Sleepy Mice Case Study: Implementation and Assessment.

Case studies are a valuable teaching tool to engage students in course content using real-world scenarios. As part of the High-throughput Discovery Science & Inquiry-based Case Studies for Today's Students (HITS) Research Coordination Network (RCN), our team has created the Sleepy Mice Case Study for students to engage with RStudio and the Allen Institute for Brain Science's open access high-throughput sleep dataset on mice. Sleep is important for health, a familiar concern to college students, and was a basis for this case study. In this case, students completed an initial homework assignment, in-class work, and a final take-home application assignment. The case study was implemented in synchronous and asynchronous Introductory Neuroscience courses, a Biopsychology course, and a Human Anatomy and Physiology course, reflecting its versatility. The case can be used to teach course-specific learning objectives such as sleep-related content and/or science data processing skills. The case study was successful as shown by gains in student scores and confidence in achieving learning objectives. Most students reported enjoying learning about sleep deprivation course content using the case study. Best practices based on instructor experiences in implementation are also included to facilitate future use so that the Sleepy Mice Case Study can be used to teach content and/or research-related skills in various courses and modalities.

Short- and long-lasting consequences of in vivo nicotine treatment on hippocampal excitability.

The potential for relapse following cessation of drug use can last for years, implying the induction of stable changes in neural circuitry. In hippocampal slices from rats treated with nicotine for 1 week, withdrawal from nicotine in vivo produces an increase in CA1 pyramidal cell excitability that persists up to 9 months. Immediately upon drug cessation, the enhanced excitability depends on input from regions upstream of CA1, while the long-term excitability change (> 4 weeks) is expressed as an increase in the intrinsic excitability of CA1 neurons. Re-exposure to nicotine in vitro restores hippocampal function to control levels via activation of high-affinity nicotinic acetylcholine receptors after 1 d of withdrawal, but not at times >4 weeks. Thus, nicotine in vivo first induces homeostatic adaptations followed by other more robust neural changes. These mechanisms may contribute to hippocampal localized cue-motivated reinstatement of drug-seeking and/or cognitive deficits observed during withdrawal.

Cellular events in nicotine addiction.

In the 25 years since the observation that chronic exposure to nicotine could regulate the number and function of high affinity nicotine binding sites in the brain there has been a major effort to link alterations in nicotinic acetylcholine receptors (nAChRs) to nicotine-induced behaviors that drive the addiction to tobacco products. Here we review the proposed roles of various nAChR subtypes in the addiction process, with emphasis on how they are regulated by nicotine and the implications for understanding the cellular neurobiology of addiction to this drug.