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Ulrich-Lai, Y. M.

Publications and source records attributed to Ulrich-Lai, Y. M..

2 recordsLinked to original sources

Extended Pavlovian conditioned approach training and devaluation in Long-Evans rats using time-restricted feeding

Pavlovian conditioned approach (PCA) is a useful tool in studying compulsive- and addictive-like behaviors. PCA pairs a cue with reward delivery and rats typically differentiate into three phenotypes (sign-trackers, goal-trackers, and intermediates) based on behavior during the reward-paired cue presentation. Sign-trackers, who preferentially interact with the cue, are more likely to engage in compulsive behaviors and have decreased behavioral flexibility compared to goal-trackers, who preferentially interact with the food cup. However, one limitation to PCA is the use of food deprivation conditions that maintain rats at 80-90% of ad libitum weight, likely increasing stress which may bias animals towards sign-tracking behavior. Furthermore, most behavioral analysis only examines lever pressing and food cup entry, overlooking other behaviors that may better define phenotypes. In the current study male and female Long-Evans rats underwent an extended PCA training paradigm followed by satiety-induced reward devaluation under time-restricted feeding (TRF) conditions. Under TRF, rats continued to gain weight across PCA training and maintained caloric intake relative to ad libitum intake. Expanding the scope of behavioral analysis increased the proportion of ST rats in both early and late PCA training. Rats also increased the time spent interacting with the food cup during the inter-trial interval across extended PCA training. All rats were sensitive to satiety-induced reward devaluation, regardless of sex or devaluation condition. This study helps establish a PCA method optimized for Long-Evans rats with relevance for identifying PCA phenotypes contribution to dysregulated behavior in the context of chronic stress and obesity.

neuroscience↗

Prefrontal Cortex Regulates Chronic Stress-Induced Cardiovascular Susceptibility

The medial prefrontal cortex (mPFC) is necessary for appropriate appraisal of stressful information, as well as coordinating visceral and behavioral processes. However, prolonged stress impairs mPFC function and prefrontal-dependent behaviors. Additionally, chronic stress induces sympathetic predominance, contributing to health detriments associated with autonomic imbalance. Previous studies identified a subregion of rodent prefrontal cortex, infralimbic cortex (IL), as a key regulator of neuroendocrine-autonomic integration after chronic stress, suggesting that IL output may prevent chronic stress-induced autonomic imbalance. In the current study, we tested the hypothesis that the IL regulates hemodynamic, vascular, and cardiac responses to chronic stress. To address this hypothesis, a viral-packaged siRNA construct was used to knockdown vesicular glutamate transporter 1 (vGluT1) and reduce glutamate packaging and release from IL projection neurons. Male rats were injected with a vGluT1 siRNA-expressing construct or GFP control into the IL and then remained as unstressed controls or were exposed to chronic variable stress (CVS). IL vGluT1 knockdown increased heart rate and mean arterial pressure (MAP) reactivity, while CVS increased chronic MAP only in siRNA-treated rats. In a separate cohort, CVS and vGluT1 knockdown interacted to impair both endothelial-dependent and endothelial-independent vasoreactivity ex vivo. Furthermore, vGluT1 knockdown and CVS increased histological markers of fibrosis and hypertrophy. Thus, knockdown of glutamate release from IL projection neurons indicates that these cells are necessary to prevent the enhanced physiological responses to stress that promote susceptibility to cardiovascular pathophysiology. Ultimately, these findings provide evidence for a neurobiological mechanism mediating the relationship between stress and poor cardiovascular health outcomes.\n\nClinical perspectiveWhat is new? O_LIKnockdown of glutamate release from infralimbic cortex increases heart rate and arterial pressure reactivity\nC_LIO_LIDecreased infralimbic glutamate output leads to vascular dysfunction after chronic stress\nC_LIO_LIThese functional changes associate with histological indicators of cardiac hypertrophy, as well as vascular hypertrophy and fibrosis\nC_LI\n\nWhat are the clinical implications? O_LIThese studies provide a neurobiological mechanism that may account for the link between long-term stress and increased cardiovascular disease risk\nC_LI

neuroscience↗