[FoRK] Success by degree
meltsner at alum.mit.edu
Wed Dec 4 14:37:23 PST 2013
Mazal Tov! As rites of passage go, this one is up there with ritual
scarring and adult (male) circumcision.
(a few weeks past the 26th anniversary of mine)
On Wed, Dec 4, 2013 at 4:19 PM, 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.
> 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
> 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
> 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
> 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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