Launching a Peer Supplemental Instruction Program for an Introductory Biology Course

For the first time at Georgia Gwinnett College, a supplemental instruction (PSI) program was designed to provide peer-led instruction on a) principles of biology, chemistry, mathematics and b) academic skills e.g. self-regulated learning, strategies in studying and test-taking. PSI for Principles of Biology (BIOL1107K) was carried out by PSI leaders who previously earned a grade of ‘A’ or ‘B’ in BIOL1107K, received training on tutoring practices and worked with faculty to develop active learning exercises/worksheets for PSI sessions. PSI was open only to students who earned a grade of ≤ 75% on the first exam across four BIOL1107K sections. Comparison of exam grades revealed that PSI student performance was not significantly different from control (students who earned a grade of ≤ 75% on the first exam but did not enroll in PSI). The challenges at an institution lacking a PSI culture and strategies to encourage student commitment will be discussed

Boundary Crossing by a Community of Practice: Tibetan Buddhist Monasteries Engage Science Education

As a globalized world struggles with division and disinformation, engaging across difference has emerged as a major challenge to communication and collaborative action needed to address growing global challenges. As such, the initiative by Tibetan Buddhist leaders to incorporate western science in curricula for monastic education may serve as an important case study that illuminates the conditions and processes at work in genuine cultural outreach and exchange. That project, spearheaded in the Emory-Tibet Science Initiative (ETSI), involves reaching out across two quite different communities of practice, Tibetan Buddhism and science, and the willingness and ability of individuals to cross the boundaries between them. In the study reported here, we apply existing understandings of communities of practice and of learning mechanisms that mediate boundary crossing to probe for presence of conditions and processes that promote effective outreach among Tibetan Buddhist monastic students. We deploy analysis of qualitative survey, interview, and self-report data from monastic students shortly after ETSI began (2009) and after science education had been rolled out in the monasteries (2019) to, first, identify initial cultural conditions related to outreach and engagement with science, and, second, probe for post-rollout presence of boundary crossing learning mechanisms among monastic students which facilitate communication from one community of practice to another. We found a range of robust initial cultural conditions (e.g., perceived overlap in subjects and methods of inquiry), along with strong presence of mechanisms that facilitate boundary crossing (e.g., reflection, transformation) and operate through time. We observed cascading effects of these conditions and mechanisms on student engagement with science. Furthermore, interactions of these conditions and mechanisms allow monastic students to engage with science on their own Buddhist terms and to regard learning science as potentially beneficial rather than threatening to their personal or collective Buddhist goals

Boundary Crossing by a Community of Practice: Tibetan Buddhist Monasteries Engage Science Education

As a globalized world struggles with division and disinformation, engaging across difference has emerged as a major challenge to communication and collaborative action needed to address growing global challenges. As such, the initiative by Tibetan Buddhist leaders to incorporate western science in curricula for monastic education may serve as an important case study that illuminates the conditions and processes at work in genuine cultural outreach and exchange. That project, spearheaded in the Emory-Tibet Science Initiative (ETSI), involves reaching out across two quite different communities of practice, Tibetan Buddhism and science, and the willingness and ability of individuals to cross the boundaries between them. In the study reported here, we apply existing understandings of communities of practice and of learning mechanisms that mediate boundary crossing to probe for presence of conditions and processes that promote effective outreach among Tibetan Buddhist monastic students. We deploy analysis of qualitative survey, interview, and self-report data from monastic students shortly after ETSI began (2009) and after science education had been rolled out in the monasteries (2019) to, first, identify initial cultural conditions related to outreach and engagement with science, and, second, probe for post-rollout presence of boundary crossing learning mechanisms among monastic students which facilitate communication from one community of practice to another. We found a range of robust initial cultural conditions (e.g., perceived overlap in subjects and methods of inquiry), along with strong presence of mechanisms that facilitate boundary crossing (e.g., reflection, transformation) and operate through time. We observed cascading effects of these conditions and mechanisms on student engagement with science. Furthermore, interactions of these conditions and mechanisms allow monastic students to engage with science on their own Buddhist terms and to regard learning science as potentially beneficial rather than threatening to their personal or collective Buddhist goals

Emory-Tibet Science Initiative: Changes in Monastic Science Learning Motivation and Engagement During a Six-Year Curriculum

Led by His Holiness the Dalai Lama, the initiative taken by the Tibetan Buddhist monastic community to connect with western science and scientists presents a unique opportunity to understand the motivations and engagement behaviors that contribute to monastic science learning. In this study, we draw on quantitative data from two distinct surveys that track motivations and engagement behaviors related to science education among monastic students. The first survey was administered at one monastic university in 2018, and the second follow-up survey was completed by students at two monastic universities in 2019. These surveys assessed the reception of science education related to motivations among monastics and their demonstration of engagement-with-science behaviors. We also tested for variation over time by surveying students in all years of the science curriculum. We identified that monastic students are motivated by their perception that studying science has an overall positive effect and benefits their Buddhist studies, rather than negatively affecting their personal or collective Buddhist goals. In accordance with this finding, monastics behave in ways that encourage fellow scholars to engage with science concepts. Survey responses were disaggregated by years of science study and indicated changes in motivation and engagement during the six-year science curriculum. These insights support the relevance of considering motivation and engagement in a novel educational setting and inform ongoing work to expand the inclusiveness of science education. Our findings provide direction for future avenues of enhancing exchange of knowledge and practice between Buddhism and science

Amphetamine-induced axon terminal injury modulates Pavlovian conditioning

Substituted amphetamines such as methamphetamine (METH) and 3,4-methylenedioxymethamphetamine (MDMA/Ecstasy) are currently major psychostimulants of abuse. Continuous use leads to addiction and can produce severe dopamine (DA) and serotonin (5-HT) neurotoxicity in humans. Clinical testing has revealed that METH and MDMA abusers consistently exhibit impairments in attention, decision-making, learning and memory. It is not clear whether this cognitive disturbance is a direct consequence of the neurotoxic potential of amphetamines or mere amphetamine exposure and the mechanisms by which this could occur are unknown. We generated mouse models of: (1) DA neurotoxicity induced by METH, (2) 5-HT neurotoxicity by fenfluramine (FEN) and (3) dual DA and 5-HT neurotoxicity by MDMA, all of which endured diminished levels of transporter densities and neurotransmitter and metabolite concentrations. These models of amphetamine-induced neurotoxicity were examined using Pavlovian conditioning paradigms that required incentive-based learning. Appetitive conditioning by drug reward was impaired by METH neurotoxicity, and enhanced by FEN neurotoxicity. Aversive conditioning by lithium chloride was impaired by MDMA neurotoxicity. Locomotor activity studies revealed that amphetamine-induced neurotoxicity did not disrupt normal sensitization to exposure to psychostimulants. The involvement of N-methyl-D-aspartate receptor (NMDAR) activation in the impairment of appetitive conditioning by METH neurotoxicity was tested. Pharmacological stimulation of NMDAR by D-cycloserine and N-acetylcysteine restored behavioral deficits after METH neurotoxicity. These data indicate that (a) amphetamines have the potential to injure DA and 5-HT axon terminals; (b) amphetamine-induced dopaminergic and serotonergic neurotoxicity exert opposing influences on appetitive conditioning by drug reward; and (c) amphetamine-induced neurotoxicity impairs Pavlovian conditioning via disruption of glutamate receptor activation. Furthermore, since enhancing NMDAR activity restored deficient appetitive conditioning, it is likely that cognitive impairments as a result of amphetamine-induced neurotoxicity may be amenable to pharmacological intervention

Methamphetamine and MDMA (ecstasy) neurotoxicity: 'of mice and men'

Methamphetamine (METH) and 3,4-meythylenedioxymethamphetamine (MDMA; 'ecstasy') are currently major drugs of abuse. One of the major concerns of amphetamines abuse is their potential neurotoxic effect on dopaminergic and serotonergic neurons. Although data from human studies are somewhat limited, compelling evidence suggests that these drugs cause neurotoxicity in rodents and primates. Recent studies in transgenic and knockout mice identified the role of dopamine transporters, nitric oxide, apoptotic proteins, and inflammatory cytokines in amphetamines neurotoxicity. Further research into the mechanisms underlying the dopaminergic and serotonergic neurotoxicity and the behavioral corollaries of these neuronal insults could facilitate our understanding of the consequences of human abuse of METH and MDMA on cognition, drug-seeking behavior, extinction and relapse

Neuromelanin, one of the most overlooked molecules in modern medicine, is not a spectator

The loss of pigmented neurons from the human brain has long been the hallmark of Parkinson's disease (PD). Neuromelanin (NM) in the pre-synaptic terminal of dopamine neurons is emerging as a primary player in the etiology of neurodegenerative disorders including PD. This mini-review discusses the interactions between neuromelanin and different molecules in the synaptic terminal and describes how these interactions might affect neurodegenerative disorders including PD. Neuromelanin can reversibly bind and interact with amine containing neurotoxins, e.g., MPTP, to augment their actions in the terminal, eventually leading to the instability and degeneration of melanin-containing neurons due to oxidative stress and mitochondrial dysfunction. In particular, neuromelanin appears to confer susceptibility to chemical toxicity by providing a large sink of iron-bound, heme-like structures in a pi-conjugated system, a system seemingly purposed to allow for stabilizing interactions including pi-stacking as well as ligand binding to iron. Given the progressive accumulation of NM with age corresponding with an apparent decrease in dopamine synthetic pathways, the immediate question of whether NM is also capable of binding dopamine, the primary functional monoamine utilized in this cell, should be raised. Despite the rather glaring implications of this finding, this idea appears not to have been adequately addressed. As such, we postulate on potential mechanisms by which dopamine might dissociate from neuromelanin and the implications of such a reversible relationship. Intriguingly, if neuromelanin is able to sequester and release dopamine in membrane bound vesicles, this intracellular pre-synaptic mechanism could be the basis for a form of chemical memory in dopamine neurons

#46 - Anti-Inflammatory Agents Modulate Phagocytic Activity of Alpha-Synuclein Stimulated Microglial Cells

Parkinson’s disease (PD) is a neurodegenerative disorder characterized by tremors, spasms, involuntary movements and the loss of dopaminergic neurons. The degeneration of dopamine neurons during PD is concurrent with the release of pro-inflammatory cytokines that cause inflammation in the brain. This can reduce the neuroprotective effects of the microglia, by inhibiting their phagocytic response. With this in mind, we investigated the ability of nicotine and ibuprofen (a non-steroidal anti-inflammatory drug) to stimulate the release of anti-inflammatory cytokines and stabilize the phagocytic activity of microglia in an inflamed environment. Nicotine has long been thought to be a carcinogen found in tobacco cigarettes and more recently E-cigarettes. Although public consensus shows a negative reception, recent in vivo and in vitro studies have supported the use of low doses of nicotine as a potentially anti-inflammatory compound. Epidemiological studies suggest that smokers tend to have a lower incidence of PD. BV-2 microglial cells were first treated with nicotine or ibuprofen at concentrations 1 µM, 10 µM and 100 µM. Following a 24-hour incubation period, cells were then treated with an α-synuclein peptide and left to incubate for another 24 hours. Phagocytic activity was measured using fluorescently-tagged E. coli particles and quantified using ImageJ. Our experiments found that specific doses of nicotine and ibuprofen stabilized phagocytic activity in microglia incubated in neurotoxic environments induced by α-synuclein. These data support the utility of anti-inflammatory compounds in the regulation of phagocytosis in microglia and their potential as a mechanism for therapeutic treatments of PD

Differential effects of amphetamines-induced neurotoxicity on appetitive and aversive Pavlovian conditioning in mice

The abuse of substituted amphetamines such as methamphetamine (METH) and 3,4-methylenedioxymethamphetamine (MDMA/Ecstasy) can result in neurotoxicity, manifested as the depletion of dopamine (DA) and 5-hydroxytriptamine (5-HT; serotonin) axon terminal markers in humans and animal models. Human METH and MDMA users exhibit impairments in memory and executive functions, which may be a direct consequence of the neurotoxic potential of amphetamines. The objective of this study was to investigate the influence of amphetamines-induced neurotoxicity on Pavlovian learning. Using mouse models of selective DA neurotoxicity (METH; 5 mg/kg x 3), selective 5-HT neurotoxicity (fenfluramine /FEN; 25 mg/kg x 4) and dual DA and 5-HT neurotoxicity (MDMA; 15 mg/kg x 4), appetitive and aversive conditioning were investigated. Dopaminergic neurotoxicity significantly impaired METH and cocaine conditioned place preference (CPP), but had no effect on LiCl-induced conditioned place aversion (CPA). In contrast, serotonergic neurotoxicity significantly enhanced CPP, and had no effect on CPA. Dual dopaminergic/serotonergic neurotoxicity had no apparent effect on CPP; however, CPA was significantly attenuated. Postmortem analysis revealed that significantly diminished levels of DA and 5-HT markers persisted in the striatum, frontal cortex, hippocampus, and amygdala. These findings suggest that amphetamines-induced dopaminergic and serotonergic neurotoxicity exert opposing influences on the affective state produced by subsequent drug reward, while dual dopaminergic/serotonergic neurotoxicity impairs associative learning of aversive conditioning. Furthermore, results revealed that amphetamines-induced DA and 5-HT neurotoxicity modulates appetitive Pavlovian conditioning similar to other DA and 5-HT neurotoxins. Modulation of Pavlovian conditioning by amphetamines-induced neurotoxicity may be relevant to compulsive drug-seeking behavior in METH and MDMA abusers