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Serotonin receptor and dendritic plasticity in the spinal cord mediated by chronic serotonergic pharmacotherapy combined with exercise following complete SCI in the adult rat
Journal article   Open access   Peer reviewed

Serotonin receptor and dendritic plasticity in the spinal cord mediated by chronic serotonergic pharmacotherapy combined with exercise following complete SCI in the adult rat

Patrick D Ganzer, Carl R Beringer, Jed S Shumsky, Chiemela Nwaobasi and Karen A Moxon
Experimental neurology, v 304, pp 132-142
Jun 2018
DOI: https://doi.org/10.1016/j.expneurol.2018.03.006
PMID: 29526741
Featured in Collection :   UN Sustainable Development Goals @ Drexel
url
https://europepmc.org/articles/pmc5915900View
Accepted (AM)Open Access (License Unspecified),  Open

Abstract

Aging Animals Female Neuronal Plasticity - drug effects Neuronal Plasticity - physiology Physical Conditioning, Animal - methods Quipazine - pharmacology Rats Rats, Sprague-Dawley Recovery of Function - drug effects Recovery of Function - physiology Serotonin Receptor Agonists - pharmacology Spinal Cord - drug effects Spinal Cord - physiopathology Spinal Cord Injuries - physiopathology
Severe spinal cord injury (SCI) damages descending motor and serotonin (5-HT) fiber projections leading to paralysis and serotonin depletion. 5-HT receptors (5-HTRs) subsequently upregulate following 5-HT fiber degeneration, and dendritic density decreases indicative of atrophy. 5-HT pharmacotherapy or exercise can improve locomotor behavior after SCI. One might expect that 5-HT pharmacotherapy acts on upregulated spinal 5-HTRs to enhance function, and that exercise alone can influence dendritic atrophy. In the current study, we assessed locomotor recovery and spinal proteins influenced by SCI and therapy. 5-HT, 5-HT R, 5-HT R, and dendritic densities were quantified both early (1 week) and late (9 weeks) after SCI, and also following therapeutic interventions (5-HT pharmacotherapy, bike therapy, or a combination). Interestingly, chronic 5-HT pharmacotherapy largely normalized spinal 5-HTR upregulation following injury. Improvement in locomotor behavior was not correlated to 5-HTR density. These results support the hypothesis that chronic 5-HT pharmacotherapy can mediate recovery following SCI, despite acting on largely normal spinal 5-HTR levels. We next assessed spinal dendritic plasticity and its potential role in locomotor recovery. Single therapies did not normalize the loss of dendritic density after SCI. Groups displaying significantly atrophied dendritic processes were rarely able to achieve weight supported open-field locomotion. Only a combination of 5-HT pharmacotherapy and bike therapy enabled significant open-field weigh-supported stepping, mediated in part by restoring spinal dendritic density. These results support the use of combined therapies to synergistically impact multiple markers of spinal plasticity and improve motor recovery.

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26 citations in Web of Science
28 citations in Scopus

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