseilikman, O., Komelkova, M., Lapshin, M. S., Vasilyeva, M., Zavjalov, E., Shevelev, O., Khotskin, N., Koncevaya, G., Khotskina, A. S., Moshkin, M., Cherkasova, O., Sarapultsev, A., Ibragimov, R., Kritsky, I., Fegert, J. M., Tseilikman, V., and Yehuda, R.

Abstract

Variations in anxiety-related behavior are associated with individual allostatic set-points in chronically stressed rats. Actively offensive rats with the externalizing indicators of sniffling and climbing the stimulus and material tearing during 10 days of predator scent stress had reduced plasma corticosterone, increased striatal glutamate metabolites, and increased adrenal 11-dehydrocorticosterone content compared to passively defensive rats with the internalizing indicators of freezing and grooming, as well as to controls without any behavioral changes. These findings suggest that rats that display active offensive activity in response to stress develop anxiety associated with decreased allostatic set-points and increased resistance to stress. © 2020 by the authors. Licensee MDPI, Basel, Switzerland.

Published
2020

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