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Neuroscience PhD at Wake Forest University at Wake Forest University

Wake Forest University Graduate School » Neuroscience PhD at Wake Forest University

Mark Ferris

Mark Ferris
The primary theme of the research in Dr. Ferris’ laboratory is to understand the neurobiology of reward and reinforcement learning and how learning-induced changes in neurobiology shape goal-directed / motivated behavior and habit formation.  We seek to understand the function of specific receptors (e.g., nicotinic receptors) and rapid neurotransmitter signaling (particularly interactions of dopamine and acetylcholine) under normal learning conditions and in neuropsychiatric disorders like drug addiction, Parkinson’s disease, and HIV-associated neurocognitive disorder.  We use a number of techniques in the laboratory including (but not limited to) drug and natural reward self-administration in rodents, voltammetry in freely-behaving rodents to detect rapid dopamine signals in real time as they interact with their environment, voltammetry in brain slices and anesthetized preparations, microdialysis coupled to high-pressure liquid chromatography (HPLC), viral-mediated gene transfer technologies, histochemistry, microscopy, and various behavioral assays (e.g., locomotor activity and conditioned learning).  We detect neurotransmitters en passant as animals interact with their environment or we stimulate neurotransmitter release using traditional pharmacology, electrical stimulation of specific brain regions, or light-stimulation with optogenetics.


  • Siciliano CA, Jones SR, Ferris MJ. Beta2 subunit containing nicotinic acetylcholine receptors exert opposing actions on rapid dopamine signaling in the nucleus accumbens of drug use prone and resilient animals.  Under Revision.
  • Melchior JR, Ferris MJ, Stuber GD, Riddle DR, Jones SR (2015). Optogenetic stimulation of dopamine terminals in the nucleus accumbens reveals local modulation of presynaptic release.  Journal of Neurochemistry, in press.
  • Ferris MJ, Calipari ES, Rose JH, Siciliano CA, Sun H, Chen R, Jones SR (2015). A single amphetamine infusion reverses deficits in dopamine nerve-terminal function caused by a history of cocaine self-administration. Neuropsychopharmacology, 40(8): 1826-1836.
  • Ferris MJ, España RA, Locke J, Konstantopoulos JK, Rose JH, Chen R, Jones SR (2014). Dopamine transporters govern diurnal variation in extracellular dopamine tone. Proceedings of the National Academy of Sciences, USA, 111(26):E2751-2759.
  • *Featured in: Research Highlights. Bray, N. (2014) Dopamine tone depends on DAT. Nature Reviews    Neuroscience, 15: 495.
  • Daigle TL, Ferris MJ, Gainetdinov RR, Sotnikova TD, Urs NM, Jones SR, Caron MG (2014). Selective deletion of GRK2 causes distinct alterations in dopamine-dependent behaviors and neurotransmission. Neuropsychopharmacology, 39(10): 2450-2462.
  • Ferris MJ, Milenkovic M, Mielnik CA, John CE, España RA, Gulerson M, Sotnikova TD, Gainetdinov RR, Jones SR, Ramsey AJ (2014). NMDA receptor hypofunction remodels the dopamine system and impairs phasic signaling. European Journal of Neuroscience, 40(1):2255-2263.
  • Ferris MJ, Calipari ES, Melchior JR, Roberts DC, España RA, Jones SR. (2013). Paradoxical tolerance to cocaine after initial supersensitivity in drug use prone animals. European Journal of Neuroscience, 38(4): 2628-2636.
  • Calipari ES, Ferris MJ. (2013). Amphetamine mechanisms and actions at the dopamine terminal revisited. Journal of Neuroscience, 33(21): 8923-8925.
  • Ferris MJ, Calipari ES, Yorgason JT, Jones SR. (2013). Examining the complex regulation and drug-induced plasticity of dopamine release and uptake using voltammetry in brain slices. ACS Chemical Neuroscience, 4(5): 693-703.
  • Ferris MJ, Calipari ES, Melchior JR, Roberts DC, Jones SR. (2012). Cocaine self-administration produces pharmacodynamic tolerance: Differential effects on the potency of dopamine transporter blockers, releasers, and methylphenidate. Neuropsychopharmacology, 37(7): 1708-1716.
  • Ferris MJ, Mateo Y, Roberts DC, Jones SR. (2011). Cocaine-insensitive dopamine transporters with intact substrate transport produced by self-administration. Biological Psychiatry, 69(3): 201-207.
  • Ferris MJ, Frederick-Duus D, Fadel J, Mactutus CF, Booze RM. (2009). The HIV-1 associated protein, Tat1-86, impairs dopamine transporters and interacts with cocaine to reduce nerve terminal function. Neuroscience, 159(4):1292-1299.
  • Ferris MJ, Mactutus CF, Booze RM. (2008). Neurotoxic profiles of HIV, psychostimulant drugs of abuse, and their concerted effect of the brain: Current status of dopamine system vulnerability in NeuroAIDS. Neuroscience and Biobehavioral Reviews, 32(5):883-909.