Biology Theses and Dissertations
Permanent URI for this collectionhttp://hdl.handle.net/1903/2749
Browse
3 results
Search Results
Item Neuroendocrine mechanisms underlying paternal experience-induced plasticity of the hippocampus(2016) Hyer, Molly Melissa; Glasper, Erica R; Neuroscience and Cognitive Science; Digital Repository at the University of Maryland; University of Maryland (College Park, Md.)Evidence suggests that males, like females, undergo altered structure and function of the hippocampus postpartum, a brain region that regulates certain aspects of emotion, learning, and memory. These behaviors are beneficial for successful parenting. In maternal rodents, offspring contact contributes to postpartum hippocampal plasticity in both mothers and offspring. Fathers do not undergo pregnancy, parturition, or lactation, therefore, the impact of offspring on hippocampal plasticity is less clear. California mouse (Peromyscus californicus) fathers are highly paternal, making this monogamous species a good model of paternal care. In this species, between postnatal days 15 and 21 paternal behavior becomes more active (i.e. increased pup retrievals) to care for pups that are beginning to explore outside of the nest. I observed reduced anxiety-like behavior in fathers specifically within this temporal window. Concomitant with attenuated anxiety-like behavior, I found that fathers maintain survival of adult born neurons in the dentate gyrus of the hippocampus. Enhanced hippocampal plasticity is not restricted to adult neurogenesis, as dendritic spine density in the dentate gyrus is increased in fathers at this same time – an effect that lasts until weaning. When permanently separated from their offspring, fathers show increased passive stress coping and reduced spine density in the DG. Taken together, these data suggest that the degree of active father-offspring interaction significantly alters hippocampal plasticity in the father. Estradiol and its receptors have been implicated in alterations to anxiety and adult neurogenesis in both males and females. I observed that estrogen receptor β (Erβ) mRNA expression was elevated in whole hippocampal homogenates at PND 16 in fathers. Similarly, circulating estradiol was elevated at both PND 2 and PND 16. After inhibition of Erβ with the drug tamoxifen, the number of surviving adult born neurons was suppressed in fathers alone. Taken together, these data suggest that in fathers, hippocampal plasticity occurs concomitantly with active father-offspring contact and that this plasticity, at least structural, is driven by activation of Erβ. Understanding paternal experience-induced plasticity and the mechanisms that drive it, may help to prevent deficits in paternal behavior that can disrupt offspring development and contribute to emotional dysregulation in fathers.Item The effect of mental stress on brain dynamics and performance related to attention control during a vigilance task: An electroencephalographic investigation(2013) Russell, Bartlett Anne Healy; Hatfield, Bradley D; Neuroscience and Cognitive Science; Digital Repository at the University of Maryland; University of Maryland (College Park, Md.)Anxiety can increase distractibility and undermine the quality of psychomotor performance. Models of attention processing postulate that anxiety consumes limited executive resources necessary for maintaining goal-oriented, "top-down" attention control and suppressing stimulus-driven "bottom-up" distraction. Attention Control Theory (ACT) predicts that anxiety adversely affects the efficiency, and particularly inhibitory components of executive, frontally mediated top-down attention control. We used two approaches for examining this model. First, though attention affects synchrony among neural structures, information regarding how human oscillatory patterns (measured with electroencephalography, EEG) change as state anxiety increases is limited. Second, while anxiety affects the balance between top-down and bottom-up mechanisms, to our knowledge no one has yet measured anxiety's effect on attention using a neural measure of top-down control in conjunction with more traditional bottom-up measures of attention capture (e.g., the P3 event related potential, or ERP). Purpose: Study 1 examines the oscillatory patterns (spectral dynamics) of the cortex in order to investigate whether frontal regions exhibit patterns of reduced efficiency and altered networking with posterior regions during threat of shock. In order to assess the relationship between top-down and bottom-up attention dynamics, Study 2 uses the same threat protocol to measure attention-directed top-down modulation of sensory signaling (steady-state visual evoked potential, or ssVEP modulation) and of bottom-up attention capture by discrete targets and distractors (Event Related Potentials, ERPs). Results: The spectral analyses in Study 1 suggest decreased processing efficiency and decreased frontal networking (coherence) with more posterior regions as anxiety increased. Reduced coherence, however, could indicate either increased or decreased top-down focus; Study 2 provides more insight. Neural responses to task-relevant targets (ERPs) diminished as threat increased, while responses to task-irrelevant distractors remained unchanged. Contrary to what ACT would predict, we observed an increase in attention modulation of an ssVEP frequency associated with amplifying the task-relevant signal and no change in an ssVEP associated with inhibiting task-irrelevant stimuli. These findings suggest top-down attention control increased under threat, but was not enough to prevent degraded processing of task-relevant targets coincident with reduced efficiency on task performance. Implications and suggestions for refining ACT are discussed.Item Developmental Alterations in Inhibitory Neurotransmission in the Fragile X Syndrome Mouse Basolateral Amygdala(2012) Kratovac, Sebila; Corbin, Joshua G; Biology; Digital Repository at the University of Maryland; University of Maryland (College Park, Md.)Fragile X Syndrome, caused by Fmr1 gene inactivation, is characterized by symptoms including enhanced fear, hyperactivity, social anxiety, and autism, pointing to synaptic and neural circuit defects in the amygdala. Previous studies in Fmr1 knockout (KO) mice have demonstrated alterations in GABAA receptor (GABAAR) function in the basolateral amygdala during early postnatal development. In this study, we sought to determine whether these early defects in GABAAR function are accompanied by changes in protein expression of GABAAR alpha 1, 2, and 3 subunits, the pre-synaptic GABA-synthesizing proteins GAD65 and 67 (GAD65/67), and the post-synaptic GABAAR-clustering protein gephyrin. We found that the developmental trajectory of protein expression is altered in knockout mice for all tested proteins except GABAAR alpha 3 and GAD 65/67. Our results suggest that alterations in the timing of inhibitory synapse protein expression in early postnatal development could contribute to observed inhibitory neurotransmission deficits in the KO mouse basolateral amygdala.