Student buy-in as a key mechanism for student engagement and performance in an active-learning context is explored. This paper provides the first operational definition of student buy-in to in-class activities, in this case characterizing the complex nature of students’ responses in an active-learning classroom.

Predictors of student commitment and engagement in an undergraduate science course featuring active learning are explored. The study identified student trust in the instructor as an important predictor of student commitment and engagement in an active-learning context.

A linear third-order model of the ocular motor plant for horizontal saccadic eye movements is presented consisting of a linear ocular motor plant and a time-optimal saccadic controller based on physiological considerations. The ocular motor plant consists of the eyeball and two extraocular muscles. All parameters and initial conditions are estimated or measured from physiological data. The neural inputs are described by pulse-slide-step waveforms with a post inhibitory rebound burst and based on a time-optimal controller. Model parameters are estimated using the system identification technique. The static and dynamic behaviors of the model are in excellent agreement with the experimental data.

We sought to understand mechanisms underlying glucose sensing in Drosophila melanogaster. We found that adult insulin producing cells (IPCs) respond to glucose and glibenclamide with a burst-like pattern of activity. Under control conditions IPCs have a resting membrane potential of −62 ± 4 mV. In response to glucose or glibenclamide IPCs generate action potentials at a threshold of −36±1.4 mV with an amplitude of 46±4 mV and width of 9.3±1.8 ms. Real-time Ca 2+ imaging confirms that IPCs respond to glucose and glibenclamide with increased intracellular Ca 2+ . These results provide the first detailed characterization of electrical properties of adult Drosophila IPCs and suggest that these cells sense glucose by a mechanism similar to mammalian pancreatic β cells.

Dravet syndrome (DS) is a form of epilepsy with a high incidence of sudden unexpected death in epilepsy (SUDEP). Respiratory failure is a leading cause of SUDEP, and DS patients’ frequently exhibit disordered breathing. Despite this, mechanisms underlying respiratory dysfunction in DS are unknown. We found that mice expressing a DS-associated Scn1a missense mutation (A1783V) conditionally in inhibitory neurons (Slc32a1cre/+::Scn1aA1783V fl/+; defined as Scn1aΔE26) exhibit spontaneous seizures, die prematurely and present a respiratory phenotype including hypoventilation, apnea, and a diminished ventilatory response to CO2. At the cellular level in the retrotrapezoid nucleus (RTN), we found inhibitory neurons expressing the Scn1a A1783V variant are less excitable, whereas glutamatergic chemosensitive RTN neurons, which are a key source of the CO2/H+-dependent drive to breathe, are hyper-excitable in slices from Scn1aΔE26 mice. These results show loss of Scn1a function can disrupt respiratory control at the cellular and whole animal levels.