J.B. Winsløws vej 21, st.
Phone: 6550 9188
Our research interests are to unravel the mechanisms underlying motor deficits induced by spinal cord injury and brain injury. Injury of the central nervous system usually causes motor deficits at different degrees. The symptoms include, among others, reduced muscle activity, such as paralysis, and/or increased muscle tone, such as hypertonia. Spasticity is a symptom of altered skeletal muscle performance with a combination of paralysis, increased tendon reflex activity, and hypertonia (Wikipedia). So far the mechanisms of pathophysiology of spasticity are not fully understood. They may involve reduced inhibition of motor neurons in the spinal cord from supra spinal sources, increased sensory activity of afferent signals from periphery, and/or plastic changes of spinal network in the spinal cord below the lesion. To understand the mechanisms of its pathogenesis is essential for developing strategies to treat or alleviate this disorder.
1. Plasticity of monoamine system in the spinal cord following spinal cord injury: In this project we use different spinal cord injury models, including hemisection, contusion and complete spinal transection models to study plastic changes of monoamine system in the spinal cord. At present our focus is on serotonin and dopamine system, including the transmitter and their receptors. In addition, we will also study intrinsic spinal sensory neurons, including cerebral spinal fluid-contacting neurons, and try to reveal their anatomical distribution and functions at normal and different pathological situations.
2. Mechanisms of hypotension following spinal cord injury: A symptom following spinal cord injury is the lowered blood pressure especially in its acute and subacute phase. Often the patients experience hypotension when the body position is changed – so called orthostatic hypotension. Although there are some hypotheses the exact mechanism is still not clear. We will investigate the mechanism behind this cardiovascular functional change using spinal cord injured animal models. A candidate to potentially regulate the blood pressure in the spinal cord may be cerebrospinal fluid-contacting neurons around the central canal. Since these neurons are mechanosensitive, they may detect the pressure changes in the spinal cord/cerebrospinal fluid and further act on the sympathetic neurons to regulate hemodynamics.
3. Motor deficits following traumatic brain injury: Traumatic brain injury is a complex injury with a broad spectrum of symptoms and disabilities, which include a variety of physical and psychological effects. Motor deficits are commonly seen following traumatic brain injury. One of the physical changes is abnormal posturing, especially when the injury is severe. In collaboration with Prof. Georgy Bakalkin from Uppsala University and Prof. Jens Schouenborg we try to investigate a spinal mechanism underlying the formation of abnormal posture using a rat model. Recently we also found that the neuroendocrine system may play a critical role for the formation of postural deficits following brain injury. We are trying to find out which neurohormones are involved and what are the acting mechanisms for these substances. Our ultima aim will be to find a pharmacotherapy to treat or alleviate abnormal postural symptom induced by brain injury.
Mengliang Zhang received his education in medicine in China at Jinzhou Medical University from 1981 to 1986. He obtained his Master degree in neuroanatomy at Dalian Medical University in China in 1991. He got his PhD in neurophysiology at Lund University in Sweden in 2001 under the supervision from Prof. Jonas Broman. From 2001 to 2004 he did a 3-year postdoc at Pennsylvania State University, USA, with Prof. Kevin Alloway, working on neuronal synchronization from sensorimotor cortex. In 2004, as a research associate professor, Mengliang Zhang joined “Motor Control of Movement Group in Copenhagen” at University of Copenhagen directed by Prof. Hans Hultborn, where he worked until 2016. Here he got several research grants independently or collaboratively and developed his own research direction – plasticity of monoamine system in the spinal cord following spinal cord injury. From 2013, as a researcher, Mengliang Zhang also part-timely worked at Neuronano Research Center at Lund University directed by Prof. Jens Schouenborg. He became a reader (docent) in 2017 at Lund University. Mengliang Zhang was recruited as an associate professor in anatomy and neurobiology to the Dept. of Molecular Medicine at the University of Southern Denmark in 2018.
- The Faculty of Health Sciences, University of Southern Denmark
- Lund University
- Sacrifice Foundation (Offerfonden)
- Novo Nordisk Foundation
- Lundbeck Foundation-Danish Society for Neuroscience stipend
- Mengliang Zhang, associate professor, group leader
- Hiroyuki Watanabe, assistant professor
- Marlene Storm Andersen, PhD student
- Xiaohe Liu, PhD student
- Karen Kalhøj Rich, laboratory technician
- Tobias Christian Mogensen, laboratory technician
- Bachelor and Master students (2-3 per year)
Applied methodologies, techniques and facilities
- Small animal microsurgery – spinal cord injury and brain injury model preparation in rats and mice
- Animal behavioral analysis
- In vivo electrophysiology: electromyography, extracellular neural recording, etc.
- Light microscopy (fluorescent, confocal, etc.)
- Electron microscopy
- Western blotting
- In situ hybridization
Courses and teaching
My specialty in teaching is human anatomy. In addition, I am also specialist in neuroscience (neuroanatomy, neurophysiology, etc.). So far, I participate in teaching of human anatomy in the following courses. The students include those majoring in medicine, biomedicine, and chiropractor.
- Modul B6: Nutrition and growth
- Modul B7: Reproduction and pharmacodynamic
- University of Southern Denmark, Odense, Denmark
- University of Copenhagen, Copenhagen, Denmark
- Lund University, Lund, Sweden
- Uppsala University, Uppsala, Sweden
- German Primate Center, Göttingen, Germany
- Drexel University, Philadelphia, USA
- Bakalkin G, Lukoyanov N, Lavrov I, Zhang M. The left-right side-specific endocrine signaling: implications for neurological deficits in stroke and neurodevelopmental disorders. Submitted to Neural Regeneration Research. 2022. In press.
- Lukoyanov N, Watanabe H, Carvalho L, Kononenko O, Sarkisyan D, Zhang M, Andersen MS, Lukoyanova EA, Galatenko V, Tonevitsky A, Bazov I, Iakovleva T, Schouenborg J, Bakalkin G. Humoral signaling from unilaterally injured brain enables contralateral motor responses. Elife. 2021 Aug 10;10:e65247.
- Carvalho L, Brito HM, Lukoyanova EA, Maia GH, Sarkisyan D, Nosova O, Zhang M, Lukoyanov N, Bakalkin G. Asymmetric neurological deficits in the offspring induced by unilateral brain injury to pregnant rats. Eur J Neurosci. 2021; 53(11):3621-3633.
- Watanabe H, Nosova O, Sarkisyan D, Andersen MS, Zhang M, Rorick-Kehn L, Clausen F, Gawel K, Kehr J, Hallberg M, Schouenborg J, Marklund N, Bakalkin G. Ipsilesional versus contralesional postural deficits induced by unilateral brain trauma: a side reversal by opioid mechanism. Brain Commun. 2020 Dec 13;2(2):fcaa208.
- Zhang M, Watanabe H, Sarkisyan D, Storm Andersen M, Nosova O, Galatenko V, Carvalho L, Lukoyanov N, Thelin J, Schouenborg J, Bakalkin G. Hindlimb motor responses to unilateral brain injury: spinal cord encoding and left-right asymmetry, Brain Communications, 2020, 2: fcaa055.
- Ren L-Q, Chen M, Hultborn H, Guo S, Zhang Y, Zhang M. Heterogeneous distribution of aromatic L-amino acid decarboxylase cells in the rat spinal cord. Front Integr Neurosci. 2017; 11:31.
- Zhang M. Two-step production of monoamines in monoenzymatic cells in the spinal cord: a different control strategy of neurotransmitter supply? Neural Regen Res. 2016; 11:1904-1909.
- Ren L-Q, Wienecke J, Hultborn H, Zhang M. Production of dopamine by aromatic L-amino acid decarboxylase cells after spinal cord injury. Journal of Neurotrauma, 2016 33:1150-1160.
- Zhang M. Normal distribution and Recovery of Motor Function in Spinal Cord Injury, 978-953-51-2497-9. InTech publisher, Pp: 95-135, 2016.
- Wienecke J, Ren L-Q, Hultborn H, Chen M, Møller M, Zhang Y, Zhang M. Spinal cord injury potentiates the ability of aromatic L-amino acid decarboxylase cells to provide monoamines. Journal of Neuroscience, 2014; 34: 11984-12000.
- Ren L, Wienecke J, Chen M, Møller M, Hultborn H, Zhang M. The time course of serotonin 2C receptor expression after spinal transection of rats: an immunohistochemical study. Neuroscience, 236:31-46, 2013.
- Kong X-Y, Wienecke J, Chen M, Hultborn H, Zhang M. The time course of serotonin 2A receptor expression after spinal transection of rats: an immunohistochemical study. Neuroscience, 177:114-126, 2011.
- Kong X-Y, Wienecke J, Hultborn H, Zhang M. Robust upregulation of serotonin 2A receptor immunoreactivity after chronic spinal transection of rats. Brain Research, 1320:60-68, 2010.
- Sukiasyan N, Hultborn H, Zhang M. Expression of calcium channel CaV1.3 in rat spinal cord and brain stem. Neuroscience, 159:217-235, 2009.
- Zhang M, Møller M, Broman J, Sukiasyan N, Wienecke J, Hultborn H. Expression of calcium channel CaV1.3 in cat spinal cord – a light and electron microscopic immunohistochemical study. Journal of Comparative Neurology, 507:1109-1127, 2008.