@article {1679, title = {The marmoset monkey as a model for visual neuroscience.}, journal = {Neurosci Res}, volume = {93}, year = {2015}, month = {2015 Apr}, pages = {20-46}, abstract = {

The common marmoset (Callithrix jacchus) has been valuable as a primate model in biomedical research. Interest in this species has grown recently, in part due to the successful demonstration of transgenic marmosets. Here we examine the prospects of the marmoset model for visual neuroscience research, adopting a comparative framework to place the marmoset within a broader evolutionary context. The marmoset{\textquoteright}s small brain bears most of the organizational features of other primates, and its smooth surface offers practical advantages over the macaque for areal mapping, laminar electrode penetration, and two-photon and optical imaging. Behaviorally, marmosets are more limited at performing regimented psychophysical tasks, but do readily accept the head restraint that is necessary for accurate eye tracking and neurophysiology, and can perform simple discriminations. Their natural gaze behavior closely resembles that of other primates, with a tendency to focus on objects of social interest including faces. Their immaturity at birth and routine twinning also makes them ideal for the study of postnatal visual development. These experimental factors, together with the theoretical advantages inherent in comparing anatomy, physiology, and behavior across related species, make the marmoset an excellent model for visual neuroscience.

}, keywords = {Animals, Biological Evolution, Brain, Callithrix, Color Perception, Color Vision, Exploratory Behavior, Macaca, Models, Animal, Social Behavior, Vision, Binocular, Vision, Ocular, Visual Perception}, issn = {1872-8111}, doi = {10.1016/j.neures.2015.01.008}, author = {Mitchell, Jude F and Leopold, David A} } @article {142, title = {Selection, gene interaction, and flexible gene networks.}, journal = {Cold Spring Harb Symp Quant Biol}, volume = {74}, year = {2009}, month = {2009}, pages = {131-8}, abstract = {

Recent results from a variety of different kinds of experiments, mainly using behavior as an assay, and ranging from laboratory selection experiments to gene interaction studies, show that a much wider range of genes can affect phenotype than those identified as "core genes" in classical mutant screens. Moreover, very pleiotropic genes can produce specific phenotypes when mild variants are combined. These studies also show that gene networks readily change configuration and the relationships between interacting genes in response to the introduction of additional genetic variants, suggesting that the networks range widely and have a high degree of flexibility and malleability. Such flexibility, in turn, offers a plausible mechanism for the molding of phenotypes through microevolution, as a prerequisite to making a suitable environment for the acceptance of newly arising large-effect mutations in the transition from microevolution to macroevolution.

}, keywords = {Animals, Biological Evolution, Drosophila melanogaster, Epistasis, Genetic, Escherichia coli, Female, Gene Regulatory Networks, Genes, Insect, Genetic Association Studies, Male, Models, Genetic, Mutation, Selection, Genetic}, issn = {1943-4456}, doi = {10.1101/sqb.2009.74.029}, author = {Greenspan, R J} } @article {144, title = {Serotonin and neuropeptide F have opposite modulatory effects on fly aggression.}, journal = {Nat Genet}, volume = {39}, year = {2007}, month = {2007 May}, pages = {678-82}, abstract = {

Both serotonin (5-HT) and neuropeptide Y have been shown to affect a variety of mammalian behaviors, including aggression. Here we show in Drosophila melanogaster that both 5-HT and neuropeptide F, the invertebrate homolog of neuropeptide Y, modulate aggression. We show that drug-induced increases of 5-HT in the fly brain increase aggression. Elevating 5-HT genetically in the serotonergic circuits recapitulates these pharmacological effects, whereas genetic silencing of these circuits makes the flies behaviorally unresponsive to the drug-induced increase of 5-HT but leaves them capable of aggression. Genetic silencing of the neuropeptide F (npf) circuit also increases fly aggression, demonstrating an opposite modulation to 5-HT. Moreover, this neuropeptide F effect seems to be independent of 5-HT. The implication of these two modulatory systems in fly and mouse aggression suggest a marked degree of conservation and a deep molecular root for this behavior.

}, keywords = {Aggression, Analysis of Variance, Animals, Behavior, Animal, Biological Evolution, Brain, Drosophila melanogaster, Drosophila Proteins, Gene Silencing, Neuropeptides, Reverse Transcriptase Polymerase Chain Reaction, Serotonin}, issn = {1061-4036}, doi = {10.1038/ng2029}, author = {Dierick, Herman A and Greenspan, Ralph J} }