Research & Projects

Ongoing Projects

Neuroendocrine consequences of early life adversity

Broadly, my Ph.D. work focuses on the effects of early life adversity (ELA), in the form of maternal separation, on the development of the neuroendocrine system in rodent models. Specifically, I investigate how CRHR1 receptor trafficking acts as a molecular bridge connecting early stress to accelerated puberty and altered anxiety circuit development in adolescence. I am using behavioral, cellular, molecular, and circuit-based techniques to identify key therapeutic targets to mitigate the effects of ELA on pubertal development, adolescent and adult anxiety-related behavior, and the underlying neural activity in rats. Looking ahead, I plan to explore how these pubertal shifts may carry metabolic consequences well into old age and contribute to aging-related deficits.

Past Projects

Exploring cellular and behavioral consequences of serotonergic psychedelics in rodent models of anxiety

Supervisor: Dr. Vidita Vaidya, Tata Institute of Fundamental Research

This work contributed to my Master's thesis. Anxiety is the world's most prevalent mental health disorder, yet the neural circuits underlying its treatment remain poorly understood. Using immunohistochemical and behavioral analysis in rodents, I investigated how the serotonergic psychedelic DOI reduces anxiety, finding that it selectively activates parvalbumin-positive inhibitory neurons in the ventral hippocampal CA1/subiculum, suppressing local activity in a pattern sufficient to drive anxiolysis. These findings offer a mechanistic foundation for understanding how psychedelics may treat anxiety disorders. Follow this work

Noradrenergic Regulation of Mitochondrial Function in the Hippocampus

Supervisor: Dr. Vidita Vaidya, Tata Institute of Fundamental Research

While monoaminergic signaling is well known to influence mood and cognition, its role in cellular energetics remains underexplored. Using qPCR, I contributed to characterizing how noradrenergic signaling modulates mitochondrial biogenesis and bioenergetic capacity in the hippocampus, revealing a novel link between neuromodulatory signaling and cellular energy metabolism (Kapri et al., under review, Neuropsychopharmacology). These findings highlight mitochondrial pathways as potential therapeutic targets in stress-related and neurodegenerative disorders.

Early-Life GPCR Signaling Imbalance Programs Adult Affective Behavior and Glial Dysfunction

Supervisor: Dr. Vidita Vaidya, Tata Institute of Fundamental Research

Early-life adversity is known to alter monoaminergic GPCR signaling, but how these perturbations program long-term brain outcomes remains poorly understood. Using a chemogenetic (DREADDs) approach in Dr. Vidita Vaidya's laboratory, I helped investigate how selectively enhancing Gq- or Gi-coupled signaling in forebrain excitatory neurons during critical postnatal windows shapes adult behavior and neuron–glia interactions. I contributed through glial immunohistochemistry and quantitative cell counting, revealing that enhanced early-life Gq signaling is sufficient to drive persistent anxiety-like behavior and lasting changes in astroglial gene expression and metabolism. These findings implicate Gq/Gi imbalance as a key mechanism in the developmental programming of affective circuits, identifying GPCR pathways as potential targets for mood disorder intervention. Follow this work

Developmental Chemogenetic Modulation of Forebrain Circuits and Its Impact on Adult Affective Behavior

Supervisor: Dr. Vidita Vaidya, Tata Institute of Fundamental Research

Early-life stress is known to alter GPCR signaling and program adult affective behavior, but the specific contributions of inhibitory Gi-coupled pathways remain unclear. In Dr. Vidita Vaidya's laboratory, I used a chemogenetic (hM4Di-DREADD) approach to selectively enhance Gi signaling in CaMKIIα-positive forebrain excitatory neurons during postnatal and juvenile windows. I contributed through immunohistochemistry, confocal imaging, and behavioral assays, including open field, elevated plus maze, light-dark box, and sensorimotor gating paradigms. Contrary to prevailing hypotheses, enhanced early-life Gi signaling did not significantly alter adult anxiety-, despair-like behavior, or sensorimotor gating, providing critical negative evidence that constrains models of GPCR-mediated circuit development and underscoring the importance of pathway-specific and temporal precision in developmental programming. Follow this work

Role of Ascorbate Peroxidase and Proline as destressors for plant abiotic stress

Supervisor: Dr. Neha Ahir, Ramnarain Ruia Autonomouse College

Abiotic stressors like salinity and drought significantly threaten crop productivity, particularly in regions like India where such conditions are widespread. This study examined how increasing salinity (2–10%) and drought (5–25%) conditions over 15 days affected levels of Ascorbate peroxidase (APX) and Proline in two varieties of Sorghum bicolor (M-35-1 and E-36-1). We found an inverse relationship between stress levels and APX, and a direct relationship with Proline across both varieties, with E-36-1 demonstrating greater stress tolerance than M-35-1. Under drought, Proline acted as the primary stress responder, while salinity additionally triggered APX upregulation to counter ROS-induced osmotic imbalance. These findings suggest that a combined Proline–APX response mitigates abiotic stress, opening avenues for stress-relief cocktails or targeted GM crop development with enhanced resilience. Follow this work

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