Interactive Methods for Teaching Action Potentials, an Example of Teaching Innovation from Neuroscience Postdoctoral Fellows in the Fellowships in Research and Science Teaching (FIRST) Program

Acquiring a faculty position in academia is extremely competitive and now typically requires more than just solid research skills and knowledge of one’s field. Recruiting institutions currently desire new faculty that can teach effectively, but few postdoctoral positions provide any training in teaching methods. Fellowships in Research and Science Teaching (FIRST) is a successful postdoctoral training program funded by the National Institutes of Health (NIH) providing training in both research and teaching methodology. The FIRST program provides fellows with outstanding interdisciplinary biomedical research training in fields such as neuroscience. The postdoctoral research experience is integrated with a teaching program which includes a How to Teach course, instruction in classroom technology and course development and mentored teaching. During their mentored teaching experiences, fellows are encouraged to explore innovative teaching methodologies and to perform science teaching research to improve classroom learning. FIRST fellows teaching neuroscience to undergraduates have observed that many of these students have difficulty with the topic of neuroscience. Therefore, we investigated the effects of interactive teaching methods for this topic. We tested two interactive teaching methodologies to determine if they would improve learning and retention of this information when compared with standard lectures. The interactive methods for teaching action potentials increased understanding and retention. Therefore, FIRST provides excellent teaching training, partly by enhancing the ability of fellows to integrate innovative teaching methods into their instruction. This training in turn provides fellows that matriculate from this program more of the characteristics that hiring institutions desire in their new faculty

Role of ghrelin in food reward: impact of ghrelin on sucrose self-administration and mesolimbic dopamine and acetylcholine receptor gene expression

The decision to eat is strongly influenced by non-homeostatic factors such as food palatability. Indeed, the rewarding and motivational value of food can override homeostatic signals, leading to increased consumption and hence, obesity. Ghrelin, a gut-derived orexigenic hormone, has a prominent role in homeostatic feeding. Recently, however, it has emerged as a potent modulator of the mesolimbic dopaminergic reward pathway, suggesting a role for ghrelin in food reward. Here, we sought to determine whether ghrelin and its receptors are important for reinforcing motivation for natural sugar reward by examining the role of ghrelin receptor (GHS-R1A) stimulation and blockade for sucrose progressive ratio operant conditioning, a procedure used to measure motivational drive to obtain a reward. Peripherally and centrally administered ghrelin significantly increased operant responding and therefore, incentive motivation for sucrose. Utilizing the GHS-R1A antagonist JMV2959, we demonstrated that blockade of GHS-R1A signaling significantly decreased operant responding for sucrose. We further investigated ghrelin's effects on key mesolimbic reward nodes, the ventral tegmental area (VTA) and nucleus accumbens (NAcc), by evaluating the effects of chronic central ghrelin treatment on the expression of genes encoding major reward neurotransmitter receptors, namely dopamine and acetylcholine. Ghrelin treatment was associated with an increased dopamine receptor D5 and acetylcholine receptor nAChRβ2 gene expression in the VTA and decreased expression of D1, D3, D5 and nAChRα3 in the NAcc. Our data indicate that ghrelin plays an important role in motivation and reinforcement for sucrose and impacts on the expression of dopamine and acetylcholine encoding genes in the mesolimbic reward circuitry. These findings suggest that ghrelin antagonists have therapeutic potential for the treatment of obesity and to suppress the overconsumption of sweet food

The Ghrelin Signalling System Is Involved in the Consumption of Sweets

The gastric-derived orexigenic peptide ghrelin affects brain circuits involved in energy balance as well as in reward. Indeed, ghrelin activates an important reward circuit involved in natural- as well as drug-induced reward, the cholinergic-dopaminergic reward link. It has been hypothesized that there is a common reward mechanism for alcohol and sweet substances in both animals and humans. Alcohol dependent individuals have higher craving for sweets than do healthy controls and the hedonic response to sweet taste may, at least in part, depend on genetic factors. Rat selectively bred for high sucrose intake have higher alcohol consumption than non-sucrose preferring rats and vice versa. In the present study a group of alcohol-consuming individuals selected from a population cohort was investigated for genetic variants of the ghrelin signalling system in relation to both their alcohol and sucrose consumption. Moreover, the effects of GHS-R1A antagonism on voluntary sucrose- intake and operant self-administration, as well as saccharin intake were investigated in preclinical studies using rodents. The effects of peripheral grelin administration on sucrose intake were also examined. Here we found associations with the ghrelin gene haplotypes and increased sucrose consumption, and a trend for the same association was seen in the high alcohol consumers. The preclinical data show that a GHS-R1A antagonist reduces the intake and self-administration of sucrose in rats as well as saccharin intake in mice. Further, ghrelin increases the intake of sucrose in rats. Collectively, our data provide a clear indication that the GHS-R1A antagonists reduces and ghrelin increases the intake of rewarding substances and hence, the central ghrelin signalling system provides a novel target for the development of drug strategies to treat addictive behaviours