Previous research conducted in the early 20th century presented data on the habituation of hydra towards repeated mechanosensory stimulus. However, it is yet unknown whether hydra display similar results towards repeated light stimulus. At the present, there’s no research into the learning and memory abilities of hydra. As such, this project aims to address the knowledge gap and shed further insight into the behavior of hydra vulgaris. The experiment is conducted with LED light stripe that stimulates the hydra with a certain color of light for certain period of time. The behavior of the hydra is then recorded and observed. The project is ongoing and has yet to produce statistically significant results. The significance of this project is that it looks at a knowledge gap that exists in existing literature about hydra vulgaris and it seeks to evaluate whether simple organisms like hydra can be habituated towards a stimuli.

Stroke is a leading cause of disability and death. In the first weeks post-stroke, the brain has increased neuroplasticity and responsiveness to rehabilitation methods. Dry electroencephalography (EEG) is a non-invasive bedside tool that tracks event-related desynchronization (ERD) in the beta (β) frequency band, a neuronal behavior observed during voluntary movement. However, existing research lacks precise monitoring of ERDs post-stroke. This project attempts to fill this gap by capturing short-term changes early post-stroke by measuring β-ERD. Brain activity is recorded using a 32-lead dry EEG cap while subjects perform hand contractions at 20% of their maximum voluntary contraction. Stroke patients are assessed every other day; controls will soon be enrolled and will be tested 5 times to control for learning effects. Quantifications of cortical activity will be measured using analysis of ERD. Preliminary results show reduced β-ERD over the stroke-affected hemisphere compared to expected patterns in healthy controls. Some stroke patients show increased ERD over time, potentially reflecting motor cortex reorganization. These results suggest that β-ERD could act as a biomarker for stroke recovery and neuroplasticity. Future directions include incorporating control subjects to assess the significance and validity of our findings. This project aims to provide a deeper understanding of neuroplasticity during stroke recovery and direct sub-acute post-stroke rehabilitation methods.

Microglia, the resident immune cells in the central nervous system, primarily serve in neuroinflammation and synaptic pruning. Microglial dysregulation is associated with neurodevelopmental disorders, including Autism Spectrum Disorder (ASD). Mutations that cause haploinsufficiency in chromodomain helicase DNA-binding protein 8 (CHD8) are known to cause ASD. This study examines the effects of lipopolysaccharide (LPS), a bacterial endotoxin commonly used to trigger immune activation, on the morphological responses of human stem cell-derived microglia with and without CHD8 mutations. Through immunohistochemical staining, confocal imaging, and quantitative analysis with CellProfiler software, morphological features and lysosomal content of microglial cells were extracted to assess structural changes caused by increased LPS doses. Both control and CHD8 mutant lines experienced significant morphological changes, becoming more rod-like, particularly after adding 100 ng/ml LPS. Additionally, the introduction of LPS caused a decrease in relative lysosomal area per cell among both test groups. This suggests that microglia with CHD8 haploinsufficiency mutations may not experience dramatic changes to their inflammatory responses compared to non-mutated microglia. Our next steps involve refining data analysis by excluding outliers and adjusting the dataset to more accurately represent observed changes, while also assessing the effects of microglial interactions with neurons carrying ASD-risk mutations.

Many sleep disorders show pronounced sex differences in prevalence and severity, often accompanied by comorbid conditions such as depression and metabolic syndrome. These disparities may stem from sex-specific regulation of sleep and circadian processes by reproductive hormones and sex chromosomes. While prior studies have shown that estrogens and androgens influence sleep-wake architecture and homeostasis, the independent role of the sex chromosome complement remains underexplored. This study uses the four core genotype (FCG) mouse model to dissociate the effects of sex chromosomes from gonadal hormones on estrogen receptor (ERα) expression in sleep-regulating regions of the brain: the ventrolateral preoptic nucleus (VLPO), suprachiasmatic nucleus (SCN), and medial preoptic area (mPOA). FCG mice will be sacrificed at mid-rest phase, and brains will be rapidly dissected, frozen and stored for analysis. Brain regions containing the SCN, VLPO, and mPOA will be sectioned using a cryostat, and fluorescence in situ hybridization (FISH) will be used to visualize and quantify ERα expression. We hypothesize that sex chromosome complement will influence ER expression independently of circulating hormones. By clarifying the genetic contributions to estrogen signaling in key sleep-related brain areas, this study may provide new insights into the biological basis of sex differences in sleep and inform the development of more tailored interventions for sleep disorders.

My research project investigates the brain mechanisms that support goal-directed behavior and habit formation in mice, focusing on how 2 major neuronal subtypes in the dorsomedial striatum (DMS)-D1 and A2A neurons-contribute to the behavioral shift from goal-directed to habits. Goal-directed behavior involves making decisions based on the expected outcomes of actions, while habits allow for routine tasks to be performed efficiently without considering consequences. Maintaining a balance between these 2 strategies is crucial for adaptive behavior, and disruptions in this balance may result in psychiatric disorders & addiction. Previous work from Dr. Malvaez has shown that D1 neurons are crucial for sustaining goal-directed behavior even after extensive training, while A2A neurons support only early goal-directed learning & may disengage as habits form. However, their specific roles in habit expression remain unclear. To test my hypothesis that A2A neurons are necessary for habit use while D1 neurons are not, I used chemogenetics to selectively inhibit D1 neuron activity during a behavioral paradigm that promotes habit formation. Surprisingly, my results showed that inhibiting D1 neurons disrupted habitual response, suggesting they remain active in habit use, while A2A inhibition had no significant effect. These findings refine our understanding of striatal circuitry & its role in behavioral flexibility, which may inform future treatments for disorders characterized by maladaptive habits, such as OCD & substance use disorders.