Marcia G. Honig, PhD

Education

• PhD Institution: Yale University, Department of Biology
• Postdoctoral: State University of New York at Stony Brook, Department of Neurobiology and Behavior; University of Michigan, Department of Biology

Research Interests

The research in my laboratory is focused on examining the behavioral consequences of traumatic brain injury (TBI) and the associated pathological changes, through the use of a mouse model.  We create the injury by delivering a high-pressure air blast to a restricted part of one side of the cranium, after anesthetizing and stabilizing the mouse to restrict its movement and shielding the rest of the head and the entire body from the blast.  In terms of the biomechanical forces produced by the air blast, the functional deficits exhibited by the mice, and the widespread axonal injury later observed with histological analysis, our model very much mimics the mild TBI (i.e. concussion) sustained by humans during traumatic incidents such as sports injuries, motor vehicle accidents, and falls, where the skull remains intact.  Accompanying the initial axonal injury, microglia become activated and the ensuing neuroinflammation contributes to further pathogenesis.

We are currently pursuing this in two ways.  First, we are utilizing a pharmacological agent that modulates microglia in such a way as to improve the outcome from TBI, and may also provide benefit in neurodegenerative diseases such as Alzheimer’s and ALS where neuroinflammation contributes to disease progression.  Secondly, we are examining how neuroinflammatory responses contribute to long-term decline, particularly with regard to cognitive function and following multiple traumatic events.

Recent Publications

• Honig MG, Del Mar NA, Henderson DL, Ragsdale TD, Doty JB, Driver JH, Li C, Fortugno AP, Mitchell WM, Perry AM, Moore BM, Reiner A. Amelioration of visual deficits and visual system pathology after mild TBI via the cannabinoid Type-2 receptor inverse agonism of raloxifene. Exp Neurol. 2019 Dec;322:113063. doi: 10.1016/j.expneurol.2019.113063. Epub 2019 Sep 10. PubMed PMID: 31518568.
• Guley NM, Del Mar NA, Ragsdale T, Li C, Perry AM, Moore BM, Honig MG, Reiner A. Amelioration of visual deficits and visual system pathology after mild TBI with the cannabinoid type-2 receptor inverse agonist SMM-189. Exp Eye Res. 2019 May;182:109-124. doi: 10.1016/j.exer.2019.03.013. Epub 2019 Mar 26. PubMed PMID: 30922891; PubMed Central PMCID: PMC6504571.
• Liu Y, McAfee SS, Guley NM, Del Mar N, Bu W, Heldt SA, Honig MG, Moore BM 2nd, Reiner A, Heck DH. Abnormalities in Dynamic Brain Activity Caused by Mild Traumatic Brain Injury Are Partially Rescued by the Cannabinoid Type-2 Receptor Inverse Agonist SMM-189. eNeuro. 2017 Aug 18;4(4). pii: ENEURO.0387-16.2017. doi: 10.1523/ENEURO.0387-16.2017. eCollection 2017 Jul-Aug. PubMed PMID: 28828401; PubMed Central PMCID: PMC5562300.
• Bu W, Ren H, Deng Y, Del Mar N, Guley NM, Moore BM, Honig MG, Reiner A. Mild Traumatic Brain Injury Produces Neuron Loss That Can Be Rescued by Modulating Microglial Activation Using a CB2 Receptor Inverse Agonist. Front Neurosci. 2016 Oct 6;10:449. eCollection 2016. PubMed PMID: 27766068; PubMed Central PMCID: PMC5052277.
• Guley NH, Rogers JT, Del Mar NA, Deng Y, Islam RM, D'Surney L, Ferrell J, Deng B, Hines-Beard J, Bu W, Ren H, Elberger AJ, Marchetta JG, Rex TS, Honig MG, Reiner A. A Novel Closed-Head Model of Mild Traumatic Brain Injury Using Focal Primary Overpressure Blast to the Cranium in Mice. J Neurotrauma. 2016 Feb 15;33(4):403-22. doi: 10.1089/neu.2015.3886. Epub 2015 Dec 17. PubMed PMID: 26414413; PubMed Central PMCID: PMC4761824.
• del Mar N, von Buttlar X, Yu AS, Guley NH, Reiner A, Honig MG. A novel closed-body model of spinal cord injury caused by high-pressure air blasts produces extensive axonal injury and motor impairments. Exp Neurol. 2015 Sep;271:53-71. doi: 10.1016/j.expneurol.2015.04.023. Epub 2015 May 7. PubMed PMID: 25957630; PubMed Central PMCID: PMC4586366.

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