About

Vineet Augustine is an Assistant Professor who completed his PhD at the California Institute of Technology in 2019 and holds a BS-MS degree from IISER-Kolkata, earned in 2013. His professional contact is vaugustine@ucsd.edu. The information provided highlights his academic background and current position but does not include specific details about his research focus or key contributions.

Research topics

• Internal medicine
• Neuroscience
• Medicine
• Biology
• Materials science
• Endocrinology

Selected publications

• A triple-node heart-brain neuroimmune loop underlying myocardial infarction

  Cell · 2026-01-27 · 6 citations

  articleSenior author
  PublisherDOI

• Defining cardioception: Heart-brain crosstalk

  Neuron · 2024-11-01 · 18 citations

  reviewSenior author
  PublisherDOI

• Phosphorylation of pyruvate dehydrogenase inversely associates with neuronal activity

  Neuron · 2024-01-23 · 55 citations

  articleOpen access

  For decades, the expression of immediate early genes (IEGs) such as FOS has been the most widely used molecular marker representing neuronal activation. However, to date, there is no equivalent surrogate available for the decrease of neuronal activity. Here, we developed an optogenetic-based biochemical screen in which population neural activities can be controlled by light with single action potential precision, followed by unbiased phosphoproteomic profiling. We identified that the phosphorylation of pyruvate dehydrogenase (pPDH) inversely correlated with the intensity of action potential firing in primary neurons. In in vivo mouse models, monoclonal antibody-based pPDH immunostaining detected activity decreases across the brain, which were induced by a wide range of factors including general anesthesia, chemogenetic inhibition, sensory experiences, and natural behaviors. Thus, as an inverse activity marker (IAM) in vivo, pPDH can be used together with IEGs or other cell-type markers to profile and identify bi-directional neural dynamics induced by experiences or behaviors.

  PublisherOA PDFDOI

• Phosphorylation of pyruvate dehydrogenase marks the inhibition of <i>in vivo</i> neuronal activity

  bioRxiv (Cold Spring Harbor Laboratory) · 2023-03-14 · 2 citations

  preprintOpen access

  Summary For decades, the expression of immediate early genes (IEGs) such as c- fos has been the most widely used molecular marker representing neuronal activation. However, to date, there is no equivalent surrogate available for the decrease of neuronal activity (i.e., inhibition). Here, we developed an optogenetic-based biochemical screen in which population neural activities can be controlled by light with single action potential precision, followed by unbiased phosphoproteomic profiling. We identified that the phosphorylation of pyruvate dehydrogenase (pPDH) inversely correlated with the intensity of action potential firing in primary neurons. In in vivo mouse models, monoclonal antibody-based pPDH immunostaining detected neuronal inhibition across the brain induced by a wide range of factors including general anesthesia, sensory experiences, and natural behaviors. Thus, as an in vivo marker for neuronal inhibition, pPDH can be used together with IEGs or other cell-type markers to profile and identify bi-directional neural dynamics induced by experiences or behaviors.

  PublisherOA PDFDOI

• Vagal sensory neurons mediate the Bezold–Jarisch reflex and induce syncope

  Nature · 2023 · 98 citations

  Senior authorCorresponding
  • Neuroscience
  • Medicine
  • Biology

  to show that VSNs that express neuropeptide Y receptor Y2 (NPY2R) predominately connect the heart ventricular wall to the area postrema. Optogenetic activation of NPY2R VSNs elicits the classic triad of BJR responses-hypotension, bradycardia and suppressed respiration-and causes an animal to faint. Photostimulation during high-resolution echocardiography and laser Doppler flowmetry with behavioural observation revealed a range of phenotypes reflected in clinical syncope, including reduced cardiac output, cerebral hypoperfusion, pupil dilation and eye-roll. Large-scale Neuropixels brain recordings and machine-learning-based modelling showed that this manipulation causes the suppression of activity across a large distributed neuronal population that is not explained by changes in spontaneous behavioural movements. Additionally, bidirectional manipulation of the periventricular zone had a push-pull effect, with inhibition leading to longer syncope periods and activation inducing arousal. Finally, ablating NPY2R VSNs specifically abolished the BJR. Combined, these results demonstrate a genetically defined cardiac reflex that recapitulates characteristics of human syncope at physiological, behavioural and neural network levels.

  PublisherOA PDFDOI

• Neural Control and Modulation of Thirst, Sodium Appetite, and Hunger

  Cell · 2020 · 142 citations

  1st authorCorresponding
  • Biology
  • Endocrinology
  • Internal medicine
  PublisherOA PDFDOI

• Temporally and Spatially Distinct Thirst Satiation Signals

  Neuron · 2019-05-29 · 83 citations

  articleOpen access1st author
  PublisherOA PDFDOI

• Neural Architecture Underlying Thirst Regulation

  2019-01-01

  dissertation1st authorCorresponding

  An important aspect of thirst is its quick quenching. When thirsty, you drink a glass of water for a few seconds; the water travels from the mouth to the stomach and you are satiated. The water has not yet been absorbed into the blood, so the brain needs to have mechanisms to signal stopping of drinking. It cannot simply depend on the body, as the body takes a good 15 - 30 minutes to even start absorption. In this dissertation, I describe dynamic thirst circuits that integrate the homeostatic-instinctive requirement for fluids, the consequent drinking behavior, and reward processing to maintain internal water balance. In Chapter 1, I show how neural populations in the lamina terminalis, a forebrain structure, form a hierarchical circuit architecture to regulate thirst. Among them, excitatory neurons in the median preoptic nucleus (MnPO) are essential for the integration of signals from the thirst-driving neurons of the subfornical organ (SFO). Thirst-driving neurons in the SFO receive temporarily distinct preabsorptive inhibition by drinking action and gastrointestinal osmolality sensing. A distinct inhibitory circuit, involving MnPO GABAergic neurons that express glucagon-like peptide 1 receptor (GLP1R), is activated immediately upon drinking and monosynaptically inhibits SFO thirst neurons. These responses are induced by the ingestion of fluids but not solids, and are time-locked to the onset and offset of drinking. Furthermore, loss-of-function manipulations of these neurons lead to a polydipsic, overdrinking phenotype. These neurons therefore facilitate rapid satiety of thirst by monitoring real-time fluid ingestion. In Chapters 2 and 3, I talk about how thirst triggers a strong motivational state that drives animals toward drinking behavior. The consequent fluid intake provides both satiation and pleasure of drinking to animals. However, how these two factors are processed and represented by the brain remains poorly understood. Here I will use in vivo optical recording, genetics, and intragastric infusion approaches to dissect thirst satiation circuits and their contribution to reward signals. Thirst-driving neurons in the subfornical organ (SFO) receive multiple temporally-distinct satiation signals prior to the homeostatic recovery: oropharyngeal stimuli induced by drinking action and gastrointestinal sensing of osmolality changes. In chapter 1, I have shown that drinking action is represented by inhibitory neurons in the median preoptic nucleus (MnPO). Here, I demonstrate that gut osmolality signals are mediated by specific GABAergic neurons in the SFO. These neurons were selectively activated by hypo-osmotic stimuli in the gut independent of drinking action. Optogenetic gain- and loss-of-function of this inhibitory population suppressed and increased water intake in thirsty animals, respectively. These results indicate that oropharyngeal- and gastrointestinal-driven satiation signals are transmitted to thirst neurons through different neural pathways. Furthermore, I investigated the contribution of thirst satiation signals to the reward circuit using a genetically-encoded ultrafast dopamine (DA) sensor. Interestingly, oral ingestion but not gut osmolality changes triggered robust DA release. Importantly, chemogenetic activation of thirst-quenching neurons did not induce DA release in water-deprived animals. Together, this dissected genetically-defined thirst satiation circuits, the activity of which are functionally separable from reward-related brain activity. Taken together, these finding provide answers to some longstanding questions in the neural control of fluid intake, and appetite in general.

  PublisherDOI

• Neural populations for maintaining body fluid balance

  Current Opinion in Neurobiology · 2019-03-02 · 15 citations

  reviewOpen access
  PublisherOA PDFDOI

• Chemosensory modulation of neural circuits for sodium appetite

  Nature · 2019-03-27 · 73 citations

  articleOpen access
  PublisherOA PDFDOI

Frequent coauthors

• Jingrui Ma

  University of California, San Diego

  8 shared

• Li Ye

  Scripps Research Institute

  7 shared

• Yuki Oka

  California Institute of Technology

  7 shared

• Zhengyuan Pang

  Scripps Research Institute

  7 shared

• Tianbo Qi

  Scripps Research Institute

  7 shared

• Sangjun Lee

  Pohang University of Science and Technology

  5 shared

• Yunxiao Zhang

  4 shared

• Shawn Zheng Kai Tan

  4 shared

Labs

• The Augustine LabPI

Education

• PhD, Computation and Neural Systems

  California Institute of Technology

  2019

• BS-MS, Biological Sciences

  Indian Institute of Science Education and Research Kolkata

  2013

Awards & honors

• Scripps Fellowship