[FoRK] Success by degree

Dr. Ernie Prabhakar drernie at radicalcentrism.org
Wed Dec 4 17:20:19 PST 2013

Woot! Congratulations to both of you. 

Sent from my iPhone

> On Dec 4, 2013, at 14:19, Wayne Baisley <baisley at alumni.rice.edu> wrote:
> By PhD, in particular.  I'm excessively proud to report that my daughter defended in Madison today. Glory details, below.
> Cheers,
> Wayne
> Greetings,
> Please join the Neuroscience Training Program for Sarah Baisley's public thesis defense seminar on Wednesday, December 4, 2013 at 11:00 AM in the Biotechnology Auditorium, Room 1111, Genetics and Biotechnology Center (425 Henry Mall). Details for her defense as well as her thesis abstract are below.
> NTP Ph.D. Candidate: Sarah Baisley
> Research conducted in the lab of Vaishali Bakshi, Ph.D.
> Title: "Modulation of Prepulse Inhibition and Ingestive Behavior by Nucleus Accumbens AMY-1 Amylin Receptors"
> Wednesday, December 4
> 11:00
> Biotechnology Auditorium, Room 1111, Genetics and Biotechnology Center (425 Henry Mall)
> Thesis Abstract:
> Amylin is a feeding-modulatory pancreatic peptide that crosses the blood-brain barrier to access receptors localized within specific sites across the neural axis. Among the densest concentrations of amylin receptors (AMY-Rs) is found in the nucleus accumbens shell (AcbSh). The AcbSh represents an interface between the limbic cortex and di/mesencephalic behavior effector systems, and plays a role in both complex motivated behaviors, and more basic information-processing functions (namely, pre-attentional sensorimotor gating). Hence, we investigated the role of AcbSh AMY-Rs in both functional realms.
> In the first set of experiments, we measured sensorimotor gating using the prepulse inhibition (PPI) paradigm, in which sub-threshold auditory stimuli (“prepulses”) negatively modulate the behavioral responses to subsequent superthreshold stimuli. AcbSh amylin infusions partially reversed PPI deficits created by the psychotomimetic drug amphetamine. These effects were limited to the AcbSh, where we also found high levels of mRNA for RAMP-1 and CT-R, the two genetic components of the high-affinity AMY-1 amylin receptor. In addition, blockade of AcbSh AMY-R receptors created PPI deficits that were reversed by the antipsychotic haloperidol. This suggests that there is an endogenous amylinergic ‘tone’ in the AcbSh that regulates PPI via interactions with dopamine receptors. Because AMY-R are almost absent outside of the medial AcbSh, drugs affecting AMY-1 receptors could provide a means of selectively targeting the ventral striatum and thereby avoid dorsal striatum-mediated side effects. Amylin is also a satiety factor, so its use as an adjunct antipsychotic could counteract the diabetes, obesity, and other metabolic side effects commonly seen with existing antipsychotic treatments.
> In the second set of experiments, we explored AcbSh amylin’s role in appetitively motivated behavior, by examining interactions between AcbSh-localized AMY-Rs and mu-opioid receptors (µ-OR). Amylin infusions in the AcbSh, but not the anterodorsal striatum, potently decreased µ-OR stimulation-induced hyperphagia at doses far lower than needed to reduce non-opioid-driven feeding. Conversely, blockade of AcbSh AMY-Rs significantly reversed the ability of pre-feeding to suppress µ-OR stimulation-induced hyperphagia. This effect of AMY-R blockade was present only after eating, when circulating amylin levels are highest. This represents the first demonstration that endogenous AMY-R signaling negatively modulates µ-OR-mediated appetitive responses at the level of the AcbSh.
> Taken together, the results from this thesis suggest that AcbSh AMY-1 stimulation may have antipsychotic potential, and that an endogenous telencephalic amylinergic ‘tone’ regulates sensorimotor gating and appetitive behavior.
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