<p> Basal forebrain corticopetal cholinergic neurons are critical for contextual and cued fear memory in the conditioned suppression paradigm, but neural mechanisms that alter these neurons in fear memory remain unknown. Interestingly, basal forebrain cholinergic lesions have no effect on behavioral performance in commonly-studied fear conditioning paradigms like Pavlovian conditioned freezing or fear-potentiated startle, yet impair fear memory in the conditioned suppression paradigm. Many studies conducted have experimented with lesions of cell bodies of corticopetal cholinergic neurons in the nucleus basalis magnocellularis (NBM), but there is a void in the literature defining which specific projections may be responsible for their discrepant role in different fear memory paradigms. The basal forebrain projects to the anterior cingulate cortex (ACC), a subregion of the medial prefrontal cortex. The ACC is a well-established portion of the fear circuit across all fear conditioning paradigms and has a clear role in decision-making in the conditioned suppression paradigm. Given the role in choice conflict that the ACC plays in operant tasks involved in the conditioned suppression paradigm, it is plausible that it may be a region that allows basal forebrain cholinergic neurons to alter a fear memory in the conditioned suppression paradigm. The goal of this study is to examine the specific roles that basal forebrain cholinergic projections to the ACC play in fear memory, specifically in the conditioned suppression paradigm. These lesions may target specific cholinergic input to the ACC from the NBM in the basal forebrain and this may isolate a specific fear circuit involved in fear memory in the conditioned suppression paradigm. Data have suggested that ACC lesioned animals demonstrate less fear-conditioned suppression over sham animals, but further experiments and cohorts of animals are required. If ACC cholinergic lesions are shown to produce deficits in fear memory in the conditioned suppression paradigm, it may suggest that the presence of the appetitive task, which only occurs in the conditioned suppression paradigm and not in any of the other commonly studied fear paradigms, may be able to elicit changes in functional connectivity to incorporate this projection from the NBM to the ACC to the fear circuit. Discrepancies in fear memory between fear conditioning paradigms demand to be addressed because assumptions about functional connectivity across different paradigms are assumed to be similar in the literature. If the notion of paradigmdependent functional connectivity presented here is true, deductions about this functional connectivity may only be made in the context of one fear paradigm and may not necessarily be applicable across paradigms. In other words, to say that Pavlovian fear conditioning and fear-potentiated startle are indicative of the broad neurobiology of fear memory would only be looking at a fraction of the reality behind how fear circuitry operates. In order to further the literature to propose holistic circuits, molecular processes and constructs that apply to all fear memory regardless of protocol or paradigm, it is necessary to investigate neural involvement across alternative fear paradigms, like conditioned suppression. This study supports the novel idea that neural circuitry that supports fear can expand with new learning tasks or events and therefore, may be more susceptible to change than previously considered, but future studies are required</p><p>

<p> When someone hears regular, periodic sounds, such as drum beats, footsteps, or stressed syllables in speech, these individual stimuli tend to be grouped into a perceived rhythm. One of the hallmarks of rhythm perception is that the listener generates expectations for the timing of upcoming stimuli, which theorists have described as endogenous periodic modulations of attention around the time of anticipated sounds. By constructing an internal representation of a rhythm, perceptual processes can be augmented by proactively deploying attention at the expected moment of an upcoming stressed syllable, the next step in an observed stride, or during the stroke of a co-speech hand gesture. A hypothetical benefit of this anticipatory allocation of attention is that it might facilitate temporal integration across the senses, binding multisensory aspects of our experiences into a unified &ldquo;now,&rdquo; anchored by temporally-precise auditory expectations. The current dissertation examines this hypothesis, exploring the effects of auditory singletons, and auditory rhythms, on electrophysiological indices of perception and attention to a visual stimulus, using the flash-lag paradigm. An electroencephalography study was conducted, where sounds, either isolated or presented rhythmically, occurred in alignment with a task-relevant visual flash. Results suggest a novel dissociation between the multisensory effects of discrete and rhythmic sounds on visual event perception, as assessed by the N1 component of the event-related potential, and by oscillatory power in the beta (15&ndash;20 Hz) frequency range. This dissociation is discussed in the context of classic and contemporary research on rhythm perception, temporal orienting, and temporal binding across the senses, and contributes to a more refined understanding of rhythmically-deployed attention. </p><p>

The influence of trauma on neuroendocrine functions and related problems with declarative memory (short term verbal memory) has been documented in several studies focused on adult survivors of trauma. However, the impact of trauma on neuroendocrine and cognitive development of children and adolescents has not yet been explored. Declarative memory functioning, cortisol reactivity and psychological symptoms were examined in nineteen adolescent female survivors (nine depressed and ten non-depressed) of emotional, physical, and sexual abuse and compared to eleven non-abused controls. Salivary cortisol measurements (initial baseline assessment, assessment after an emotionally challenging task, followed by second baseline one week later) were used to assess cortisol reactivity. The relationship between patterns of cortisol reactivity and declarative memory functioning was examined, as assessed by scores on selected subtests of the California Verbal Learning Tests. Similarly, the relationship between patterns of cortisol reactivity and psychological symptoms, as reported on the Trauma Symptom Checklist for Children, was also assessed. Results indicated the presence of different patterns of cortisol reactivity during a challenging task for the girt survivors of chronic trauma (depressed and non-depressed) as compared to controls. The abused girls most frequently exhibited increased cortisol release from the initial baseline to the subsequent measurement times, whereas cortisol levels generally decreased in the control group. Furthermore, in girl survivors of chronic trauma, the larger increases in cortisol release were related to lower declarative memory scores and to more symptoms of dissociation, depression, posttraumatic stress, anger, and anxiety. Although the subject sample was small, the results supported the existence of a link between exposure to trauma, adrenocortical reactivity, and to a lesser extent, declarative memory functioning. Similar results have been widely documented in adults with Post Traumatic Stress Disorder. These findings have implications in terms of understanding of neurobiological development of trauma survivors. Indeed, neurohormonal alterations (changes in cortisol reactivity) influence response to stress, emotional regulation, and behavioral adjustment. Therefore, understanding of the relationship of cortisol reactivity with cognitive and emotional symptoms in young trauma survivors will enhance the identification of at-risk individuals and will help in preventing the development of long lasting deficits in emotional and behavioral functioning.

In addition to physiological functions, the neuropeptide hormone, arginine vasopressin (AVP) facilitates the mammalian central nervous system (CNS) regulation of cognitive function and social behaviors. V 1A receptors mediate these effects. Although distribution patterns of AVP-producing neurons and fibers are similar among mammals, CNS V1A receptor patterns are species-specific. Here, rhesus (Macaca mulatta) central V1A receptors were mapped using receptor autoradiography techniques. By incubating 20 μm tissue sections with 125I-lin-AVP (125I-Phenylacetyl-D-Tyr(Me)-Phe-Gln-Asn-Arg-Pro-Arg-Tyr-NH 2 linear vasopressin V1A receptor antagonist) AVP binding sites were detected. A V1A agonist ([d(Ch2)5[Tyr(Me)]AVP) displaced the 125I-lin-AVP tracer in all sites, providing support for verification of the sites as V1A receptors. V1A receptors were localized within pyriform, entorhinal, cingulate and insular cortices, the presubiculum, bed nucleus of the stria terminalis (BNST), lateral septum (LS), mammillary bodies and within several structures of the amygdala, hypothalamus, hippocampus, thalamus and brain stem. The rhesus V1A receptor map is relevant to recent research in human learning, memory and emotion. Particularly pertinent are those receptors found in the amygdala, mammillary bodies, medial temporal lobe structures, and cingulate cortex. Comparison of this rhesus V1A receptor map to those previously reported for nonprimates revealed that all had V1A receptors in the BNST, central amygdala, diagonal band of Broca, LS, and solitary tract. Marmosets shared similar binding patterns in the BNST, but densities differed in SCN, LS, and various amygdala and hypothalamus regions. In presubiculum, supraoptic nucleus, cortical regions, and mammillary bodies, areas dense with V1A receptors in rhesus, marmosets revealed none. Such differences may reflect species-specific memory capabilities.

Both coping behaviors and physiological vulnerability to stress have been found to be associated with the development of psychopathology; however, less is known about the interrelations between coping and physiological stress responses. This study explored relations between late adolescents' styles of coping with distress and their physiological reactivity and recovery to negotiating conflict with their romantic partners. Partners' coping styles and the interaction between partners' coping styles were also examined as predictors of stress responses. One hundred and ninety couples were asked to discuss and attempt to resolve a conflictual issue that they had disagreed about in the previous month. Physiological reactivity was assessed using samples of salivary cortisol, a primary hormonal product of one of the major stress response systems. A salivary cortisol sample at entry, a pre-task anticipatory sample, and 5 post-task samples were collected. Growth modeling of the cortisol data indicated that dyadic coping was a better predictor of cortisol reactivity and recovery during relationship conflict than individual coping behaviors alone. In addition, relations among coping and physiological stress responses were found to be significantly different for males and females.

Irritable Bowel Syndrome (IBS) is a disorder characterized by abdominal pain and altered bowel habits (diarrhea and/or constipation) occurring in the absence of abnormalities on both physical and laboratory investigations. This study examined the effects of respiration biofeedback to decrease abdominal pain, anxiety levels, and medication intake in participants with IBS, using a multiple-baseline design across 10 participants. The STAI-Trait Anxiety Inventory, and the Nijmegen Questionnaire for Hyperventilation were administered at baseline and follow-up to determine decreases in anxiety and hyperventilation. It was hypothesized that respiration biofeedback training would produce significant decreases in pain, anxiety, and medication intake during treatment, as well as decreases in the State-Trait and Nijmegen Questionnaire scores at follow-up. Decreases in pain levels were obtained in 70% of the participants, and 30% of the participants showed decreases in anxiety levels. Four of the 5 participants (80%) who recorded medication intake showed decreases in medication. Findings are interpreted and future research is suggested.

<p> This dissertation aims to address a gap in the literature regarding the effect of the achievement-focused student identity on prosocial values and behaviors, specifically among students who predominantly value prosociality. Largely, research on identity and motivation addresses academic outcomes and psychological well-being outcomes (Settles, Sellers, &amp; Damas, 2002; Jaret &amp; Reitzes, 2009) while more recent literature that has addressed prosocial motives (Yeager, et al., 2015) has solely assessed academic performance outcomes. Drawing upon values literature (Schwartz, 1992) it can be inferred that the achievement-focused student identity may inhibit or decrease prosocial values and behaviors. Further, this may be particularly deleterious for the psychological well-being of students who hold prosociality as a central guiding feature of their self-concept. First, I examine whether certain social identities tend to have a higher tendency towards prosociality (Study 1). Second, I assess how a salient achievement-focused identity affects student behaviors (with particular attention to more prosocially inclined students) during a stressful academic situation (Study 2a &amp; 2b). Next, I devise a novel measure to assess the centrality of prosociality to the self and perceptions of conflict between prosocial values and achievement-focused settings (Study 3). Then, I assess how a salient achievement-focused identity impacts prosocial values and behaviors, and offer a new "integrated" approach to the student identity. Last, I assess how this expanded and "integrated" identity influences students' academic perceptions and psychological well-being, specifically for those students who are more prosocially inclined (e.g., women and lower income) as well as for those who perceive higher levels of prosocial-achievement conflict (Study 4).</p>

<p> The study investigated the indicators of acculturative stress among immigrants, and the stereotypes associated with immigrants as portrayed by American movies. The purposive sample (N=10) consisted of movies about immigrants produced in America between 2002 and 2017. Thus, drawing from the findings of previous studies on acculturation, the researcher developed a set of acculturative stress indicators (Socialization, Religion, Nutrition, Education, Language, and Citizenship). Also, the immigrant protagonist's race/ethnicity was a key factor that was considered because it is one of the primary basis for their identification in the movies. The ethnicity identified from the movies spread across 8 countries, which were classified into three ethnic categories: Asian, White, and Hispanic or Latino. Based on the results and findings of the study, the movies were found to portray more Socialization Stress Indicators and very little Religion Stress Indicators. There was a significant difference in the portrayal of the Language Stress Indicator between immigrant lead characters from Hispanic or Latino ethnicity and other ethnicities. The implications of movie based stereotypes about immigrants were discussed with regards to accurate and culturally appropriate portrayals. Therefore, the study highlights the need for extensive evidence-based research on the portrayal of immigrants in the movies, especially due to the high level of media consumption in recent times.</p><p>

<p> Recent research has associated obesity with cognitive impairments and alterations in brain-derived neurotrophic factor (BDNF), with the majority of studies examining this in older adult or aging animals. To expand upon these efforts, two experiments were performed to examine the effects of diet-induced obesity (DIO) on spatial performance and hippocampal BDNF expression in young adult female and male rats. To expand upon these efforts, we examined these effects over dietary interventions of differing durations. To investigate these issues rats (female rats in Experiment 1 and male rats in Experiment 2) were assigned to either a standard chow condition or a DIO condition and remained on these diets for 4-, 8- or 12-weeks. Compared to their chow-fed counterparts, female DIO rats consumed significantly more average weekly calories, weighed significantly more, and exhibited significant alterations in glucose metabolism. However, these obesity-related physiological changes were not associated with concurrent impairments in spatial ability as measured using the Morris water maze, and only the 4-week DIO dietary intervention demonstrated a difference in hippocampal BDNF mRNA expression. Compared to their chow-fed counterparts, male DIO rats consumed significantly more average weekly calories than their chow-fed counterparts, weighed significantly more, and exhibited significant alterations in glucose metabolism. However, obesity-related physiological alterations were not associated with concurrent impairments in spatial ability or differences in BDNF mRNA expression, with the exception of the 12-week DIO animals performing significantly better than their chow-fed counterparts during the reversal probe trial on the final day of training. These findings were unexpected and will be discussed further later in the thesis. </p><p>

Psychological and physiological effects of nitrous oxide resemble those of eight other drug categories. Lipid solubility or hydrate microcrystal theories correlate behavioral measures with measurable parameters of the molecule N20. N20, a spindle poison, halts mitosis in metaphase, producing widespread physiological consequences. N20 affects the microtubules of the spindle in a number of specific ways. Microtubules are utilized in other parts of eukaryotic cells, in a wide variety of functions. In neurons, microtubules build and maintain dendritic sensory processes. Since microtubules are built of two dissimilar proteins, constantly assemble and disassemble, and maintain a more negative interior potential, they would be responsive to changes in summed post-synaptic dendritic potential. Microtubules respond to N20 with a loss of communication between subcellular components, and between cells. Chromosomes, proteins, and ATP are no longer transported efficiently. Such fundamental changes might explain nitrous oxide's effects in "potentiating" other drugs, and upon perception and memory.