The John B. Pierce Laboratory


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A study by scientists Ivan de Araujo, Wenfei Han, and team suggests the origin of hunting behavior may come from two set of neurons tucked deep in the forebrain of most vertebrates

(Yale Press Release)

Activating these neurons in living mice prompt them to pursue never seen before prey and to bite everything in their path, even sticks and bottle caps, the researchers report in the January 12, 2017 issue of the journal Cell.

“This area, the central amygdala, seems to allow the animal precise control over the muscles involved in pursuing and capturing prey,’’ said Ivan de Araujo, associate fellow at The John B. Pierce Laboratory, associate professor of psychiatry at Yale School of Medicine, and senior author of the paper.

In their experiments, de Araujo and colleagues used light-based technique called optogenetics to specifically activate neurons of the central amygdala, an almond-shaped structure involved in emotion and motivation. They found that one set of neurons prompted mice to pursue moving objects, while a second set of neurons seemed to activate jaw muscles involved in biting.

Normally behaving lab mice “jump on inanimate objects and bite them” when both sets of neurons are activated, de Araujo said. Activating these neurons also increased the efficiency with which mice hunt and capture live insects, in addition to make them pursue and attack animate toy insects. The two sets of neurons seem to act as relay stations that trigger hunting behavior after the animal detects visual signals of nearby moving prey.

These areas of the amygdala are preserved in almost all vertebrates, attesting to their importance in evolution.  Interestingly, these regions seem to be absent in brains of some species such as lampreys, which have no jaws, de Araujo noted.  His lab studies feeding behaviors of mice in the lab but felt “we needed to truly understand how an animal pursues food in a natural environment.”

Dr. Usselman’s published work chosen as an APSselect Paper

Charlotte Usselman, PhD has been a Post Doctoral Fellow in Dr. Nina Stachenfeld’s laboratory since November, 2015.  Before coming to the Pierce Laboratory, Dr. Usselman trained in Kevin Shoemaker’s laboratory at Western University (Canada), one of the most prestigious laboratories in the world studying neurovascular control of blood pressure.  A paper recently published from her work in that laboratory, Hormone phase influences sympathetic responses to high levels of lower body negative pressure in young healthy women was recently published in Am J Physi – Reg, Integrative Comp Physiol (http://ajpregu.physiology.org/content/311/5/R957).  This paper was chosen by the Journal as an APSselect Paper.

APSselect: The editorial team carefully selects from the top articles nominated each month across the 10 APS (American Physiological Society) research journals that highlight, promote, and rapidly disseminate some of the most stimulating original research.  This is a rare and exciting honor, especially for a scientist in the early phase of what is obviously a promising career in physiology.

This study examined the role that circulating sex hormones play on maintaining blood pressure during orthostatic challenges.  Orthostatic challenges are those which encourage the pooling of blood in the lower body, such as standing for a long time, or moving from seating or lying to standing.  Usselman et al. found that high female sex hormone conditions were associated with greater peripheral blood pooling, likely the result of estrogen as a dilator of peripheral blood vessels. One unexpected finding was that women taking hormonal contraceptives experienced a fall in blood pressure at the highest level of lower body negative pressure, implying that hormone exposure may reduce orthostatic tolerance in young women. Together, these data improve our understanding of the role of sex hormones on the regulation of blood pressure, and provide some insight into the mechanisms by which young women have an increased risk for orthostatic intolerance but are protected from hypertension.

Research Scientists develop model for studying Alzheimer’s disease

By Ziba Kashef

The vast majority of Alzheimer’s disease cases are not directly inherited but linked to environmental and genetic factors. Yet most models used for studying Alzheimer’s in animals mimic the inherited form of the disease.

Yale researchers developed a novel model that may prove useful to the study of Alzheimer’s at its earliest stages. Led by associate professor of neuroscience Justus Verhagen of The John B. Pierce Laboratory and research scientist Alla Ivanova, the researchers studied mice lacking a protein, Fus1, that helps regulate mitochondria — the structures that maintain the balance of critical functions within cells.

In tests, these animals exhibited a loss of smell as well as spatial memory — early signs of Alzheimer’s in people. If confirmed in further studies, the model could serve as an additional tool for understanding the role of Fus1 and mitochondria in the development of Alzheimer’s, said the researchers.

Read the full study published in Frontiers in Aging Neuroscience.