Twitter(X): @audrey_medeiros

ORCID: 0000-0002-5562-4772

Hi all! I am a senior graduate student in the lab interested in how synaptic architecture relates to synapse function. My main area of study in the lab is how the organization of calcium channels and their auxiliary subunits contribute to the neurotransmitter release properties of a synapse.

Background: I have my B.S. in Pathobiology from the University of Connecticut, where I was an undergraduate researcher in Dr. Pinar Zorlutuna’s lab. During my year in the lab, I fabricated microfluidic devices to use in the study of cardiac ischemic injury with the goal of reducing our dependence on animal models. When the Zorlutuna lab moved to Notre Dame in 2014, I started my journey into neuroscience through a summer position in Dr. Elizabeth Jonas’s lab of Yale University. Working with Dr. Jonas, I cultured hippocampal neurons for live confocal imaging in long-term potentiation (LTP) studies. The goal of this work was to induce LTP in ATP-FRET-expressing neurons, a technique that relies on excitation of a donor molecule for fluorescence, to identify mutations that disrupt LTP. After graduation, I conducted research in Dr. Jennifer Morgan’s lab at the Marine Biological Laboratory as a research assistant where my projects centered on the presynaptic protein α-synuclein, whose atypical aggregation is linked to compromised neurotransmission and disease pathogenesis in Parkinson’s Disease. In my 3 years in the Morgan lab I explored how unique conformations (monomer, dimer, and brain-derived) of α-synuclein influence synaptic structure using transmission electron microscopy of the lamprey giant reticulospinal synapse (see references below).

Current Work: I joined the O’Connor-Giles lab in 2018 where I use genetic tools, including CRISPR gene editing to endogenously tag synaptic proteins, and confocal and superresolution microscopy to study synapse structure-function relationships at the Drosophila neuromuscular junction (NMJ). I study two distinct motor neuronal subtypes that innervate most muscles and drive locomotion, a functionally phasic neuron that terminates in “small” boutons (type Is) and a functionally tonic neuron that forms “big” boutons (type Ib). These two subtypes form synapses with distinct release probabilities, where type Is synapses have a higher probability of release and higher action potential induced calcium influx than type Ib. I use these two motor neuron subtypes as a model to study how the organization of calcium channel complexes contributes to  distinct release properties, and how these differences are regulated in adaptive plasticity. I also use electron microscopy to study the ultrastructural effects of mutant/null alleles of proteins important for synapse assembly and function.

Outside lab: Outside of lab I like going skiing in the winter, hiking around New England, and love to travel! My favorite places I’ve visited so far are Madeira in Portugal, Cinque Terre and Amalfi in Italy, Banff National Park in Canada, and Jackson Hole in Wyoming USA.


Medeiros AT., O’Connor-Giles KM. (2023). To b or not to b: transcriptional regulation of tonic type Ib vs. phasic type Is motor neurons. Neuron Preview 2023;111(22):3497-3499.

Medeiros AT., Gratz J, Delgado A, Ritt JT, O’Connor-Giles KM. (2023). Molecular and organizational diversity intersect to generate functional synaptic heterogeneity within and between excitatory neuronal subtypes. eLife, 12:RP88412.

Banks SML, Medeiros AT, Sousa R, Lafer EM, Morgan JR. (2021). Chaperone proteins as ameliorators of α-synuclein-induced synaptic pathologies: insights into Parkinson’s disease. Neural Regen Res 16(6):1198-1199.

Román-Vendrell C, Medeiros AT, Sanderson JB, Jiang H, Bartels T, Morgan JR. (2021). Effects of excess brain-derived human α-synuclein on synaptic vesicle trafficking. Front. Neurosci. 15:639414.

Soll L, Eisen J, Vargas K, Medeiros AT, Hammar KM, Morgan J. α-Synuclein-112 impairs synaptic vesicle recycling consistent with its enhanced membrane binding properties. Front. Cell Dev. Biol., 8(405).

Banks SML*, Medeiros AT*, McQuillan M, Busch D, Ibarraran-Vinegra AS, Roy S, Sousa R, Lafer EM, Morgan JR. (2020). Hsc70 Ameliorates the Vesicle Recycling Defects Caused by Excess α-Synuclein at synapses, eNeuro.0448-19.2020. *Indicates equal contribution. 

Medeiros AT, Bubacco L, Morgan JR. (2018). Impacts of increased α-synuclein on clathrin-mediated endocytosis at synapses: implications for neurodegenerative diseases. Neural Regen Res 2018;13:647-8.

Medeiros AT, Soll LG, Tessari I, Bubacco L, & Morgan JR. (2017). α-Synuclein Dimers Impair Vesicle Fission during Clathrin-Mediated Synaptic Vesicle Recycling. Front. Cell Neurosci., 11:388.