Does Insomnia Cause Revenge Seeking Behavior? Using a Puzzle-Based Sleep Lab Educational Escape Room to Teach Circadian Rhythms in a Large Introductory Neuroscience Course.

Traditional large lecture classes can be passive experiences for students. Instead, imagine that several of those learners work at a sleep laboratory and admit four new patients. Within hours, the entire facility is on lockdown, and a mysterious voice on the intercom proclaims that all researchers will lose their ability to sleep within the next hour.

Huntingtin Plays a Role in the Physiological Response to Ethanol in Drosophila.

Background: Huntingtin (htt) protein is an essential regulator of nervous system function through its various neuroprotective and pro-survival functions, and loss of wild-type htt function is implicated in the etiology of Huntington's disease. While its pathological role is typically understood as a toxic gain-of-function, some neuronal phenotypes also result from htt loss. Therefore, it is important to understand possible roles for htt in other physiological circumstances.

The secret life of baby turtles: A novel system to predict hatchling emergence, detect infertile nests, and remotely monitor sea turtle nest events.

Current understanding of sea turtle nesting, hatching, and emergence events has been largely limited to observable events on the surface of the sand, though recent approaches using audio or visual equipment have allowed scientists to better understand some underground nest phenomena. We used a technology-based approach to define motion-related Caretta caretta hatching and emergence nest events. We describe a novel low-cost, accelerometer-based system called TurtleSense that can detect movement and temperature within sea turtle nests remotely.

Acute ethanol exposure during late mouse neurodevelopment results in long-term deficits in memory retrieval, but not in social responsiveness.

Objective: Prenatal alcohol exposure can result in neurological changes in affected individuals and may result in the emergence of a broad spectrum of neurobehavioral abnormalities termed fetal alcohol spectrum disorders (FASD). The effects of ethanol exposure during development are both time and dose dependent. Although many animal models of FASD use more chronic ethanol exposure, acute developmental alcohol exposure may also cause long-lasting neuronal changes.

Using Rubrics as a Scientific Writing Instructional Method in Early Stage Undergraduate Neuroscience Study.

Scientific writing is an important communication and learning tool in neuroscience, yet it is a skill not adequately cultivated in introductory undergraduate science courses. Proficient, confident scientific writers are produced by providing specific knowledge about the writing process, combined with a clear student understanding about how to think about writing (also known as metacognition). We developed a rubric for evaluating scientific papers and assessed different methods of using the rubric in inquiry-based introductory biology classrooms.

Huntington's disease: the past, present, and future search for disease modifiers.

Huntington's disease (HD) is an autosomal dominant genetic disorder that specifically causes neurodegeneration of striatal neurons, resulting in a triad of symptoms that includes emotional, cognitive, and motor disturbances. The HD mutation causes a polyglutamine repeat expansion within the N-terminal of the huntingtin (Htt) protein. This expansion causes aggregate formation within the cytosol and nucleus due to the presence of misfolded mutant Htt, as well as altered interactions with Htt's multiple binding partners, and changes in post-translational Htt modifications.

Pericytes derived from adipose-derived stem cells protect against retinal vasculopathy.

Background: Retinal vasculopathies, including diabetic retinopathy (DR), threaten the vision of over 100 million people. Retinal pericytes are critical for microvascular control, supporting retinal endothelial cells via direct contact and paracrine mechanisms. With pericyte death or loss, endothelial dysfunction ensues, resulting in hypoxic insult, pathologic angiogenesis, and ultimately blindness.

Deletion of the huntingtin proline-rich region does not significantly affect normal huntingtin function in mice.

The N-terminus of Huntingtin, the protein encoded by the Huntington's disease gene, contains a stretch of polyglutamine residues that is expanded in Huntington's disease. The polyglutamine stretch is flanked by two conserved protein domains in vertebrates: an N1-17 domain, and a proline-rich region (PRR). The PRR can modulate the structure of the adjacent polyglutamine stretch, and is a binding site for several interacting proteins.

Deletion of the huntingtin polyglutamine stretch enhances neuronal autophagy and longevity in mice.

Expansion of a stretch of polyglutamine in huntingtin (htt), the protein product of the IT15 gene, causes Huntington's disease (HD). Previous investigations into the role of the polyglutamine stretch (polyQ) in htt function have suggested that its length may modulate a normal htt function involved in regulating energy homeostasis. Here we show that expression of full-length htt lacking its polyglutamine stretch (DeltaQ-htt) in a knockin mouse model for HD (Hdh(140Q/DeltaQ)), reduces significantly neuropil mutant htt aggregates, ameliorates motor/behavioral deficits, and extends lifespan in comparison to the HD model mice (Hdh(140Q/+)).

Deletion of the triplet repeat encoding polyglutamine within the mouse Huntington's disease gene results in subtle behavioral/motor phenotypes in vivo and elevated levels of ATP with cellular senescence in vitro.

Huntingtin (htt), the protein encoded by the Huntington's disease (HD) gene, contains a polymorphic stretch of glutamines (polyQ) near its N-terminus. When the polyQ stretch is expanded beyond 37Q, HD results. However, the role of the normal polyQ stretch in the function of htt is still unknown.