Biology subjects

Hwa, L. S.

Publications and source records attributed to Hwa, L. S..

4 recordsLinked to original sources

bioRxiv2020

Activation of the kappa opioid receptor / dynorphin system alters stress and threat responding during acute withdrawal from intermittent alcohol drinking in male mice.

The dynorphin/kappa opioid receptor (KOR) system in the brain regulates both stressful experiences and negative, aversive states during withdrawal from drugs of abuse. We explored the role of this system during acute withdrawal from long-term alcohol drinking. Male C57BL/6J mice were subjected to repeated forced swim tests, home cage exposure to a predator odor, and a visual threat after intermittent access to alcohol or water. Systemic injection of KOR antagonist norBNI reversed alcohol-related differences in immobility time during the second swim test and reduced burying behavior in response to predator odor, but did not affect behavioral response to visual threat. HighlightsO_LIIntermittent alcohol drinking changed stress reactions in mice. C_LIO_LIKOR antagonist norBNI altered some, but not all, stress responses in alcohol drinkers C_LI

neuroscience↗

bioRxiv2019

Extended Amygdala Kappa Opioid Receptor Signaling Gates Alcohol-induced Stress Impairments in Mice

"The authors have withdrawn their manuscript because they identified errors in the methods and data reporting that make the results and conclusions unreliable. The published version of this preprint has already been retracted. Therefore, the authors do not wish this work to be cited as reference for the project. If you have any questions, please contact the corresponding author."

neuroscience↗

bioRxiv2018

Chronic inflammatory pain drives alcohol drinking in a sex-dependent manner

Sex differences in chronic pain and alcohol abuse are not well understood. The development of rodent models is imperative for investigating the underlying changes behind these pathological states. However, past attempts have failed to produce drinking outcomes similar to those reported in humans. In the present study, we investigated whether hind paw treatment with the inflammatory agent Complete Freunds Adjuvant (CFA) could generate hyperalgesia and alter alcohol consumption in male and female C57BL/6J mice. CFA treatment led to greater nociceptive sensitivity for both sexes in the Hargreaves test, and increased alcohol drinking for males in a continuous access two-bottle choice (CA2BC) paradigm. Regardless of treatment, female mice exhibited greater alcohol drinking than males. Following a 2-hour terminal drinking session, CFA treatment failed to produce changes in alcohol drinking, blood ethanol concentration (BEC), and plasma corticosterone (CORT) for both sexes. 2-hr alcohol consumption and CORT was higher in females than males, irrespective of CFA treatment. Taken together, these findings have established that male mice are more susceptible to escalations in alcohol drinking when undergoing pain, despite higher levels of total alcohol drinking and CORT in females. Furthermore, the exposure of CFA-treated C57BL/6J mice to the CA2BC drinking paradigm has proven to be a useful model for studying the relationship between chronic pain and alcohol abuse. Future applications of the CFA/CA2BC model should incorporate manipulations of stress signaling and other related biological systems to improve our mechanistic understanding of pain and alcohol interactions.

animal behavior and cognition↗

bioRxiv2018

Predator odor increases glutamatergic synaptic transmission in the prelimbic cortex via corticotropin-releasing factor receptor 1 signaling

The authors have withdrawn their manuscript because the University of North Carolina at Chapel Hill conducted a research misconduct proceeding and concluded that research misconduct occurred involving results presented in this preprint. Hence, the results and conclusions of the preprint article are no longer reliable. The published version of this preprint (Neuropsychopharmacology, doi: 10.1038/s41386-018-0279-2) is being retracted as well. Therefore, the authors do not wish this work to be cited as reference for the project. If you have any questions, please contact the corresponding author.

neuroscience↗