Vickie Liu, Psychology and Education
Helping Parents to Transit During COVID-19 Through Learning Tools
Project Advisor: Jennifer Jacoby
Most parenting guides in China are either highly theoretical or cover mostly on academic development and ignore the rest. Last summer, I worked with Di Zhao, a phd candidate at Beijing Normal University to translate academic findings from early childhood theory into a digestible and comprehensive parenting guide that covered aspects from cognitive development, social emotional development and body development etc. In the parenting guide, we also designed home learning games for parents (whose children are 3-5 years old). In order to boost reading ability, we designed a parenting guide in a cartoon narrative with storylines and pictures. Our handout was very popular among parents given that the pandemics has made home learning much more commonplace, and our handbook reached 10000 families with the help of our ngo partners.
Kessh Bhasiin, Neuroscience and Behavior
The Effect of Glial Tau Expression on Blood Brain Barrier Integrity Post-Traumatic Injury in Drosophila melanogaster
Project Advisor: Dr. Kenneth Colodner
Consisting of tight seals between and low levels of transport across the cells that constitute the brain’s blood vessels, the blood-brain barrier (BBB) allows for the maintenance of precise ionic concentrations within and the exclusion of inflammatory mediators and pathogens from the central nervous system (CNS)1 . Given that dysfunction of this barrier can alter the finely regulated environment of the CNS, BBB breakdown is often a feature of neurodegenerative diseases. One such condition is Chronic Traumatic Encephalopathy, a disease associated with traumatic brain injury, which is characterized by abnormal accumulation of the microtubule-stabilizing protein tau in astrocytes 2 . Interestingly, tau aggregation is found in glial cells juxtaposed with blood vessels, leading to the question of whether the presence of glial tau alongside the vasculature could be contributing to BBB disruption and subsequent cognitive decline.
In an effort to elucidate the role of glial tau in the BBB disruption post traumatic injury, we used a Drosophila melanogaster model of glial tauopathy3 . The fly’s ‘BBB’ consists of two layers of glial and has properties and a molecular composition homologous to the vertebrate barrier. As such, we subjected flies overexpressing tau in their glial cells to traumatic injury, dissected their brains and assessed BBB integrity. Preliminary analysis revealed the need to optimize our methodology to preserve BBB integrity, and I will discuss the optimization process and the refined technique that will allow us to answer our central research question.
1. Daneman, R., & Prat, A. (2015). The blood-brain barrier. Cold Spring Harbor Perspectives in Biology,
2. McKee, A. C., Cairns, N. J., Dickson, D. W., Folkerth, R. D., Dirk Keene, C., Litvan, I., ... Gordon, W. A. (2016). The first NINDS/NIBIB consensus meeting to define neuropathological criteria for the diagnosis
of chronic traumatic encephalopathy. Acta Neuropathologica, 131(1).
3. Colodner, K. J., & Feany, M. B. (2010). Glial fibrillary tangles and JAK/STAT-mediated glial and neuronal cell death in a Drosophila model of glial tauopathy. Journal of Neuroscience, 30(48),
Liz Roy, Neuroscience and Behavior
Anxiety and Schizophrenia are Reflected in the Mismatch Negativity ERP Component
Project advisor: Jane Couperus
The mismatch-negativity (MMN) is a component of event-related potentials (ERPs) that can be used to assess pre-attentive auditory processing of information. This component, which can be mapped to the fronto-central region of the brain, corresponds to the behavioral discrimination threshold and can be elicited when stimuli do not match an echoic memory trace of expected auditory cues.1 This is observed in the ERP as a difference in wave amplitude between expected and deviant/target stimuli responses.
Previous studies have established a relationship between MMN amplitude and anxiety-related behavioral and psychiatric disorders, including generalized anxiety, post-traumatic stress disorder, and schizophrenia, however the actual effect is unclear2 . This project analyses ERP data from 199 college-age participants using two psychological inventories for perceived stress (Perceived Stress Scale) and anxiety (Beck Anxiety Inventory) and an auditory oddball paradigm. Results showed a negative relationship between MMN amplitude and BAI score, however a statistically significant relationship was not found between MMN amplitude and PSS score. These data indicate that anxiety may have an attenuating effect on pre-attentive auditory processing, which perceived stress does not appear to strongly effect. Furthermore, this presentation aims to review and assess current findings relating the MMN to conditions such as 22q11.b deletion syndrome and genetically-related schizophrenia, which have also reflected pre-perceptual auditory processing issues.
1 Pazo-Alvarez, P., Cadaveira, F., & Amenedo, E. (2003). MMN in the visual modality: a review. Biological
psychology, 63(3), 199–236.
2 Fucci, E., Abdoun, O., & Lutz, A. (2019). Auditory perceptual learning is not affected by anticipatory anxiety in the healthy population except for highly anxious individuals: EEG evidence. Clinical Neurophysiology: Of icial Journal of the International Federation of Clinical Neurophysiology, 130(7), 1135–1143.
Saee Chitale, Neuroscience and Behavior
Role of the Hippocampus in Behavioural Adjustment and Drug Associated Memory Following Reward Devaluation
Project Advisors: Marta Sabariego, André White
Frustration is defined as an aversive emotional state triggered by situations involving reward loss1. Despite compelling epidemiological and clinical evidence associating reward loss with the etiology of anxiety and depression, the neural correlates that underlie adaptation to reward changes remain largely unidentified. Previous experiments conducted in our lab have demonstrated that hippocampal lesions impair the ability of rats to adjust to changes in reward. However, full lesions of the hippocampus could have disrupted other neural circuits and interfered with learning before the reward manipulation. Moreover, it is still unclear whether the impairment seen in these hippocampal lesioned rats was due to a lack of emotionality (i.e. lesioned rats not feeling frustrated after reward loss) or a lack of cognitive flexibility (i.e. lesioned rats not being able to modify previously learned responses). In order to address these questions, I exposed the rats to a conditioned place preference (CPP) task alongside a reward-loss maze paradigm. In the CPP task, I first trained rats to associate a context with cocaine (a drug that engages key pleasure centers in the brain by blocking dopamine reuptake). Rats demonstrated that they acquired this context-drug association by spending more time in the context paired with the drug. In the following days, I conducted extinction sessions, where rats were exposed to the context, but the drug was not administered. This decreased preference for the previously drug- associated context, demonstrating that animals learned about this new association (context- no drug). If hippocampal inactivation precludes the ability to feel frustration, then a reward devaluation (on the maze paradigm) should not cause any behavioral change in the drug- association paradigm (CPP). However, if the problem is linked to cognitive flexibility, then we should observe signs of frustration and a concomitant increase in preference for the previously cocaine-associated context. I therefore inactivated excitatory neurons in the dorsal hippocampus of rats using designer receptor exclusively activated by designer drugs (DREADD) and found that, while hippocampal-inactivated rats did not adapt their response to environmental changes related to reward downshifts, they showed behavioral signs of negative emotion in the CPP task. In particular, a sudden reduction in the amount of an expected food reward caused a spontaneous recovery of the extinguished context- cocaine association. This indicates that animals with a dysfunctional hippocampus do not lack emotionality but rather experience cognitive inflexibility. This research will contribute to revealing the function of neural circuits for reward loss, a critical step for developing treatments to prevent or ameliorate emotional and cognitive problems in anxiety, depression, and stress-related disorders.
1 Torres, & Papini, M. R. (2017). Incentive relativity. Encyclopedia of comparative cognition and behavior, 1-13.