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Michelle Hook, PhD

Michelle Hook
Michelle Hook, PhD

Associate Professor

Contact

Neuroscience & Experimental Therapeutics
8447 Riverside Pkwy
Bryan, TX 77807
michellehook@tamu.edu
Phone: 979.436.0568
Fax: 979.436.0086

Education and Training

  • University of New England, PhD, 1998

Research Interests

  • Effects of opioids on the prognosis for recovery after SCI. Morphine is one of the most frequently prescribed analgesics for the treatment of pain immediately after a spinal cord injury (SCI). We have shown, however, that irrespective of the route of administration morphine administered in the acute phase of a spinal cord injury significantly undermines recovery of locomotor function, decreases general health and produces symptoms of paradoxical pain in a rat model. The adverse effects of morphine on locomotor recovery may be mediated, at least in part, by increased neuronal death with drug administration. We have also shown that morphine is not the only opioid to produce adverse effects after SCI. Oxycodone and fentanyl, that are often used in pain management, also undermine recovery. We have begun to elucidate the molecular mechanisms underlying these adverse effects. Our data suggest that kappa-opioid receptors mediate the morphine-induced attenuation of recovery, and that glial cells may be involved in opioids adverse effect. We are extending these studies to test the effects of blocking the kappa opioid receptor when administering fentanyl and oxycodone. Oure goal is to identify an adjuvant that can be administered with opioids to provide safe and effective pain management after a spinal cord injury.
  • Identifying the molecular mechanisms contributing to depression and cognitive impairment after spinal cord injury (SCI). The incidence of depression is significantly increased in spinally injured patients, relative to the general population. My lab has shown that depression-like behaviors are also increased in rats with SCI. We developed and validated a method for characterizing depression-like behavior in SCI rats, and have shown in preliminary studies that depression-like behavior is associated with non-subjective measures of physiological function (increased heart-rate, decreased heart-rate variability, decreased hippocampal neurogenesis) as well as elevated pro-inflammatory cytokine levels and decreased serotonin in the cortex. Importantly, as seen in humans, not all rats develop depression-like behavior following injury. Approximately one-third of the rats display depression behaviors, while two-thirds do not. Interestingly, the rats that develop depression-like behavior also show impairments on tests of spatial learning. We are now exploring the role of the gut in the development of depression-like behavior, as well as focusing on strategies that increase neurogenesis in the hippocampus, as a potential strategy for reversing cognitive deficits and depression. These innovative studies lay the foundation for a new area of research in neurotrauma models, and address a consequence of spinal injury that significantly impacts quality of life and likely impacts successful rehabilitation after injury. Understanding the molecular mechanisms underlying decreased psychological well-being will be important not only for SCI, but for a range of inflammatory based conditions including traumatic brain injury, stroke and multiple sclerosis.
  • Factors contributing to bone loss after SCI. After spinal cord injury, 80% of individuals are diagnosed with osteopenia or osteoporosis. The dramatic loss of bone after SCI increases the potential for fractures 100-fold, with post-fracture complications occurring in 54% of cases. Numerous factors have been implicated in SCI-induced bone loss, but to date no effective therapies have been developed to either decrease the acute loss of bone or to facilitate bone formation in chronic phases of injury. My lab has started to investigate the SCI-induced changes that might contribute to the dramatic loss of bone after injury. Specifically we are focused on changes in the bone marrow niche induced by uncontrolled and increased sympathetic innervation below the level of injury. We hypothesize that increased sympathetic drive leads to changes in the activity of osteoblasts and osteoclasts, bone forming and resorbing cells respectively, as well and hematopoietic stem and precursor cells, that drive increased bone loss after injury.

Representative Publications

  • Rau, J., Weise, L., Moore, R., Terminel, M., Brakel, K., Cunningham, R., Bryan, J., Stefanov, A., Hook, M.A. (2023). Intrathecal minocycline does not block the adverse effects of repeated, intravenous morphine administration on recovery of function after SCI. Exp Neurol. 359:114255. doi: 10.1016/j.expneurol.2022.114255. Epub 2022 Oct 22. PMID: 36279935.
  • Terminel, M.N., Bassil, C., Rau, J., Trevino, A., Ruiz, C., Alaniz, R., Hook, M.A. (2022). Morphine-induced changes in the function of microglia and macrophages after acute spinal cord injury. BMC Neurosci. 23(1):58. doi: 10.1186/s12868-022-00739-3. PMID: 36217122; PMCID: PMC9552511.
  • Metzger, C., Rau, J., Stefanov, A., Joseph, R.M., Allaway, H.C., Allen M.R., Hook, M.A. (2022). Inflammaging and bone loss in a rat model of spinal cord injury. J Neurotrauma. 40(9-10):901-917.  doi: 10.1089/neu.2022.0342. PMID: 36226413.
  • Rau, J., Hemphill, A., Araguz, K., Cunningham, R., Stefanov, A., Weise, L., Hook, M.A. (2022). Adverse Effects of Repeated, Intravenous Morphine on Recovery after Spinal Cord Injury in Young, Male Rats Are Blocked by a Kappa Opioid Receptor Antagonist. J Neurotrauma. 39(23-24):1741-1755. doi: 10.1089/neu.2022.0208. PMID: 35996351.
  • Stampas, A., Hook, M., Korupolu, R., Jethani, L., Kaner, M.T., Pemberton, E., Li, S., Francisco, G.E. (2022) Evidence of treating spasticity before it develops: a systematic review of spasticity outcomes in acute spinal cord injury interventional trials. Ther Adv Neurol Disord.15:17562864211070657. doi: 10.1177/17562864211070657. PMID: 35198042; PMCID: PMC8859674.
  • Hook, M.A., Falck, A., Dundumulla, R., Terminel, M., Cunningham, R., Sefiani, A., Callaway, K., Gaddy, D., & Geoffroy, C. G. (2022). Osteopenia in a Mouse Model of Spinal Cord Injury: Effects of Age, Sex and Motor Function. Biology, 11(2), 189. https://urldefense.com/v3/__https://doi.org/10.3390/biology11020189__;!!KwNVnqRv!GXQXoLESdErt_yBuOl1l2Vuh_3lvcybZhWjg2u2k2xoKX9gzODx13Vj_qXXYCaYtga36wYCtY4cpcsEUodA$
  • Brakel, K., Aceves, M. Garza, A., Yoo, C., Escobedo, G., Panchani, N., Shapiro, L., Hook, M. (2021). Inflammation increases the development of depression behaviors in male rats after spinal cord injury. Brain, Behavior, & Immunity - Health, Volume 14, 100258.
    8. Shon, A., Brakel, K., Hook, M., and Park, H. (2021). Closed-loop plantar cutaneous augmentation by electrical nerve stimulation increases ankle plantarflexion during treadmill walking. IEEE Transactions on Biomedical Engineering, 68 (9): 2798-2809.
  • Shon, A., Brakel, K., Hook, M., and Park, H. (2021). Fully Implantable Plantar Cutaneous Augmentation System for Rats using Closed-loop Electrical Nerve Stimulation. IEEE Transactions on Biomedical Circuits and Systems, 15 (2): 326-338.
  • Zarate SM, Pandey G, Chilukuri S, Garcia JA, Cude B, Storey S, Salem NA, Bancroft EA, Hook M, Srinivasan R.J (2020). Cytisine is neuroprotective in female but not male 6-hydroxydopamine lesioned parkinsonian mice and acts in combination with 17-β-estradiol to inhibit apoptotic endoplasmic reticulum stress in dopaminergic neurons. Neurochem. 2020 Dec 23. doi: 10.1111/jnc.15282.
  • Stampas, A., Pedroza, C., Bush, J., Ferguson, A., Kramer, J., and Hook, M. (2020). The First 24 hours: Opioid Administration in People with Spinal Cord Injury and Neurologic Recovery. Spinal Cord, 58(10):1080-1089.
  • Strain, M.M., Hook, M.A., Reynolds, J.D., Huang, Y.J., Henwood, M.K., and Grau, J.W. (2019). A brief period of moderate noxious stimulation induces hemorrhage and impairs locomotor recovery after spinal cord injury. (2019). Physiology and Behavior, 212:112695.
  • Brakel, K., Aceves, A., Aceves, M., Hierholzer, A., Nguyen, N., and Hook, M. (2019). Depression-like behavior corresponds with cardiac changes in a rodent model of spinal cord injury. Experimental Neurology, 320: 112977.
  • Brakel, K., and Hook, M. (2019). Brakel, K., and Hook, M. (2019). SCI and Depression: Does Inflammation Commandeer the brain?. Experimental Neurology, 320:112977.
    15. Aceves, M., Terminel, M.N., Okoreeh, A., Aceves, A.R., Gong, Y., Polanco, A., Sohrabji, F. and Hook, M.A. (2019). Morphine increases macrophages at the lesion site following spinal cord injury: Protective effects of minocycline. Brain, Behavior and Immunity, 79: 125-138.
  • Metzger, C.E., Gong, S., Aceves, M., Bloomfield, S.A., and Hook MA. (2018). Osteocytes reflect a pro-inflammatory state following spinal cord injury in a rodent model. Bone. 20, 465-475.
  • Grau, J.W., Huang, Y-J., Turtle, J.D., Strain, M.M., Miranda, R.M., Garraway, S.M., Hook, M.A. (2017). When pain hurts: Nociceptive stimulation induces a state of maladaptive plasticity and impairs recovery after spinal cord injury. J Neurotrauma, 34(10):1873-1890.
  • Turtle, J.D., Strain, M.M., Huang, Y-J., Reynolds, J.A., Hook, M.A., and Grau, J.W. (2017). Pain input impairs recovery after spinal cord injury: Treatment with lidocaine. J Neurotrauma, 34(6):1200-1208.
  • Aceves, M., Bancroft, E.A., Aceves, A.R., and Hook, M.A. NorBNI Blocks the Adverse Effects of Morphine Following Spinal Cord Injury. (2017). J Neurotrauma, 34(6):1164-1174.
  • Hook, M.A., Woller, S.A., Aceves, M., Bancroft, E., Funk, M.K., Hartman, J., Garraway, S. (2017). Neurobiological consequences of morphine following spinal cord injury. J Neurotrauma, 34(3):632-644.
  • Aceves, M., Mathai, B., Hook, M.A. (2016). Evaluation Of The Effects Of Specific Opioid Receptor Agonists In A Rodent Model Of Spinal Cord Injury, Spinal Cord, 54(10):767-777. doi: 10.1038/sc.2016.28.
  • Maldonado-Bouchard, S., Peters, K., Woller, S.A., Madahiaz, B., Faghihi, U., Patel, S., Bake, S., Hook, M.A. (2016) Inflammation is Increased with Anxiety- And Depression-Like Signs in a Rat Model of Spinal Cord Injury. Brain, Behavior and Immunity, 51: 176-195.
  • Woller, S.A., Malik, J.S., Aceves, M., and Hook, M.A. (2014). Morphine self-administration following spinal cord injury. Journal of Neurotrauma, 31(18): 1570-1583
  • Maldonado Bouchard, S. and Hook, M.A. (2014). Psychological stress as a modulator of functional recovery following spinal cord injury. Frontiers in Neurology, 5: 44
  • Luedtke, K., Maldonado Bouchard, S., Woller, S.A., Funk, M.K., Aceves, M., and Hook M.A. (2014). Assessment of depression in a rodent model of spinal cord injury. Journal of Neurotrauma, 31(12):1107-21.
  • Woller, S.A. & Hook, M.A. (2013). Opioid administration following spinal cord injury: Implications for pain and motor recovery. Experimental Neurology, 247: 328-341.
  • Woller, S.A., Moreno, G.L., Hart, N., Wellman, P.J., Grau, J.W., & Hook, M.A. (2012). Analgesia or addiction: implications for morphine use after spinal cord injury. Journal of Neurotrauma, 9(8):1650-62.

Current Funding

2023-2024        WoodNext Foundation: Brain-gut interactions in a rat model of SCI (Principal          Investigator)            

2022-2025        Department of Defense: Opioid-Immune interactions and their implications for long term recovery after SCI (Principal Investigator)

2022-2024        Department of Defense: Therapeutic Potential of Increasing Lymphangiogenesis in a Mouse Model of ALS (Co-Investigator)

2022-2023        Mission Connect: Does loss of sympathetic nerve signaling underly acute, rapid bone loss after spinal cord injury? (Principal Investigator)

2022-2024        Texas A&M University Seedling Grant: Bone marrow (BM) transplants to reduce the risk of osteoporosis after spinal cord injury (SCI) (Principal Investigator)

2022-2024        International Spinal Research Trust: Local and sustained release of Chondroitinase ABC-37 (Co-Investigator)