Chase Francis, Ph.D.

@article{Francis:2018aa,

title = {Synaptic and intrinsic plasticity in the ventral tegmental area after chronic cocaine.},

author = {Tanner Chase Francis and Stephanie C Gantz and Khaled Moussawi and Antonello Bonci},

url = {https://www.ncbi.nlm.nih.gov/pubmed/30237117},

doi = {10.1016/j.conb.2018.08.013},

issn = {1873-6882 (Electronic); 0959-4388 (Linking)},

year  = {2018},

date = {2018-09-17},

journal = {Curr Opin Neurobiol},

volume = {54},

pages = {66--72},

address = {Intramural Research Program, Synaptic Plasticity Section, National Institute on Drug Abuse, US National Institutes of Health, Baltimore, MD 21224, USA.},

abstract = {Cocaine exposure induces persistent changes in synaptic transmission and intrinsic properties of ventral tegmental area (VTA) dopamine neurons. Despite significant progress in understanding cocaine-induced plasticity, an effective treatment of cocaine addiction is lacking. Chronic cocaine potentiates excitatory and alters inhibitory transmission to dopamine neurons, induces dopamine neuron hyperexcitability, and reduces dopamine release in projection areas. Understanding how intrinsic and synaptic plasticity interact to control dopamine neuron firing and dopamine release could prove useful in the development of new therapeutics. In this review, we examine recent literature discussing cocaine-induced plasticity in the VTA and highlight potential therapeutic interventions.},

keywords = {},

pubstate = {published},

tppubtype = {article}

}

@article{Francis:2017aa,

title = {Molecular basis of dendritic atrophy and activity in stress susceptibility.},

author = {T C Francis and R Chandra and A Gaynor and P Konkalmatt and S R Metzbower and B Evans and M Engeln and T A Blanpied and M K Lobo},

url = {https://www.ncbi.nlm.nih.gov/pubmed/28894298},

doi = {10.1038/mp.2017.178},

issn = {1476-5578 (Electronic); 1359-4184 (Linking)},

year  = {2017},

date = {2017-11-01},

journal = {Mol Psychiatry},

volume = {22},

number = {11},

pages = {1512--1519},

address = {Department of Anatomy and Neurobiology, University of Maryland School of Medicine, University of Maryland, Baltimore, MD, USA.},

abstract = {Molecular and cellular adaptations in nucleus accumbens (NAc) medium spiny neurons (MSNs) underlie stress-induced depression-like behavior, but the molecular substrates mediating cellular plasticity and activity in MSN subtypes in stress susceptibility are poorly understood. We find the transcription factor early growth response 3 (EGR3) is increased in D1 receptor containing MSNs of mice susceptible to social defeat stress. Genetic reduction of Egr3 levels in D1-MSNs prevented depression-like outcomes in stress susceptible mice by preventing D1-MSN dendritic atrophy, reduced frequency of excitatory input and altered in vivo activity. Overall, we identify NAc neuronal-subtype molecular control of dendritic morphology and related functional adaptations, which underlie susceptibility to stress.},

keywords = {},

pubstate = {published},

tppubtype = {article}

}

@article{Francis:2015aa,

title = {Nucleus accumbens medium spiny neuron subtypes mediate depression-related outcomes to social defeat stress.},

author = {Chase T Francis and Ramesh Chandra and Danielle M Friend and Eric Finkel and Genesis Dayrit and Jorge Miranda and Julie M Brooks and Sergio D Iniguez and Patricio O'Donnell and Alexxai Kravitz and Mary Kay Lobo},

url = {https://www.ncbi.nlm.nih.gov/pubmed/25173629},

doi = {10.1016/j.biopsych.2014.07.021},

issn = {1873-2402 (Electronic); 0006-3223 (Linking)},

year  = {2014},

date = {2014-07-21},

journal = {Biol Psychiatry},

volume = {77},

number = {3},

pages = {212--222},

address = {Department of Anatomy and Neurobiology, University of Maryland School of Medicine, Baltimore.},

abstract = {BACKGROUND: The nucleus accumbens is a critical mediator of depression-related outcomes to social defeat stress. Previous studies demonstrate distinct neuroplasticity adaptations in the two medium spiny neuron (MSN) subtypes, those enriched in dopamine receptor D1 versus dopamine receptor D2, in reward and reinforcement leading to opposing roles for these MSNs in these behaviors. However, the distinct roles of nucleus accumbens MSN subtypes, in depression, remain poorly understood. METHODS: Using whole-cell patch clamp electrophysiology, we examined excitatory input to MSN subtypes and intrinsic excitability measures in D1-green fluorescent protein and D2-green fluorescent protein bacterial artificial chromosome transgenic mice that underwent chronic social defeat stress (CSDS). Optogenetic and pharmacogenetic approaches were used to bidirectionally alter firing of D1-MSNs or D2-MSNs after CSDS or before a subthreshold social defeat stress in D1-Cre or D2-Cre bacterial artificial chromosome transgenic mice. RESULTS: We demonstrate that the frequency of excitatory synaptic input is decreased in D1-MSNs and increased in D2-MSNs in mice displaying depression-like behaviors after CSDS. Enhancing activity in D1-MSNs results in resilient behavioral outcomes, while inhibition of these MSNs induces depression-like outcomes after CSDS. Bidirectional modulation of D2-MSNs does not alter behavioral responses to CSDS; however, repeated activation of D2-MSNs in stress naive mice induces social avoidance following subthreshold social defeat stress. CONCLUSIONS: Our studies uncover novel functions of MSN subtypes in depression-like outcomes. Notably, bidirectional alteration of D1-MSN activity promotes opposite behavioral outcomes to chronic social stress. Therefore, targeting D1-MSN activity may provide novel treatment strategies for depression or other affective disorders.},

keywords = {},

pubstate = {published},

tppubtype = {article}

}