9th Annual Meeting of the Front Range Neuroscience Group

Cognition and Behavior 1) The disruptive effect of instrumental non-contingency on executive functioning. T Gupta, R Toll. From the Department of Psychology and Neuroscience, University of Colorado at Boulder, Boulder, CO Previous research has suggested that an inability to learn how to control one’s environment (instrumental non-contingency) has negative effects on cognitive abilities, as demonstrated by impaired performance on subsequent cognitively demanding tasks. However, the nature of such cognitive impairment is poorly specified. The current study tested to the hypothesis that instrumental non-contingency leads specifically to disruption in cognitive control functioning. The sample consisted of undergraduate students (n=108) recruited from general psychology courses and randomly assigned to one of three groups: control, instrumental contingency (IC), or instrumental noncontingency (IN). Participants completed the color-word Stroop, a classic test of cognitive control, at baseline. Next, participants completed an instrumental learning task in which they either were able to learn how to control a noise stress (IC), were unable to learn how to control a noise stress (IN), or were not exposed to stress or instrumental learning demands (control). Finally, participants completed the color-word Stroop a second time. Results indicated that while the IC group showed practice-related improvements in Stroop performance, the IN group failed to show such improvements. These findings suggest that being unable to learn how to control one’s environment causes disruption to executive functioning. These results provide support for behavioral therapies that encourage instrumental learning as a strategy for protecting the individual from the negative effects of stress, and suggest that such strategies specifically protect cognitive control abilities. 2) Increased anxiety-like behavior in fibroblast growth factor 8-deficient mice. LR Brooks, CL Enix, SC Rich, CA Lowry, PS Tsai. From the Department of Integrative Physiology and Center for Neuroscience, University of Colorado, Boulder, CO. Serotonergic systems modulate mood-, stressand anxiety-related behaviors. Serotonergic (5-HT) neurons in the dorsal raphe nucleus (DRN) comprise multiple subpopulations with distinct anatomical locations, afferent inputs and efferent targets. Prior research has shown that 5-HT neurons are highly dependent on fibroblast growth factor (FGF) signaling for their prenatal development. Developmental deficiency in FGF signaling results in a significant loss of 5-HT neurons around the time of birth. However, it is unclear if specific populations of 5-HT neurons are impacted under FGF signaling deficiency, and whether these changes result in altered anxiety-like behavior in adulthood. To answer these questions, wild-type (WT) and Fgf8 heterozygous hypomorphic (Fgf8+/-) mice, which have roughly a 25% reduction of Fgf8 mRNA, were tested in the elevated plus-maze (EPM) for anxiety-like behavior. Further, we tested if their behavior is accompanied by an alteration in the organization of 5-HT neurons in the DRN. Adult male WT and Fgf8+/mice were placed on the EPM for 5 minutes and scored for the following parameters: time spent in the open, closed and center areas, and total number and percent entries into each arm. Fgf8+/mice spent significantly less time in and initiated fewer entries into the open unprotected arm than WT controls. There were no differences between genotypes in overall explorative activities as determined by the sum of all entries into either arm. This increased avoidance of the aversive properties of height and openness suggests that Fgf8+/hypomorphic male mice have increased anxiety-like behavior. Immunohistochemical staining of the serotonergic marker, tryptophan hydroxylase 2, revealed subtle changes in the organization of serotonergic neurons throughout the DRN, suggesting a neuroanatomical basis for the altered behavior. Overall, this study links alterations in developmental events to anxietylike behaviors, which suggests that disruptions of FGF signaling may be a factor to consider in the neurodevelopmental origins of anxiety and affective disorders.Sources of Support: NIH R01 HD042634; R01 MH086539 3) BXD recombinant inbred mice with low brain iron exhibit a reduced dopaminergicmediated synaptic transmission in the CA1 region of the hippocampus AB Breton, JA Fox, MP Brownson, M.D. McEchron. From the WWAMI Department, University of Wyoming, Laramie, WY. Iron deficiency (ID) is the most prevalent nutritional disorder in the world. Studies have shown that developmental ID is linked to learning impairments in humans. The BXD recombinant inbred mouse strains have been shown to have varying but consistent levels of brain iron. This could provide a useful genetic mouse model for examining the effects of ID on brain function, independent of nutritional intake. The BXD mouse strains are formed by litter mating of the inbred strains, C57BL/6J and DBA/2J. There are 28 known BXD recombinant inbred strains. The BXD 13 strain contains higher levels of brain iron when compared with the BXD 6 strain. Work has shown that the BXD 6 strain exhibits reduced levels of hippocampus-dependent learning compared to the BXD 13 strain. The present study used electrophysiological brain slice methods to examine dopaminergic-mediated synaptic efficacy in the hippocampus of BXD 13 and BXD 6 mice. Our previous work demonstrates that perinatal nutritional ID produces irreversible impairments in dopaminergic-dependent synaptic transmission in the hippocampus. Catecholamines such as norepinephrine and dopamine are known to play a pivotal role in memory consolidation. Studies have shown that catecholamine agonists produce a long lasting potentiation in synaptic transmission. Mice were maintained on a normal iron diet (90 ppm iron) through pregnancy and postnatal development. Hippocampal brain slices were prepared between postnatal day 26 and 30, and synaptic efficacy was measured in the CA1 region of the hippocampus by examining population spike amplitude. Slices were treated with the dopaminergic agonist SKF-38393 to induce modulatory increases in synaptic efficacy. Slices obtained from the high brain iron BXD 13 mice (n=10) exhibited a long-lasting increase in synaptic efficacy as the result of SKF-38393 perfusion. The low brain iron BXD 6 slices (n=10) showed little or no increase in synaptic efficacy as a result of SKF-38393 perfusion. These results demonstrate that genetic mediation of low brain iron may impair or reduce dopaminergicdependent synaptic plasticity in the hippocampus.