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Victor et al. Neuroimmunol Neuroinflammation 2020;7:234-47 Neuroimmunology
DOI: 10.20517/2347-8659.2020.02 and Neuroinflammation

Review Open Access

Microglial contributions to aberrant neurogenesis
and pathophysiology of epilepsy

Tanya R. Victor, Stella E. Tsirka

Department of Pharmacological Sciences, Stony Brook University, Stony Brook, NY 11794, USA.
Correspondence to: Dr. Stella E. Tsirka, Program in Molecular and Cellular Pharmacology, Department of Pharmacological
Sciences, Stony Brook University, 101 Nichols Rd, Stony Brook, NY 11794-8651, USA. E-mail: styliani-anna.tsirka@stonybrook.edu

How to cite this article: Victor TR, Tsirka SE. Microglial contributions to aberrant neurogenesis and pathophysiology of epilepsy.
Neuroimmunol Neuroinflammation 2020;7:234-47. http://dx.doi.org/10.20517/2347-8659.2020.02

Received: 5 Jan 2020 First Decision: 2 Mar 2020 Revised: 26 Mar 2020 Accepted: 27 May 2020 Available online: 12 Jul 2020

Academic Editor: Athanassios P. Kyritsis Copy Editor: Cai-Hong Wang Production Editor: Jing Yu

Abstract
Microglia are dynamic cells that constitute the brain’s innate immune system. Recently, research has demonstrated
microglial roles beyond immunity, which include homeostatic roles in the central nervous system. The function
of microglia is an active area of study, with insights into changes in neurogenesis and synaptic pruning being
discovered in both health and disease. In epilepsy, activated microglia contribute to several changes that occur
during epileptogenesis. In this review, we focus on the effects of microglia on neurogenesis and synaptic pruning,
and discuss the current state of anti-seizure drugs and how they affect microglia during these processes. Our
understanding of the role of microglia post-seizure is still limited and may be pivotal in recognizing new therapeutic
targets for seizure intervention.

Keywords: Microglia, epilepsy, neurogenesis, neuroinflammation, seizures

INTRODUCTION
Epilepsy is a neurological disorder characterized by recurrent seizures. Microglia, the innate immune
cells of the central nervous system (CNS), are increasingly recognized as mediators of seizures and
contributors to the epileptogenic process. The progression to epilepsy is characterized by the presence of
neuroinflammation, as well as structural and molecular alterations in the brain, that subsequently lead
to increased neuronal hyperexcitability and a lasting disposition towards spontaneous recurrent seizures
[1]
(SRS) . Microglia regulate neuroinflammation and axonal sprouting and have been reported to modulate

© The Author(s) 2020. Open Access This article is licensed under a Creative Commons Attribution 4.0
International License (https://creativecommons.org/licenses/by/4.0/), which permits unrestricted use,
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