Smoking remains the leading cause of morbidity and mortality in the United States, with less than 5% of smokers attempting to quit succeeding. This low smoking cessation success rate is thought to be due to the long-term adaptations and alterations in synaptic plasticity that occur following chronic nicotine exposure and withdrawal. Glial cells have recently emerged as active players in the development of dependence phenotypes due to their roles in modulating neuronal functions and synaptic plasticity. Fundamental studies have demonstrated that microglia and astrocytes are crucial for synapse formation and elimination in the developing brain, likely contributing to why glial dysfunction is implicated in numerous neurological and psychiatric disorders. Recently, there is increasing evidence for the involvement of glial cells in drug dependence and its associated behavioral manifestations. This review summarizes the newly evaluated role of microglia and astrocytes as molecular drivers of nicotine dependence and withdrawal phenotypes.
|State||Published - Sep 15 2020|
Bibliographical noteFunding Information:
This work was supported by federal funding from the National Institutes of Health- NIDA ( DA044311 to JRT and DA049087 to ELA) and by an IRC seed grant from the University of Kentucky .
ASJC Scopus subject areas
- Cellular and Molecular Neuroscience