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1. Projections from the Rostral Zona Incerta to the Thalamic Paraventricular Nucleus Mediate Nociceptive Neurotransmission in Mice

Author

Feng-Ling Wu, Si-Hai Chen, Jia-Ni Li, Liu-Jie Zhao, Xue-Mei Wu, Jie Hong, Ke-Hua Zhu, Han-Xue Sun, Su-Juan Shi, E Mao, Wei-Dong Zang, Jing Cao, Zhen-Zhen Kou, and Yun-Qing Li

Subjects
zona incerta, gamma–aminobutyric acid-ergic, thalamic paraventricular nucleus, GABA-A receptor, nociceptive neurotransmission, Microbiology, QR1-502
Abstract

Zona incerta (ZI) is an integrative subthalamic region in nociceptive neurotransmission. Previous studies demonstrated that the rostral ZI (ZIR) is an important gamma–aminobutyric acid-ergic (GABAergic) source to the thalamic paraventricular nucleus (PVT), but whether the ZIR–PVT pathway participates in nociceptive modulation is still unclear. Therefore, our investigation utilized anatomical tracing, fiber photometry, chemogenetic, optogenetic and local pharmacological approaches to investigate the roles of the ZIRGABA+–PVT pathway in nociceptive neurotransmission in mice. We found that projections from the GABAergic neurons in ZIR to PVT were involved in nociceptive neurotransmission. Furthermore, chemogenetic and optogenetic activation of the ZIRGABA+–PVT pathway alleviates pain, whereas inhibiting the activities of the ZIRGABA+-PVT circuit induces mechanical hypersensitivity and partial heat hyperalgesia. Importantly, in vivo pharmacology combined with optogenetics revealed that the GABA-A receptor (GABAAR) is crucial for GABAergic inhibition from ZIR to PVT. Our data suggest that the ZIRGABA+–PVT pathway acts through GABAAR-expressing glutamatergic neurons in PVT mediates nociceptive neurotransmission.

Published
2023
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8. List of Contributors

Author

Abraham, David, primary, Almeida, Maria, additional, Ambrogini, Elena, additional, Arnold, Andrew, additional, Bakos, Bence, additional, Bergwitz, Clemens, additional, Bikle, Daniel D., additional, Bilezikian, John P., additional, Binkley, Neil, additional, Bisello, Alessandro, additional, Bonewald, L.F., additional, Bou-Gharios, George, additional, Bouillon, Roger, additional, Bouxsein, Mary L., additional, Boyce, Brendan F., additional, Boyd, Steven, additional, Brandi, Maria Luisa, additional, Burr, David B., additional, Calvi, Laura M., additional, Canalis, Ernesto, additional, Cao, Xu, additional, Carmeliet, Geert, additional, Carpenter, Thomas O., additional, Chang, Wenhan, additional, Chim, Shek Man, additional, Choudhary, Shilpa, additional, Christakos, Sylvia, additional, Chun, Yong-Hee Patricia, additional, Cipriani, Cristiana, additional, Civitelli, Roberto, additional, Clemens, Thomas L., additional, Collins, Michael T., additional, Conte, Caterina, additional, Cooper, Mark S., additional, Cornish, Jillian, additional, Cremers, Serge, additional, Dawson-Hughes, Bess, additional, de Crombrugghe, Benoit, additional, DeLuca, Hector F., additional, Dempster, David W., additional, Drake, Matthew T., additional, Ducy, Patricia, additional, Ebetino, Frank H., additional, Engelke, Klaus, additional, Erben, Reinhold G., additional, Eyre, David R., additional, Farber, Charles R., additional, Feigenson, Marina, additional, Ferron, Mathieu, additional, Florenzano, Pablo, additional, Fontana, Francesca, additional, Foster, Brian L., additional, Friedman, Peter A., additional, Fukumoto, Seiji, additional, Gamer, Laura W., additional, Gardella, Thomas J., additional, Garnero, Patrick, additional, Genant, Harry K., additional, Giusti, Francesca, additional, Göbel, Andy, additional, Goltzman, David, additional, Gorski, Jeffrey P., additional, Griffith, James, additional, G Russell, R. Graham, additional, Hankenson, Kurt D., additional, Hannan, Fadil M., additional, Harris, Stephen E., additional, Hartley, Iris R., additional, Hartmann, Christine, additional, Heaney, Robert P., additional, Hendy, Geoffrey N., additional, Hilton, Matthew J., additional, Hofbauer, Lorenz C., additional, Holdsworth, Gill, additional, Hsu, Yi-Hsiang, additional, Hudson, David M., additional, Hurley, Marja, additional, Insogna, Karl L., additional, Jilka, Robert L., additional, Johnson, Mark L., additional, Johnson, Rachelle W., additional, Jones, Glenville, additional, Judex, Stefan, additional, Jüppner, Harald, additional, Kalajzic, Ivo, additional, Karsenty, Gérard, additional, Ke, Hua Zhu, additional, Khosla, Sundeep, additional, Kiel, Douglas P., additional, Klein-Nulend, J., additional, Ko, Frank C., additional, Kobayashi, Yasuhiro, additional, Konrad, Martin, additional, Kostenuik, Paul J., additional, Kovacs, Christopher S., additional, Kremer, Richard, additional, Krishnan, Venkatesh, additional, Kronenberg, Henry M., additional, Lakatos, Peter A., additional, Liberman, Uri A., additional, Lorenzo, Joseph A., additional, Lynch, Conor C., additional, Lyons, Karen M., additional, Ma, Y. Linda, additional, Maes, Christa, additional, Mannstadt, Michael, additional, Manolagas, Stavros, additional, Marcus, Robert, additional, Maridas, David E., additional, Marie, Pierre J., additional, Marini, Francesca, additional, Markovac, Jasna, additional, Martin, T. John, additional, Matthews, Brya G., additional, Maurizi, Antonio, additional, Mirfakhraee, Sasan, additional, Moe, Sharon M., additional, Monroe, David G., additional, Moreira, Carolina A., additional, Müller, Ralph, additional, Musson, David S., additional, Nakatani, Teruyo, additional, Naot, Dorit, additional, Napoli, Nicola, additional, Naveh-Many, Tally, additional, Nemeth, Edward F., additional, Nickolas, Thomas L., additional, Ominsky, Michael S., additional, Ono, Noriaki, additional, Ornitz, David M., additional, Partridge, Nicola C., additional, Patel, Vihitaben S., additional, Pike, J. Wesley, additional, Pilbeam, Carol, additional, Plum, Lori, additional, Potts, John T., additional, Puzas, J. Edward, additional, Rachner, Tilman D., additional, Rakian, Audrey, additional, Rakian, Rubie, additional, Renthal, Nora E., additional, Rhoades (Sterling), Julie A., additional, Riminucci, Mara, additional, Roberts, Scott J., additional, Robey, Pamela Gehron, additional, Rogers, Michael J., additional, Roodman, G. David, additional, Rosen, Clifford J., additional, Rosen, Vicki, additional, Rowe, David W., additional, Rubin, Janet, additional, Rubin, Clinton T., additional, Schlingmann, Karl P., additional, Seeman, Ego, additional, Seibel, Markus J., additional, Sempos, Chris, additional, Shoback, Dolores M., additional, Silve, Caroline, additional, Silver, Justin, additional, Sims, Natalie A., additional, Singer, Frederick R., additional, Stains, Joseph P., additional, Stegen, Steve, additional, Stern, Paula H., additional, Tabacco, Gaia, additional, Takacs, Istvan, additional, Takahashi, Naoyuki, additional, Tay, Donovan, additional, Teti, Anna, additional, Thakker, Rajesh V., additional, Tomlinson, Ryan E., additional, Tonelli, Francesco, additional, Towler, Dwight A., additional, Tsourdi, Elena, additional, Tu, Chia-Ling, additional, Udagawa, Nobuyuki, additional, Weaver, Connie M., additional, Wein, Marc N., additional, Weinstein, Lee S., additional, Weis, MaryAnn, additional, Whyte, Michael P., additional, Williams, Bart O., additional, Xu, Xin, additional, Yakar, Shoshana, additional, Yang, Yingzi, additional, Zanotti, Stefano, additional, and Zhou, Hong, additional

Published
2020
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10. Etelcalcetide (AMG 416), a peptide agonist of the calcium-sensing receptor, preserved cortical bone structure and bone strength in subtotal nephrectomized rats with established secondary hyperparathyroidism

Author

Li, Xiaodong, Yu, Longchuan, Asuncion, Frank, Grisanti, Mario, Alexander, Shawn, Hensley, Kelly, Han, Chun-Ya, Niu, Qing-Tian, Dwyer, Denise, Villasenor, Kelly, Stolina, Marina, Dean, Charles, Jr, Ominsky, Michael S., Ke, Hua Zhu, Tomlinson, James E., and Richards, William G.

Published
2017
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23. Proline-Rich Tyrosine Kinase 2 Regulates Osteoprogenitor Cells and Bone Formation, and Offers an Anabolic Treatment Approach for Osteoporosis

Author

Buckbinder, Leonard, Crawford, David T., Qi, Hong, Ke, Hua Zhu, Olson, Lisa M., Long, Kelly R., Bonnette, Peter C., Baumann, Amy P., Hambor, John E., Grasser,, William A., Pan, Lydia C., Owen, Thomas A., Luzzio, Michael J., Hulford, Catherine A., Gebhard, David F., Paralkar, Vishwas M., Simmons, Hollis A., Kath, John C., Roberts, W. Gregory, Smock, Steven L., Guzman-Perez, Angel, Brown, Thomas A., and Li, Mei

Published
2007
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49. Sclerostin antibody administration converts bone lining cells into active osteoblasts

Author

Kim, Sang Wan, Lu, Yanhui, Williams, Elizabeth A., Lai, Forest, Lee, Ji Yeon, Enishi, Tetsuya, Balani, Deepak H., Ominsky, Michael S., Ke, Hua Zhu, Kronenberg, Henry M., and Wein, Marc N.

Subjects
Adipogenesis, Osteoblasts, fungi, Adipocytes, Osteocytes, Article
Abstract

Sclerostin antibody (Scl-Ab) increases osteoblast activity, in part through increasing modeling-based bone formation on previously quiescent surfaces. Histomorphometric studies have suggested that this might occur through conversion of bone lining cells into active osteoblasts. However, direct data demonstrating Scl-Ab-induced conversion of lining cells into active osteoblasts is lacking. Here, we used in vivo lineage tracing to determine if Scl-Ab promotes the conversion of lining cells into osteoblasts on periosteal and endocortical bone surfaces in mice. Two independent, tamoxifen-inducible lineage tracing strategies were used to label mature osteoblasts and their progeny using the DMP1 and osteocalcin promoters. Following a prolonged ‘chase’ period, the majority of labeled cells on bone surfaces assumed a thin, quiescent morphology. Then, mice were treated with either vehicle or Scl-Ab (25 mg/kg) twice over the course of the subsequent week. After sacrifice, marked cells were enumerated, their thickness quantified, and proliferation and apoptosis examined. Scl-Ab led to a significant increase in the average thickness of labeled cells on periosteal and endocortical bone surfaces, consistent with osteoblast activation. Scl-Ab did not induce proliferation of labeled cells, and Scl-Ab did not regulate apoptosis of labeled cells. Therefore, direct reactivation of quiescent bone lining cells contributes to the acute increase in osteoblast numbers following Scl-Ab treatment in mice.

Published
2017

50. Anabolic Responses of an Adult Cancellous Bone Site to Prostaglandin E2 in the Rat

Author

Ito, Hiroshi, Ke, Hua Zhu, Jee, Webster S. S, and Sakou, Takashi

Subjects
Life Sciences (General)
Abstract

The objects of this study were to determine: (1) the response of a non-growing cancellous bone site to daily prostaglandin E2 (PGE2) administration; and (2) the differences in the effects of daily PGE2, administration in growing (proximal tibial metaphysis, PTM) and non-growing cancellous bone sites (distal tibial metaphysis, DTM). Seven-month-old male Sprague-Dawley rats were given daily subcutaneous injections of 0, 1, 3 and 6 mg PGE2/kg per day for 60, 120 and 180 days. The static and dynamic histomorphometric analyses were performed on double-fluorescent labeled undecalcified distal tibial metaphyses (DTM). No age-related changes were found in static and dynamic histomorphometry of DTM cancellous bone between 7 and 13 months of age. The DTM of 7-month-old (basal controls) rats consisted of a 24.5 +/- 7.61%-metaphyseal cancellous bone mass, and a thick trabeculae (92 +/- 12 micro-m). It also had a very low tissue-base bone formation rate (3.0 +/- 7.31%/year). Exogenous PGE2 administration produced the following transient changes in a dose-response manner between zero and 60 days: (1) increased trabecular bone mass and improved architecture (increased trabecular bone area, width and number, and decreased trabecular separation); (2) increased trabecular interconnections: (3) increased bone formation parameters; and (4) decreased eroded perimeter. A new steady state with more cancellous bone mass and higher bone turnover was observed from day 60 onward, The elevated bone mass induced by the first 60 days of PGE2 treatment was maintained by another 60 and 120 days with continuous daily PGE2 treatment. When these findings were compared to those previously reported for the PTM, we found that the DTM was much more responsive to PGE2 treatment than the PTM. Percent trabecular bone area and tissue based bone formation rate increased significantly more in DTM as compared to PTM after the 60 days of 6 mg PGE2 treatment. These observations indicate that a non-growing cancellous bone site is more responsive than growing bone site to long-term daily administration of PGE2.

Published
1993

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