Event Title

BNST PAC1 Receptor Activation May Reinstate Cocaine Seeking Behavior in Rats

Presenter Information

Sarah Brainard, Oberlin College

Location

Science Center, Bent Corridor

Start Date

10-27-2017 6:00 PM

End Date

10-27-2017 6:40 PM

Research Program

University of Vermont Summer Neuroscience Undergraduate Research Felloship (SNURF)

Poster Number

55

Abstract

Previous studies have demonstrated that in rats, stressors such as a footshock can lead to the reinstatement of cocaine seeking. However, the behavioral and neural mechanisms that underlie this reinstatement are not well understood. To determine whether drug relapse is likely mediated by PAC1 receptor activation in the Bed Nucleus of the Stria Terminalis (BNST), in experiment 1, we infused a PAC1 receptor specific agonist (maxadilan) bilaterally into the BNST after animals received 10 days of acquisition (cocaine available) training and 9-15 days of extinction (cocaine unavailable) training. Preliminary data suggests that bilateral maxadilan infusions into the BNST may cause reinstatement of cocaine seeking. In experiment 2, extracellular signal-regulated kinase (pERK), a downstream target of PAC1 receptor activation, was assessed after footshock or no footshock paired with PACAP6-38 (PAC1/VPAC2 antagonist) or vehicle infusions. If footshock leads to PACAP receptor activation, we predict that there will be increased activation of ERK in the BNST after footshock but not after PACAP6-38 infusion. Preliminary data shows that pERK staining can be seen in the BNST but further data analysis is needed to determine whether footshock or PACAP6-38 affect this activation.

Major

Neuroscience

Project Mentor(s)

Sayamwong E. Hammack and Olivia W. Miles, Psychological Science, University of Vermont

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Oct 27th, 6:00 PM Oct 27th, 6:40 PM

BNST PAC1 Receptor Activation May Reinstate Cocaine Seeking Behavior in Rats

Science Center, Bent Corridor

Previous studies have demonstrated that in rats, stressors such as a footshock can lead to the reinstatement of cocaine seeking. However, the behavioral and neural mechanisms that underlie this reinstatement are not well understood. To determine whether drug relapse is likely mediated by PAC1 receptor activation in the Bed Nucleus of the Stria Terminalis (BNST), in experiment 1, we infused a PAC1 receptor specific agonist (maxadilan) bilaterally into the BNST after animals received 10 days of acquisition (cocaine available) training and 9-15 days of extinction (cocaine unavailable) training. Preliminary data suggests that bilateral maxadilan infusions into the BNST may cause reinstatement of cocaine seeking. In experiment 2, extracellular signal-regulated kinase (pERK), a downstream target of PAC1 receptor activation, was assessed after footshock or no footshock paired with PACAP6-38 (PAC1/VPAC2 antagonist) or vehicle infusions. If footshock leads to PACAP receptor activation, we predict that there will be increased activation of ERK in the BNST after footshock but not after PACAP6-38 infusion. Preliminary data shows that pERK staining can be seen in the BNST but further data analysis is needed to determine whether footshock or PACAP6-38 affect this activation.