Colloquium Series 2022-2023 - Center for the Neurobiology of Learning and Memory

Colloquium Series
UCI Spotlight
2022-2023

CNLM Colloquium UCI Spotlight Series Flyer

Tuesday, November 8, 2022 - 11:00 AM

Alyson Zalta, Ph.D.
Associate Professor
Psychological Science
School of Social Ecology

Exploring morning light therapy as a novel treatment for traumatic stress

Trauma contributes to a wide variety of mental health problems including posttraumatic stress disorder (PTSD), depression, anxiety, substance use, and suicidality. Although front-line psychotherapies and pharmacotherapies exist for traumatic stress, evidence suggests that many individuals fail to receive treatment, remain symptomatic despite treatment, or drop out of treatment before its conclusion. Uptake of these treatments is poor for several reasons including stigma, avoidance, unpleasant side effects, and poor accessibility. New treatments are needed for traumatic stress that can overcome these critical barriers to care while targeting the underlying biological mechanisms of the pathology. Morning light treatment has good potential as a novel non-invasive, low risk, scalable treatment for traumatic stress. Evidence suggests that morning light may improve traumatic stress by reducing reactivity in the amygdala, a brain region implicated in the pathophysiology of PTSD and anatomically linked to circadian photoreceptors in the eye. This seminar will describe the results of a randomized pilot trial that provides initial proof-of-concept that light treatment can improve traumatic stress and preliminary results from an ongoing randomized clinical trial aimed at evaluating the brain mechanisms underlying morning light therapy for traumatic stress.

Tuesday, January 17, 2023 - 11:00 AM

Elizabeth Head, Ph.D.
Professor
Pathology
School of Medicine

What we can learn about Alzheimer disease from people with Down syndrome

Description

Virtually all people with Down syndrome develop Alzheimer disease neuropathology by the time they are 40 years of age. Interestingly, the first signs of cognitive decline may not occur until after 50 years of age, and some people reach their 60’s without clinical decline. By examining the brains of people with Down syndrome across the lifespan we can understand the order of events in the development of Alzheimer disease, including when and where cerebrovascular changes and neuroinflammation occur. Learning about the sequence of events of Alzheimer disease pathogenesis in Down syndrome will allow us to design prevention and treatment interventions. Information learned from people with Down syndrome may in turn, help us promote successful aging in this vulnerable group and may be translated to all people at risk of Alzheimer disease.

Tuesday, January 24, 2023 - 11:00 AM

Lisa Flanagan, Ph.D.
Professor
Neurology
School of Medicine

Regulation of early neural development by glycosylation

Description

Deciphering how neural stem cells function in early development to generate the cerebral cortex will help us better understand normal and disrupted brain formation and organization. We used neural stem cells, genetic mouse models, and innovative engineering approaches to uncover a novel role for glycosylation in directing early neural development. N-linked glycosylation of the neural stem cell plasma membrane controls neuronal and astrocytic differentiation, likely through regulation of cell surface protein binding to extracellular ligands. Increased formation of cell surface highly-branched N-glycans promotes astrocyte generation whereas loss of these glycans disrupts neuron differentiation in vitro and in vivo. Glycosylation plays a critical and previously unrecognized role in cell differentiation and early brain development and may help to explain cellular responses to extracellular cues.

Tuesday, January 31, 2023 - 11:00 AM

Javier Diaz Alonso, Ph.D.
Assistant Professor
Anatomy and Neurobiology
School of Medicine

Chasing the AMPAR slot(s). Multiple mechanisms modulate synaptic strength.

Description

Long-term potentiation (LTP) of excitatory synapses is essential for multiple forms of learning and memory formation. Pioneering work from CNLM members and others led to a model for NMDAR-dependent LTP where synaptic strengthening depends on the recruitment of AMPA receptors to the postsynapse. Despite decades of research, the molecular mechanisms underlying the activity-dependent insertion of AMPA receptors at synapses, and specifically which regions in the receptor complex are required for trafficking and docking, are not fully understood. In the past few years, we have assessed the role played by different protein domains of the AMPAR complex in these processes, focusing on: i) the sequence diverse intracellular AMPAR C-tails, ii) the extracellular ATDs, which protrude into the synaptic cleft and iii) the AMPAR auxiliary proteins TARPs, which interact with synaptic scaffolds. Our recent and ongoing work is revealing an important role for all of these 3 elements, yet our data suggests that they play different roles in different synapses and control different AMPAR-dependent processes. I will discuss our unpublished work, in collaboration with other CNLM labs, dissecting novel molecular mechanisms modulating the activity-dependent synaptic accumulation and subsynaptic positioning of AMPARs to support novelty processing, learning and memory formation.

Tuesday, February 7, 2023 - 11:00 AM

Aaron Bornstein, Ph.D.
Assistant Professor
Cognitive Sciences
School of Social Sciences

Reconciling adaptive and maladaptive responses to uncertainty: data and theory

Tuesday, February 14, 2023 - 11:00 AM

Kei Igarashi, Ph.D.
Associate Professor
Anatomy and Neurobiology
School of Medicine

Circuit mechanisms of associative memory in health and Alzheimer’s disease

Description

Mounting evidence shows that dopamine in the striatum is critically involved in reward-based reinforcement learning. However, it remains unclear how dopamine reward signals influence the entorhinal-hippocampal circuit, another brain network critical for learning and memory. Using in vivo optogenetic and electrophysiological approaches, we recently found that dopamine signals from the ventral tegmental area control encoding of cue-reward association rules in the lateral entorhinal cortex (LEC) (Lee et al., Nature, 2021). Our results suggest that LEC represent a cognitive map of abstract task rules, and LEC dopamine facilitates the incorporation of new memories into this map. I would like to discuss how we can unify the roles of two central, but previously independent, players in learning – dopamine and the entorhinal-hippocampal circuit – in future studies. In the second part of the talk, I will share our results on how neuronal activities in the entorhinal-hippocampal memory circuit are lost in a mouse model of Alzheimer’s disease (Jun et al., Neuron, 2020), and discuss how the systems neuroscience approach can contribute to the understanding of Alzheimer’s disease pathogenesis.

Reference:

Lee JY, Jun H, Soma S, Nakazono T, Shiraiwa K, Dasgupta A, Nakagawa T, Xie JL, Chavez J, Romo R, Yungblut Y, Hagihara M, Murata K, and Igarashi KM* (2021)
Dopamine facilitates associative memory encoding in the entorhinal cortex
Nature, 598:321-326

Jun H, Bramian A, Soma S, Saito T, Saido TC, Igarashi KM* (2020)
Disrupted Place Cell Remapping and Impaired Grid Cells in a Knockin Model of Alzheimer's Disease
Neuron, 107:1095-1112

Tuesday, February 28, 2023 - 11:00 AM

Georg Striedter, Ph.D.
Professor
Neurobiology and Behavior
School of Biological Sciences

Which model system is “best”? An argument from toxicology.

Description

As researchers seek to find treatments for various disorders, they tend to use diverse model systems, but which models are “best” for a given aim? Dr. Striedter has recently published a book on this topic and, in this talk, will discuss the challenges of model system selection from a perspective rarely mentioned at the CNLM, namely that of toxicology. As toxicologists examine whether a particular compound is toxic to humans, should they study cultured cells, mice, guinea pigs, monkeys, or (of course) multiple models? As the number of studied models goes up, what happens to the risk of obtaining false positives? Which research strategy is most cost effective? These questions have clear analogs when it comes to selecting models for research on human diseases, neurological or otherwise. Dr. Striedter will discuss these analogies briefly, using Alzheimer’s disease as a CNLM-relevant example. He intends to leave plenty of room for discussion.

Tuesday, March 21, 2023 - 11:00 AM

Pierre Baldi, Ph.D.
Distinguished Professor
Donald Bren School of Information and Computer Science
Professor (Joint Appointment)
Biomedical Engineering

The quest for how the brain learns

Description

We will first showcase two cutting-edge applications of modern Artificial Intelligence (AI) in biomedical imaging and in reasoning. These applications, as well as most modern AI applications (e.g., ChatGPT, AlphaFold, AlphaGO, Google Translate, Self-Driving Cars) are based on deep learning, a modern rebranding of neural networks, or connectionist methods, dating back to the 1980s, or even the 1950s. We will then briefly review the neuroscience-inspired, tortuous, historical path that has led to deep learning, and the key discoveries made along the way, highlighting the synergies and discrepancies between neuroscience and deep learning. One key conclusion is that approximate gradient descent is essential for learning. However, the standard gradient descent algorithm of deep learning called backpropagation is not biologically-plausible for multiple reasons. We will examine these reasons one-by-one and identify biologically-plausible solutions for each one of them. In particular, we will introduce and demonstrate a general class of neural architectures and learning algorithms capable of learning from data in a largely unsupervised and asynchronous manner, without the need for symmetric connectivity.

Tuesday, March 28, 2023 - 11:00 AM

Kevin T. Beier, Ph.D.
Assistant Professor
Physiology and Biophysics
School of Medicine

Molecular mechanisms of memory stability and the molecular and circuit determinants of cocaine addiction

Description

I will speak on two separate projects in our lab. First, we have uncovered the molecular mechanism by which administration of the Zeta Inhibitory Peptide (ZIP) causes memory loss. While it was previously believed that ZIP administration perturbs memory stability through disruption of constitutive kinase activity, recent studies have cast doubt on this hypothesis. However, ZIP's effects on memory stability are robust, raising the question of what the actual mechanism is by which ZIP exerts its function. We have identified the basic molecular and pathways engaged by ZIP, and use this information to identify an inhibitor that, together with ZIP, enables bidirectional modulation of synaptic plasticity. Second, we are exploring the biological factors that influence the behavioral response to the administration of drugs of abuse. Some individuals that take drugs of abuse are susceptible to developing dependence, while others are resilient. The fundamental source of this variation is not understood. We will discuss our work implicating circuit- and molecular-level changes in the globus pallidus that facilitate individual differences in response to cocaine administration, and share the identification of a novel small molecule compound, isolated from rosemary, that blunts drug reward and volitional intake.

Tuesday, April 4, 2023 - 11:00 AM

Megan Peters, Ph.D.
Assistant Professor
Cognitive Science
School of Social Sciences

Neurocomputational approaches to the study of perceptual awareness

Description

When our brains process sensory information, they transform it into a coherent, conscious experience that we use to drive adaptive decisions and learning. In this talk I will describe several ongoing lines of research in my group that focus on understanding the neural and computational substrates of our subjective sense of the world around us. Specifically, separating the study of phenomenology from the study of signal processing capacity is challenging, so our group has been focusing on how the study of metacognitive evaluation (confidence judgements in our perceptual decisions) may shine light on these processes. Using a combination of behavior/psychophysics, computational modeling, noninvasive neuroimaging, and machine learning in humans, we seek to understand how the brain is capable of efficiently using sensory information and how this ability relates to our qualitative, phenomenal experiences.

Tuesday, May 9, 2023 - 11:00 AM

Laura Ewell, Ph.D.
Assistant Professor
Anatomy and Neurobiology
School of Medicine

Sparse to dense networks: pattern separation and completion in health and epilepsy

Description

The attractor theory of memory posits that CA3, the recurrent network at the core of the hippocampus, is capable of learning, storing, and recalling ensembles of neurons that represent experience. In healthy conditions there are constraints on the CA3 network that ensure that individual neural patterns comprise a small group of neurons that do not overlap with other patterns. One critical constraint called pattern separation works at the network level – and is thought to be performed by the dentate gyrus. In this talk, I will be examining the network processes of pattern separation and pattern completion through the lens of temporal lobe epilepsy – a disease in which network codes shift from sparse to dense schemes. We will discuss single unit data from freely moving rodents (epilepsy models and healthy animals) and new tasks being developed by my laboratory to study these critical memory processes.

Tuesday, May 23, 2023 - 11:00 AM

Leslie Thompson, Ph.D.
Professor
Psychiatry & Human Behavior
School of Medicine

Huntington’s disease research and therapeutics; the long winding road

Description

Huntington’s disease is a devastating neurodegenerative disease that typically strikes in the prime of life with no disease modifying treatment. It is caused by a repeat expansion within the coding region of the protein Huntingtin which is expressed throughout the body and is required for a vast array of cellular processes. The disease mutation causes both a gain of function and loss of normal function which adds significant complexity to understanding disease mechanisms and advancing therapeutics. In this talk I will describe three vignettes relating to disease mechanisms and therapeutic approaches undertaken in the laboratory.

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Colloquium Series UCI Spotlight 2022-2023

Colloquium Series
UCI Spotlight
2022-2023