Neuroscience Seminar Series

4:00-4:30PM Presentation

Title: Exploring VNS Therapy for Autism-Related Behavioral Issues

Speaker:
Melissa Krauth - First Year Presentation
PhD Student, UT Dallas

ASD is a common neurodevelopmental disorder affecting up to 3% of children and is associated with many genetic and environmental risk factors. The most common genetic cause of ASD involves loss of function of the Fmr1 gene, which results in Fragile X Syndrome (FXS). Individuals with FXS typically present with ASD-like behaviors and co-morbid conditions and are particularly prone to high levels of anxiety which can have a negative impact on life outcomes. Vagus Nerve Stimulation (VNS) is an FDA-approved treatment which has shown intriguing preliminary effects on anxiety and other quality-of-life metrics in patients, including some with ASD. VNS also reduced anxiety in wild-type (WT) rats and improved sociability in an environmental rat model of ASD, while also producing pro-cognitive benefits. Based on these findings, we hypothesized that VNS may prove a useful approach for addressing behavioral and cognitive deficits in a rat model of FXS, the Fmr1 knock-out (KO)

4:30-5:00PM Presentation

Title: Role of VNS-Mediated BDNF Release in the Infralimbic Cortex on Extinction Learning of Cocaine Seeking

Speaker:
Lily Vu - First Year Presentation
PhD Student, UT Dallas

A major driver of relapse is the exposure of addicts to the contexts and cues associated with drug-taking. Extinction learning extinguishes the association of cues to the extreme reward experience by pairing the cues with a neutral experience. The goal of extinction learning is to reduce cravings and relapse in response to previously drug-associated cues. Previous work in our lab shows that vagus nerve stimulation (VNS) during extinction learning reduces cue-induced reinstatement of drug-seeking in a rodent model of cocaine self-administration. VNS leads to the release of Brain-Derived Neurotrophic Factor (BDNF), which acts as a key modulator of synaptic plasticity in response to experiences. Preliminary data from our lab shows that systemic injection of BDNF receptor antagonist ANA-12 prevents the effect of VNS on reinstatement. Previous research and preliminary data also suggest that VNS-evoked release of BDNF may reduce cue-induced reinstatement of drug self-administration by supporting synaptic plasticity during extinction training. However, the neural circuits through which VNS modulates drug-seeking are unclear. The infralimbic cortex (IL) within the medial prefrontal cortex is a crucial brain region for extinction learning. Previous experiments show that altering BDNF levels in the IL modulates extinction learning as well as drug-seeking. Thus, VNS may modulate drug-seeking by elevating BDNF levels in the IL. To investigate this, I injected a CRISPR-mediated adeno-associated virus (AAV) that expresses GFP and targets rat BDNF into the IL to locally knockdown BDNF to examine if local knockdown of BDNF in the IL is necessary for the effect of VNS on drug-seeking behavior. 

On December 5 2023 at 4:00 - 5:00PM
In-person in RL 3.204.

This will also be available on MS Teams.
Meeting ID: 225 457 952 537
Passcode: zr2TPn

The host for these talks is Ben Kolber, PhD.