RESEARCH ARTICLE


Synaptic Signals from Glutamate-Treated Neurons Induce Aberrant Post-Synaptic Signals in Untreated Neuronal Networks



Mary Guaraldi1, Sangmook Lee1, 2, Thomas B. Shea1, *
iD

1 Laboratory for Neuroscience, Department of Biological Sciences, University of Massachusetts Lowell, Lowell, MA 01854, USA
2 MassBiologics, Fall River, MA 02720, USA


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© 2020 Guaraldi et al.

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* Address correspondence to this author at the Laboratory for Neuroscience, Department of Biological Sciences, University of Massachusetts Lowell, Lowell, MA 01854, USA; Tel: 978-934-2881; Fax: 978-934-3044; E-mail: thomas_shea@uml.edu


Abstract

Background and Objective:

Glutamate neurotoxicity is associated with a wide range of disorders and can impair synaptic function. Failure to clear extracellular glutamate fosters additional cycles and spread of regional hyperexcitation.

Methods and Results:

Using cultured murine cortical neurons, herein it is demonstrated that synaptic signals generated by cultures undergoing glutamate-induced hyperactivity can invoke similar effects in other cultures not exposed to elevated glutamate.

Conclusion:

Since sequential synaptic connectivity can encompass extensive cortical regions, this study presents a potential additional contributor to the spread of damage resulting from glutamate excitotoxicity and should be considered in attempts to mitigate neurodegeneration.

Keywords: Glutamate, Hyperactivity, Neurotoxicity, Multi-electrode arrays, Neurodegeneration, Synaptic signaling.