- Ph.D., Neurobiology, University of Alabama at Birmingham
- B.S., Psychology and Biology, State University of New York at Binghamton
Our brain cells communicate with one another by a process known as synaptic transmission. Synaptic transmission forms the basis of our thoughts and perception. In human patients with epilepsy, aberrant synaptic transmission contributes to seizures.
The focus of my research is to: 1) to understand the molecular mechanisms of altered synaptic communication that leads to the development of epilepsy and identify targets that may serve as therapeutic targets for treatment 2) to elucidate the mechanism that make a subset of epilepsy patients refractory to treatment (patients that cannot control their seizures with common anti-epileptic drugs) and 3) to decipher the role of the gut microbiota in seizure susceptibility in acquired and idiopathic epilepsies (epilepsies of unknown cause).
Projects will aim to: 1) determine how changes in the gut microbiota influences the function of neuron and glia cells to shape synaptic function in different neuronal circuits in normal and epilepsy models, 2) examine how specific diets affects the composition of the gut microbiota and regulate neuronal function and seizure threshold, 3) decipher how bacterially released molecules such as short-chain fatty acids can regulate neuronal function to shape neuronal hyperexcitability, and 4) determine differences in the quantity and diversity of microbes in epilepsy models.
My lab utilizes a variety of methodologies including electrophysiological techniques to probe changes in the function of neuronal circuits, synapses, and synaptic receptors, modern molecular approaches, imaging, and biochemical analyses. To assess changes in gut microbes we will use 16S rRNA and metagenomic sequencing.
Ultimately, the goal is to identify the mechanisms by which the gut microbes affect seizure activity and then develop deliberate manipulation of the gut microbiota as a therapeutic strategy to ameliorate seizure activity.
1. Campbell SL, vaan Groen T, Kadisha I, Smoot LH and Bolger GB. 2017 Altered phosphorylation, electrophysiology, and behavior on attenuation of PDE4B action in hippocampus. BMC Neuroscience. 2017 Dec 2;18(1):77.
2. Robert SM, Buckingham SC, Campbell SL, Robel S, Holt KT, Ogunrinu-Babarinde T, Warren PP, White DM, Reid MA, Eschbacher JM, Berens ME, Lahti AC, Nabors LB, Sontheimer H. SLC7A11 expression is associated with seizures and predicts poor survival in patients with malignant glioma. Sci Transl Med. 2015 May 27;7(289).
3. Robel S, Buckingham SC, Boni JL, Campbell SL, Danbolt NC, Riedemann T, Sutor B, Sontheimer H. Reactive astrogliosis causes the development of spontaneous seizures. J Neurosci. 2015 Feb 25;35(8):3330-45.
4. Yokoi F, Chen HX, Dang MT, Cheetham CC, Campbell SL, Roper SN, Sweatt JD, Li Y. Behavioral and electrophysiological characterization of Dyt1 heterozygous knockout mice. PLoS One. 2015 Mar 23;10(3).
5. Campbell SL, Robel S, Cuddapah VA, Robert S, Buckingham SC, Kahle KT, Sontheimer H. GABAergic disinhibition and impaired KCC2 cotransporter activity underlie tumor-associated epilepsy. Glia. 2015 Jan;63(1):23-36.
6. Campbell SL, Hablitz JJ, Olsen ML. Functional changes in glutamate transporters and astrocyte biophysical properties in a rodent model of focal cortical dysplasia. Front Cell Neurosci. 2014 Dec 17;8:425.
7. Yokoi F, Cheetham CC, Campbell SL, Sweatt JD, Li Y. Pre-synaptic release deficits in a DYT1 dystonia mouse model. PLoS One. 2013 Aug 13;8(8).
8. Campbell SL, Buckingham SC, Sontheimer H. Human glioma cells induce hyperexcitability in cortical networks. Epilepsia. 2012 Aug;53(8):1360-70.
9. Calfa G, Chapleau CA, Campbell S, Inoue T, Morse SJ, Lubin FD, Pozzo-Miller L. HDAC activity is required for BDNF to increase quantal neurotransmitter release and dendritic spine density in CA1 pyramidal neurons. Hippocampus. 2012 Jul;22(7):1493-500.
10. Buckingham SC, Campbell SL, Haas BR, Montana V, Robel S, Ogunrinu T, Sontheimer H. Glutamate release by primary brain tumors induces epileptic activity. Nat Med. 2011 Sep 11;17(10):1269-74.
11. Xie Z, Cahill ME, Radulovic J, Wang J, Campbell SL, Miller CA, Sweatt JD, Penzes P. Hippocampal phenotypes in kalirin-deficient mice. Mol Cell Neurosci. 2011 Jan;46(1):45-54.
12. Feng J, Zhou Y, Campbell SL, Le T, Li E, Sweatt JD, Silva AJ, Fan G. Dnmt1 and Dnmt3a maintain DNA methylation and regulate synaptic function in adult forebrain neurons. Nat Neurosci. 2010 Apr;13(4):423-30.
13. Olsen ML, Campbell SC, McFerrin MB, Floyd CL, Sontheimer H. Spinal cord injury causes a wide-spread, persistent loss of Kir4.1 and glutamate transporter 1: benefit of 17 beta-oestradiol treatment. Brain. 2010 Apr;133(Pt 4):1013-25.
14. Yokoi F, Dang MT, Miller CA, Marshall AG, Campbell SL, Sweatt JD, Li Y. Increased c-fos expression in the central nucleus of the amygdala and enhancement of cued fear memory in Dyt1 DeltaGAG knock-in mice. Neurosci Res. 2009 Nov;65(3):228-35.
15. Campbell SL, Hablitz JJ. Decreased glutamate transport enhances excitability in a rat model of cortical dysplasia. Neurobiol Dis. 2008 Nov;32(2):254-61.
16. Miller CA, Campbell SL, Sweatt JD. DNA methylation and histone acetylation work in concert to regulate memory formation and synaptic plasticity. Neurobiol Learn Mem. 2008 May;89(4):599-603.
17. Olsen ML, Campbell SL, Sontheimer H. Differential distribution of Kir4.1 in spinal cord astrocytes suggests regional differences in K+ homeostasis. J Neurophysiol. 2007 Aug;98(2):786-93.
18. Campbell SL, Mathew SS, Hablitz JJ. Pre- and postsynaptic effects of kainate on layer II/III pyramidal cells in rat neocortex. Neuropharmacology. 2007 Jul;53(1):37-47.
19. Olsen ML, Higashimori H, Campbell SL, Hablitz JJ, Sontheimer H. Functional expression of Kir4.1 channels in spinal cord astrocytes. Glia. 2006 Apr 1;53(5):516-28.
20. Campbell S, Hablitz JJ. Modification of epileptiform discharges in neocortical neurons following glutamate uptake inhibition.Epilepsia.
21. Campbell SL, Hablitz JJ. Glutamate transporters regulate excitability in local networks in rat neocortex. Neuroscience. 2004;127(3):625-35.
- 3460 Litton-Reaves Hall