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Student Seminars


Research symposium in honor of Marc Schieber, MD, PHD

Marc Schieber, MD, PHD - Professor, University of Rochester

The Departments of Neuroscience and Neurology, and the Del Monte Institute for Neuroscience welcome you to a research symposium in honor of Marc Schieber, MD, PHD

Reception to follow

Speakers include:

  • Catherine Lang, PhD, Professor of Physical Therapy, Neurology and Occupational Therapy, Washington University
  • Kevin Mazurek, PhD, Assistant Professor of Neurology and Biomedical Engineering, Mayo Clinic, Rochester, MN
  • Adam Rouse, MD, PhD, Dept. Neurosurgery, University of Kansas Medical Center
  • Marco Santello, PhD, Fulton Professor of Neural Engineering, Arizona State University

 Sep 06, 2024 @ 1:00 p.m.

 Medical Center | 1-7619 Adolph Aud

Host: The Departments of Neuroscience and Neurology, and the Del Monte Institute for Neuroscience

The functional impact of cortical and retinal damage on the parallel processing streams in the early visual pathways - Thesis Defense

Jingi Yang - PhD Candidate, Neuroscience Graduate Program

The magnocellular and parvocellular pathways are the major parallel information processing streams of the early visual system. Signals relayed by these pathways from the retina to the dorsal lateral geniculate nucleus (dLGN), and then to primary visual cortex (V1) are critical for visual image processing and representation. When any of these pathways are disrupted, loss of vision occurs. The structure and function of each pathway have been well characterized. However, little is known about neurophysiological changes in these pathways following injury, such as in V1 stroke or retinal disease.

Previous work in non-human primate models of glaucoma suggests that there is a greater loss of cytochrome oxidase reactivity in parvocellular compared to magnocellular layers of the dLGN (Crawford et al., 2001, Sasaoka et al., 2008), suggesting stream-specific effects of retinal ganglion cell (RGC) degeneration. Furthermore, previous work in non-human primate models of V1 damage suggests relative preservation of visually responsive magnocellular neurons in the dLGN after long-term V1 damage (Yu et al., 2018), and visual training-induced recovery in occipital cortical stroke patients is more effective with motion stimuli, i.e., stimuli that activate the magnocellular stream. My thesis aimed to understand whether functional plasticity in the early visual pathways following cortical or retinal damage is stream-specific.

We hypothesized that both RGC loss and V1 lesions caused by stroke could differentially affect the magnocellular or parvocellular pathways. In the first study of an animal (ferret) model of RGC loss, I examined the impact of the retinal excitotoxic lesions on the physiological response properties of dLGN neurons. Although the majority of contralesional transient and sustained dLGN neurons lost tuning to contrast, sustained neurons had longer response latencies, greater variability in their responses to visual stimuli, and greater changes in their tuning preferences compared to transient neurons. In the second study of visual training-induced recovery in human stroke patients, I showed that adaptive training with static, drifting, or flickering Gabor patches of progressively lower contrasts improved contrast sensitivity for both orientation and motion discrimination in cortically-blind (vision loss due to V1 stroke) participants; however, normal contrast sensitivity was not recovered in any participant. In summary, this work suggests that: (1) More RGCs in the X (parvocellular-like) stream than those in the Y (magnocellular-like) stream degenerate following kainic acid injections into the eye, (2) sustained (parvocellular-like) neurons in the ferret dLGN appear to be less functionally resistant to degeneration 7 days following retinal lesions compared to transient (magnocellular-like) dLGN neurons, (3) lesion to V1 induces a rapid and severe impairment of contrast sensitivity for orientation and motion direction discrimination in the affected hemifield, (4) adaptive training with stimuli containing higher temporal frequencies, optimal for magnocellular pathway, is not more effective than static stimuli. Together, these findings suggest that post-injury functional plasticity in the early visual pathways depends not only on the parallel streams but also on the location of the injury and the type of the injury.

 Jul 03, 2024 @ 1:00 p.m.

 Medical Center | K-207 (2-6408)

Host: Advisors: Farran Briggs, PhD & Krystel Huxlin, PhD

Neurogenetic Mechanisms Underlying Sexually Dimorphic Behavioral States in C. elegans - Thesis Defense

Gregory Reilly, MS - PhD Candidate, Neuroscience Graduate Program

Biological sex is a fundamental dimension of internal state that can have deep influences on behavior. Understanding the mechanisms behind these influences can provide insight into how shared neural circuits are tuned to produce sex-specific behavioral variation. Biological sex can influence both short-term behaviors and longer, more persistent forms of behavior known as behavioral states. In C. elegans, persistent motor behavior, called locomotor states, is well-studied in hermaphrodites. On a patch of food, hermaphrodites will switch between two states of foraging and feeding, called roaming and dwelling respectively. However, while some work has examined motor states in males, these remain poorly characterized. Previous work from our lab has demonstrated that male locomotion is sex-specific; the sexual state of muscle tissue and the nervous system is essential for sex differences in speed and body posture. Therefore, biological sex may also similarly influence locomotor states. We trained a supervised machine learning Random Forest model to detect three locomotor states: roaming, dwelling, and tail chase. In addition, we used a dimensionality reduction analysis, Linear Discrimination Analysis (LDA), to compare the overall characteristics of these states. Furthermore, to measure the transition probability between states, we used a Markov model. While both males and hermaphrodites share the locomotor states of roaming and dwelling, the characteristics of these differ by sex- the amount of time spent in each state, state durations, and transitions between states (temporal differences), as well as the linear speed, curvature, and other characteristics (feature differences), have sexual dimorphism. To understand how sex tunes these locomotor states, we manipulated the sex determination pathway to sex reverse the nervous system in both males and hermaphrodites. Interestingly, we found that pan-neuronally feminized males had similar locomotor state characteristics to hermaphrodites; both temporal and state feature sex differences were eliminated in the feminized males. Yet, masculinized hermaphrodites were indistinguishable from their wildtype counterparts indicating that either male-specific neurons or other tissue played a role in mediating these sex differences. To uncover the mechanisms that biological sex leverages to achieve this sex-specific variance in locomotor states, various neuromodulator knockout mutants known to affect locomotor states were tested. PDFR-1 emerged as a strong candidate as it removed differences in both temporal and features of locomotor states. Preliminary data suggests that PDFR-1 signaling may regulate the temporal sex differences through daf-7, a TGF-ß signal. daf-7 knockout mutants appear to maintain differences in state features but both spend similar amounts of time roaming and dwelling. Given that PDFR-1 signaling has been implicated as the mechanism that regulates sexual dimorphism in daf-7 expression in the ASJ neuron, these results remain promising. Together, our results provide a mechanistic framework for understanding how sex-specific neuronal tuning influences behavioral states.

 Jun 14, 2024 @ 10:00 a.m.

 Medical Center | SMD Lg. Aud. (2-6424)

Host: Advisor: Doug Portman, PhD

Mechanisms of Cerebellar Microglial Dynamics and Their Influence On Behavior - Thesis Defense

Mark Stoessel, MS - PhD Candidate, Neuroscience Graduate Program

Synaptic plasticity allows the central nervous system to incorporate new sensory experiences and information, and its disruption is associated with many neurological and psychiatric disorders. Much recent work has focused on the contribution of non-neuronal central nervous system cells, especially microglia, to synaptic plasticity. Though classically defined by their immune capacities, microglia are vital to many homeostatic processes, including synaptic plasticity of nascent and adult neuronal networks. Despite the emerging consensus that microglial dynamics are critical to brain function during physiological as well as pathological conditions, it is unclear whether these microglial roles and their underlying mechanisms are universal or differ between brain regions. There is a growing body evidence to suggest microglia exhibit a high degree of regional specialization. Cerebellar microglia in particular exhibit unique transcriptional and epigenetic profiles, and distinct functional properties, such as being morphologically less ramified, and less densely distributed than cortical microglia. As a consequence, cerebellar microglia survey less of the parenchyma than cortical microglia but compensate for this by undergoing frequent somatic translocations under homeostatic conditions, a phenomenon not observed in cortex. Despite such differences, cerebellar microglia maintain common microglial functions. Two pathways of interest to cortical microglial mediated synaptic plasticity are purinergic signaling through the P2Y12 receptor and noradrenergic signaling through the β2 adrenergic receptor (β2-AR), both of which have been shown to be critically involved in microglial roles in synaptic remodeling and rapid chemotaxis to sites of injury.

To address this question of regional heterogeneity in microglial signaling we investigated the roles of P2Y12 and β2-AR in cerebellar microglial with a comparison to the known roles of these signaling pathways in cerebral cortex. We desired to understand the contribution of these pathways to the many aspects of microglial function in the adult brain and therefore characterized cerebellar microglial morphology, surveillance, injury response dynamics, gene expression patterns, and contributions to cerebellar learning and plasticity, while manipulating either microglial purinergic or adrenergic signaling. On the whole, our findings suggest that signaling pathways that are present in both cortical and cerebellar microglia may play differential roles in microglial function depending on brain area.

 Jun 12, 2024 @ 1:00 p.m.

 Medical Center | K-207 (2-6408)

Host: Advisor: Ania Majewska, PhD

NSC 503 Seminar

Amelia Hines; Andrea Campbell - PhD Candidate

Faculty Evaluators:  Jesse Schallek and Gabriella Sterne

Student Moderator:  Anthony Bryan Crum (Bryan)

 May 20, 2024 @ 4:00 p.m.

 Medical Center | K-307

Neurorehabilitation in Apraxia - “Between Thinking and Doing: Disorders at the Cognitive-motor Interface in Chronic Stroke”

Laurel Buxbaum, PsyD - Research Professor, Department of Rehabilitation Medicine, Institute Scientist, Moss Rehabilitation Research Institute

 May 15, 2024 @ 12:00 p.m.

 Medical Center | K-307 Room 3.6408

NSC 503 Seminar

Aiesha Anchan; Gavin Magill - PhD Candidate

Faculty Evaluators:  Amy Kiernan and Kenneth Henry

Student Moderator:  Alexis Feidler

 May 13, 2024 @ 4:00 p.m.

 Medical Center | K-307

Effects of Developmental Ethanol Exposure on Cerebellar Microglia and Purkinje Cells - Thesis Defense

MaKenna Cealie - PhD Candidate, Neuroscience Graduate Program

Fetal alcohol spectrum disorders (FASD), caused by prenatal alcohol exposure, are the most common cause of non-heritable, preventable mental disability and have no known cure. Physical, cognitive, and behavioral deficits have been reported in FASD, including impairments related to the cerebellum. To elucidate the mechanisms of FASD, we examined microglia, the immune cells of the central nervous system, as well as Purkinje cells, the sole output of the cerebellar cortex, which are both impacted by developmental ethanol exposure. Microglia are dynamic cells and shape neuronal circuit development and connectivity in the cerebellum. However, how cerebellar microglia dynamics and their interactions with neurons are affected by early life exposure to ethanol is unknown. We explored the impact of a third-trimester equivalent binge-level ethanol exposure on cerebellar microglia and microglia-Purkinje cell interactions in adolescent and young adult mice.

We subcutaneously injected Ai9+/-/C3xcr1G/+/L7cre mice with 5.0 g/kg/day of either ethanol or saline from postnatal (P) days 4-9. Mice were then aged to adolescence (P28) and cranial windows were implanted above the cerebellum to allow for two-photon in vivo imaging in both adolescence and young adulthood (P60). We found that in vivo cerebellar microglia dynamics, microglia morphology, and microglia-Purkinje cell interactions were largely unaffected by developmental ethanol exposure in both adolescence and young adulthood. We also examined if a “second-hit” laser ablation injury in young adulthood would uncover differences, but found no changes in cerebellar microglia injury response between ethanol- and saline-dosed animals. We collected the young adults’ brains for confocal imaging to examine a larger number of microglia and Purkinje cells. Microglia density, morphology, and interactions with Purkinje cells were largely unaltered by developmental ethanol exposure. However, Purkinje cell linear frequency was significantly decreased in ethanol-dosed mice.

Overall, we found that cerebellar microglia in adolescent and young adult mice were largely unaffected by developmental ethanol exposure, but Purkinje cells appeared to be more susceptible to its effects. Our work suggests that microglia may return to homeostasis later in life after an early life insult. This work is important to narrow down the mechanisms leading to FASD so future therapies can be developed.

 May 13, 2024 @ 11:00 a.m.

 Medical Center | Lower Adolph Aud. (1-7619)

Host: Advisor: Ania Majewska, PhD

Investigating the critical in vivo role of neuronal PP1β - Thesis Defense

Cody McKee - PhD Candidate, Neuroscience Graduate Program

Protein Phosphatase 1 (PP1) is a major Serine (Ser)/Threonine (Thr) phosphatase responsible for more than half of all Ser/Thr dephosphorylation events in eukaryotic cells. Three genes encode the three major isoforms of PP1 (α, β, and γ). While PP1α and PP1γ are considered major players in synaptic physiology, the neuronal function of PP1β is unknown. Recently, de novo mutations in PP1β have been linked to intellectual developmental disabilities in children, suggesting a critical role for PP1β in the central nervous system. While correlations between PP1 and various other neurodevelopmental/neurodegenerative diseases have been suggested, a causative role for PP1 in many of these contexts has yet to be established. The current study seeks to investigate the neuronal role of PP1β in vivo, and to uncover potential mechanisms by which PP1β influences neuronal function.

A Thy1-Cre mouse line was used to generate neuron specific PP1β conditional KO (PP1β cKO) mice. These mice exhibit a failure to thrive and typically die by 2-3 postnatal weeks. Hippocampal slice recordings demonstrated increased paired-pulse facilitation, suggesting impaired neurotransmitter release. In agreement with studies suggesting activity influences myelination within specific brain regions, we found significantly lower levels of myelin basic protein in the cortex of PP1β cKO mice. Furthermore, to assess the influence of PP1β on myelin function in a predominately activity-independent context, we measured compound action potentials (CAPs) along the optic nerve. Deficits in CAP recordings suggested impaired optic nerve myelination. However, analysis of the electron micrographs failed to detect a significant difference in myelinated axons. Using immunofluorescence, we then uncovered significantly fewer nodes of Ranvier in PP1β cKO mice that could potentially explain the CAP recordings. This deficit in nodes coincided with an increase in phosphorylation of PP1β-specific substrate, myosin light chain, which localizes to nodes of Ranvier. These data suggest a potential role for PP1β in nodal structure that could influence action potential propagation.

To then study the role of PP1β in adolescent mice, we generated a neuron specific inducible PP1β KO mouse line (iKO). These iKO mice exhibit progressive deterioration of hind limb functionality and premature demise at ~4 weeks post recombination. We then uncovered significant changes in various respiratory parameters suggesting a potential mechanism to explain the premature demise. However, while no morphological changes were observed within neuromuscular junctions in the diaphragm, it is possible that neurotransmitter release at these synapses is abrogated, and this will be investigated in the future.

These data support the hypothesis that PP1β alters action potential propagation in a way that disrupts downstream functionality. These results shed light on the role of PP1β and potential mechanisms that could be disrupted by PP1β in pathological states. Future studies will seek to uncover the molecular substrates underlying these effects and provide potential therapeutic targets for diseases in which PP1β functionality may be altered.

 May 10, 2024 @ 2:00 p.m.

 Medical Center | K-207 (2-6408)

Host: Advisor: Houhui (Hugh) Xia

NSC 503 Seminar

Aishwarya Jayan; Leah Sheppard - PhD Candidate

Faculty Evaluators:  Todd Jusko and Joog-Hoon Nam

Student Moderator:  Thomas Delgado

 May 06, 2024 @ 4:00 p.m.

 Medical Center | K-307

The Elizabeth Doty Lecture - "The Internal Focus of Attention"

Anna Christina Nobre, PhD - Wu Tsai Professor of Psychology, Director, Center for Neurocognition and Behavior, Wu Tsai Institute, Yale Univiversity

Dr. Nobre’s talk will discuss her recent studies exploring how we focus attention to contents in working memory. Her findings highlight the flexibility of the internal focus – dynamically and proactively prioritizing or shielding different contents in turn to guide future behavior – as well as its sensitivity to the temporal structure of anticipated events and tasks.


 May 02, 2024 @ 4:00 p.m.

 Medical Center | Lower Adolph Aud. (1-7619)

NSC 503 Seminar

Niki Lam; Tom Scudder - PhD Candidate

Titles:  Disentangling the contributions of enhancement and suppression to selective visual processing - Lam
Cav1.3 Ca+ Current Mediation by the PACAP peptide - Scudder

Faculty Evaluators:  Paul Kammermeir and Robert Freeman

Student Moderator:  Abigail Sawicki

 Apr 22, 2024 @ 4:00 p.m.

 Medical Center | K-307

Annual Neuroscience Retreat

Dr. Takao Hensch - Keynote Speaker

 Apr 19, 2024 @ 8:30 a.m.

 Memorial Art Gallery | 

NSC 503 Seminar

Bingyu Sun; Bryan Redmond - PhD Candidate

Titles:  ADDaPT: automated direction discrimination perimetric task for detecting blind field visual abilities - Redmond
The Mechanistic Effects of Cannabidiol in an Amyloidosis Mouse Model - Sun

Faculty Evaluators:  J. Chris Holt and Thomas O'Connor

Student Moderator:  Michael (Mike) Giannetto

 Apr 15, 2024 @ 4:00 p.m.

 Medical Center | K-307

NSC 503 Seminar

Erica Squire; Staci Rocco - PhD Candidate

Titles:  Gustatory processing in Drosophila melanogaster and the role of ‘buddy - Squire
Evaluating the Cellular and Molecular effects of Basmisanil: A Potential Rapid Antidepressant for MDD - Rocco

Faculty Evaluators:  Debroah Cory-Slechta and Samuel Norman-Haignere

Student Moderator:  Evan Newbold

 Apr 01, 2024 @ 4:00 p.m.

 Medical Center | K-307

NSC 503 Seminar

Amelia Day Hines; Sid Chittaranjan - PhD Candidate, Neuroscience Graduate Program

Titles: Astrocytes modulate synaptic plasticity via norepinephrine - Hines
The Role of Astrocytes in Acute Insulin Resistance - Chittaranjan

Faculty Evaluators:  Jean Bidlack and Brian Keane

Student Moderator:  Victoria Popov

 Mar 25, 2024 @ 4:00 p.m.

 Medical Center | K-307

Thesis Defense: "Interfacing with the Cortical Reach-to-Grasp Network using Low-Amplitude Intracortical Microstimulation"

Brandon Ruszala - PhD Candidate, Biomedical Engineering PhD Program

Abstract: Movement is the primary way people interact with the world. Injuries to the nervous system that disrupt a person’s ability to move (e.g., losing a limb or paralysis) can be devastating. However, the cortical regions that control movement often remain intact and functional offering an interesting potential treatment – communicating with those still-functional brain regions to control a machine and bypass the injuries. In other words, establishing a brain-machine interface (BMI). Focusing on upper-extremity BMIs, robotic arms can be successfully controlled by decoding neurons from motor cortex and improved by delivering sensory feedback to somatosensory cortex with intracortical microstimulation (ICMS). However, controlling BMIs with the speed, accuracy, and precision of natural movements made with native limbs remains a challenge. This dissertation identifies several features of the cortical motor system that could be leveraged to refine BMI control. First, we show that neurons in motor cortex encode instruction modality – a non-kinematic feature that may constitute noise for BMIs trained to decode movement kinematics from those neurons. Accounting for such non-kinematic variation in future decoding algorithms may allow for more accurate decoding of movement parameters from that neural activity. Second, we show low-amplitude ICMS can modulate neurons in distant cortical regions. Initially, we show ICMS delivered in primary somatosensory cortex modulates the activity of neurons across wide territories in primary motor cortex and ventral premotor cortex. Subsequently, we show distant modulation effects can be produced over even greater spatial scale across the entire cortical reach-to-grasp network. For BMIs that concurrently stimulate neurons in some cortical regions while decoding neurons in others, modulation produced by the stimulation in decoded neurons can hinder decoder performance. Incorporating information about distant modulation effects into decoding algorithms could mitigate that hindrance. Finally, we explored the cortical reach-to-grasp network for novel regions in which information can be delivered using ICMS. We found that the ventral premotor cortex and the anterior intraparietal area were effective regions for delivering information, whereas the dorsal premotor cortex and dorsal posterior parietal cortex were ineffective. Future BMIs might deliver more complex information to the brain via those former regions, expanding the bidirectional brain-machine interface.

 Mar 19, 2024 @ 10:00 a.m.

 Medical Center | K-207 (2-6408)

Zoom Link

Host: Advisor: Marc Schieber, MD, PhD

NSC 503 Seminar

Aaron Huynh; Stacey Pedraza - PhD Candidate

Extra presentation by Amber Rivera, MSW, Director of Lerner Life and Wellness

Titles:  “Approach to Evaluate Post-Stroke Motor Rehabilitation” - Huynh
“Macrocyclic Tetrapeptides to Treat Cocaine Use Disorder” - Pedraza

Faculty Evaluators:  Chris Proschel and Kerry O'Banion

Student Moderator:  Yanya Ding

 Mar 18, 2024 @ 4:00 p.m.

 Medical Center | K-307

NSC 503 Seminar

Anthony Bryan Crum (Bryan); John Gonzalez Amoretti - PhD Candidate

Faculty Evaluators:  Lars Ross and Ania Majewska

Student Moderator:  Erin Murray

 Mar 04, 2024 @ 4:00 p.m.

 Medical Center | K-307

NSC 503 Seminar

Dennisha King; Paige Nicklas - PhD Candidate

Faculty Evaluators:  Harris Gelbard and Marc Schieber

Student Moderator:  Julia Granato

 Feb 26, 2024 @ 4:00 p.m.

 Medical Center | K-307

NSC 503 Seminar

Amy Bucklaew; Renee Miller, PhD - PhD Candidate; Professor, BCS

Faculty Evaluators:  Adam Synder and Ian Fiebelkorn

Student Moderator:  Jo Fritzinger

 Feb 19, 2024 @ 4:00 p.m.

 Medical Center | K-307

NSC 503 Seminar

Daulton Myers; Jeeyun Kim - PhD Candidate

Faculty Evaluators:  Nathan Smith and Manuel-Gomes-Ramirez

Student Moderator:  Mike DuHain

 Feb 12, 2024 @ 4:00 p.m.

 Medical Center | K-307

NSC 503 Seminar

Erin Murray; Margaux Masten - PhD Candidate

Faculty Evaluators:  Juile Fudge and Manoela Fogaça

Student Moderator:  Caitlin Sharp

 Feb 05, 2024 @ 4:00 p.m.

 Medical Center | K-307

Connecting the dots between brain microstructure, function, and behavior in rodents using MRI

Tanzil Arefin, PhD - Assistant Research Professor, Biomedical Engineering, Penn State College of Engineering

 Jan 30, 2024 @ 4:00 p.m.

 Medical Center | Ryan Case Method Rm. (1-9576)

Host: Department of Neuroscience and the Del Monte Institute for Neiroscience

NSC 503 Seminar

Abigail Alpers; Tanique McDonald - PhD Candidate

Faculty Evaluators:  Michael Telias and Andrew Wojtovich

Student Moderator:  Matt Adusei

 Jan 29, 2024 @ 4:00 p.m.

 Medical Center | K-307

NSC 503 Seminars

Dominic Bunn; Mariah Marrero - PhD Candidate

Faculty Evaluators:  Liz Romanski and John Olschowka

Student Moderator:  Sarah Yabonski

 Jan 22, 2024 @ 4:00 p.m.

 Medical Center | K-307

Notter Lecture - The Bodily Senses

Fan Wang, PhD - Professor, Brain and Cognitive Sciences, McGovern Institute, MIT

The bodily sensations include touch, pain, and our senses of the body's postures and movements.  In this talk, I will describe mostly unpublished studies from my lab on neurons and circuits involved in these bodily senses. 

First, I will describe our discovery of touch neurons that tell the brain "when" is the touch onset with millisecond precision.  This is achieved using in vivo recording from ontogenetically identified touch neurons.  Second, I will talk about pain, both the sensory-discriminative and the emotional aspects of pain.  Note that emotions are inseparable from the body's autonomic responses, and we have discovered that controlling autonomic reactions can control pain perception.  Finally, I will discuss our new studies on how the brain (the sensory cortex) represents body postures and associated behaviors.  We have developed new algorithms that enables full parameterized description of the body postures in freely moving mice, and combined with in vivo recording, we have discovered posture/behavior syllable-related ensembles in the brain.

 Jan 17, 2024 @ 4:00 p.m.

 Medical Center | Ryan Case Methods Rm (1-9576)

Host: University of Rochester School of Medicine and Dentistry Department of Neuroscience and the Del Monte Institute for Neuroscience