Senior Recital: Paul Spanagel, baritone

https://digitalwindow.vassar.edu/musi_senior/1006/thumbnail.jp

Implication of Class Size Reduction for Upper Grades

Government officials, policymakers, school districts and teachers have questioned the impact of class size on students’ achievement, engagement, and behavior. This thesis project examines the challenges and benefits to class size initiatives and proposes an extension from elementary grades through high school as a means to raise student achievement and involvement. It discusses prior research efforts such as Project STAR, which was conducted in Tennessee, and its significance in establishing benchmarks for studying smaller class size with regard to ethnicity, gender, and socioeconomic status. Further historical research considers: class size reduction initiatives as they link to student achievement, comparison of students per class and cumulative grade point averages to understand trends, student to teacher ratio effects, and potential fiscal concerns for enlarging class reduction programs in the secondary levels. The study was completed in a suburban district with students of varying ethnic and socioeconomic status. The study was two-fold: district wide teacher surveys to understand class size and cumulative grade point average and year-long observation in individual math classes (two small and one large). Conclusions drawn support the concept of lowered class size to increase students’ academic achievement

Reward Sensitivity for a Palatable Food Reward Peaks During Pubertal Developmental in Rats

Puberty is a critical period for the initiation of drug use and abuse. Because early drug use onset often accounts for a more severe progression of addiction, it is of importance to understand the underlying mechanisms and neurodevelopmental changes during puberty that are contributing to enhanced reward processing in teenagers. The present study investigated the progression of reward sensitivity toward a natural food reward over the whole course of adolescence in male rats (postnatal days 30–90) by monitoring consummatory, motivational behavior and neurobiological correlates of reward. Using a limited-free intake paradigm, consumption of sweetened condensed milk (SCM) was measured repeatedly in adolescent and adult rats. Additionally, early- and mid-pubertal animals were tested in Progressive Ratio responding for SCM and c-fos protein expression in reward-associated brain structures was examined after odor conditioning for SCM. We found a transient increase in SCM consumption and motivational incentive for SCM during puberty. This increased reward sensitivity was most pronounced around mid-puberty. The behavioral findings are paralleled by enhanced c-fos staining in reward-related structures revealing an intensified neuronal response after reward-cue presentation, distinctive for pubertal animals. Taken together, these data indicate an increase in reward sensitivity during adolescence accompanied by enhanced responsiveness of reward-associated brain structures to incentive stimuli, and it seems that both is strongly pronounced around mid-puberty. Therefore, higher reward sensitivity during pubertal maturation might contribute to the enhanced vulnerability of teenagers for the initiation of experimental drug use

Engaging Students with Great Problems

The Great Problems Seminars were designed to bring first year engineering students into meaningful contact with current events, societal problems, and human needs. Key learning objectives include: introducing project team work and developing writing and presentation skills. Each seminar has focused on a large global issue: food and hunger, energy and its utilization, health and healthcare delivery, the NAE Grand Challenges. Seminars are co-taught by an interdisciplinary pair: one natural science/engineering instructor and one humanities/social science instructor. The first half of the two-term course sequence explores the depth and breadth of the problem; the second half is devoted to project work. Focus group assessment demonstrates that the GPS courses achieve the original course objectives. Student course evaluations indicate high satisfaction despite requiring significantly more work than traditional first year offerings taught within the disciplines. Comments by former GPS students demonstrate that they value how these courses prepared them for their futures

Great Problems Seminars: A New First-Year Foundation at WPI

The Great Problems Seminars are a new program designed to engage Worcester Polytechnic Institute’s first-year students with current events, societal problems, and human needs. Each seminar starts with an important global problem and helps students to find a place where they can make real progress, no matter how small, in solving the problem. Four WPI faculty representing Chemistry, Mechanical Engineering, and Humanities developed and delivered two Great Problems Seminars in 2007. Feed the World explored the chemical, ethical, physiological and economic dimensions of a (simple) question: Why do we eat what we eat? The students completed projects on subjects ranging from hunger in Worcester to controlling fertilizer runoff. Power the World focused on the physics, history, and the environmental and economic impact of energy technologies. The students completed projects ranging from an energy cost analysis of green roofs and photovoltaic systems for WPI to air pollution in China. This paper will describe the final student projects as well as the smaller projects and activities designed to help students develop the intellectual skills needed for research and professional work, including clear, succinct writing, oral presentation, pair and small group discussion, and the ability to take and understand multiple-perspectives. Perhaps the most important “finding” is that first-year students can do much more than we (or they) expect

Incentive learning underlying cocaine relapse requires mGluR5 receptors located on dopamine D1 receptor-expressing neurons

Understanding the psychobiological basis of relapse remains a challenge in developing therapies for drug addiction. Relapse in cocaine addiction often occurs following exposure to environmental stimuli previously associated with drug taking. The metabotropic glutamate receptor, mGluR5, is potentially important in this respect; it plays a central role in several forms of striatal synaptic plasticity proposed to underpin associative learning and memory processes that enable drug-paired stimuli to acquire incentive motivational properties and trigger relapse. Using cell type-specific RNA interference, we have generated a novel mouse line with a selective knock-down of mGluR5 in dopamine D1 receptor-expressing neurons. Although mutant mice self-administer cocaine, we show that reinstatement of cocaine-seeking induced by a cocaine-paired stimulus is impaired. By examining different aspects of associative learning in the mutant mice, we identify deficits in specific incentive learning processes that enable a reward-paired stimulus to directly reinforce behavior and to become attractive, thus eliciting approach toward it. Our findings show that glutamate signaling through mGluR5 located on dopamine D1 receptor-expressing neurons is necessary for incentive learning processes that contribute to cue-induced reinstatement of cocaine-seeking and which may underpin relapse in drug addiction

Adeno-associated virus (AAV)-mediated suppression of Ca2+/calmodulin kinase IV activity in the nucleus accumbens modulates emotional behaviour in mice

<p>Abstract</p> <p>Background</p> <p>Calcium/calmodulin-dependent protein kinase IV (CaMKIV) controls activity-dependent gene transcription by regulating the activity of the cyclic AMP response element binding protein (CREB). This signaling pathway is involved in gating emotional responses in the CNS but previous studies did not address the potential roles of CaMKIV in discrete brain regions. In the present study, we aimed at specifically dissecting the role of CaMKIV in the nucleus accumbens of adult mice.</p> <p>Results</p> <p>We used recombinant adeno-associated virus (rAAV)-mediated gene transfer of a dominant-negative CaMKIV variant (rAAV-dnCaMKIV) to inhibit endogenous CaMKIV in the nucleus accumbens. rAAV-dnCaMKIV treated animals were subjected to a battery of tests including, prepulse inhibition of the acoustic startle response, open field, social interaction and anxiety-related behaviour. We found that basal locomotor activity in the open field, and prepulse inhibition or startle performance were unaltered in mice infected with rAAV-dnCaMKIV in the nucleus accumbens. However, anxiogenic effects were revealed in social interaction testing and the light/dark emergence test.</p> <p>Conclusion</p> <p>Our findings suggest a modulatory role of CaMKIV in the nucleus accumbens in anxiety-like behaviour but not sensorimotor gating.</p

Are animal models of addiction useful?

Background: Preclinical research involving non-human animals has made important contributions to our understanding of risk-factors for addiction, neuroadaptations that follow chronic drug exposure, and to the development of some efficacious pharmacotherapies for addiction. Despite these contributions, we argue that animal models of addiction have impeded progress in our understanding of addiction and its treatment in humans. Argument: First of all, the majority of pharmacological treatments that were initially developed using animal models have failed to prove effective for the treatment of addiction in humans, resulting in a huge waste of resources. Secondly, we demonstrate that prevailing animal models that portray addiction as a disorder of compulsion and habit cannot be reconciled with observations that psychoactive drug use in humans is a goal-directed operant behaviour that remains under the control of its consequences, even in people who are addicted. Thirdly, addiction may be a uniquely human phenomenon that is dependent on language, which necessarily limits the validity of animal models. Finally, we argue that addicted brains must be understood as one component of broader networks of symptoms and environmental and social factors that are impossible to model in laboratory animals. Conclusions: A case can be made that animal models of addiction have not served us well in understanding and treating addiction in humans. It is important to reconsider some widely-held beliefs about the nature of addictive behaviour in humans that have arisen from the zeal to translate observations of laboratory animals

Genetic deletion of neuronal PPARγ enhances the emotional response to acute stress and exacerbates anxiety: An effect reversed by rescue of amygdala PPARγ function

PPARγ is one of the three isoforms of the Peroxisome Proliferator-Activated Receptors (PPARs). PPARγ is activated by thiazolidinediones such as pioglitazone, and it is targeted to treat insulin resistance. PPARγ is densely expressed in brain areas involved in regulation of motivational and emotional processes.Here, we investigated the role of PPARγ in the brain and explored its role in anxiety and stress responses in mice. The results show that stimulation of PPARγ by pioglitazone did not affect basal anxiety but fully prevented the anxiogenic effect of acute stress. Using mice with genetic ablation of neuronal PPARγ (PPARγ(NestinCre)), we demonstrated that a lack of receptors, specifically in neurons, exacerbated basal anxiety and enhanced stress sensitivity. The administration of GW9662, a selective PPARγ antagonist, elicited a marked anxiogenic response in PPARγ wild-type (Wt) but not in PPARγ(NestinCre) KO mice. Using c-Fos immunohistochemistry we observed that acute stress exposure resulted in a different pattern of neuronal activation in the amygdala and the hippocampus of PPARγ(NestinCre) KO mice compared with Wt mice. No differences were found between Wt and KO mice in hypothalamic regions responsible for hormonal response to stress, nor in blood corticosterone levels. Microinjection of pioglitazone, into the amygdala but not into the hippocampus abolished the anxiogenic response elicited by acute stress. Results also showed that in both regions PPARγ co-localizes with GABAergic cells. These findings demonstrate that neuronal PPARγ is involved the regulation of the stress response, and that the amygdala is a key substrate for the anxiolytic effect of PPARγ