Parvalbumin (PV) and cholecystokinin (CCK) proteins are found in the basolateral amygdala nuclei, particularly in gamma-aminobutyric acid (GABA) interneurons. PV+ neurons were localized to the basolateral amygdala and they expressed the GABA neuron marker glutamic acid decarboxylase (GAD). Here, we used Cre recombinase mouse lines to induce expression of mutant muscarinic inhibitory (hM4D) and excitatory (hM3D) receptors on PV+ or CCK+ neurons. Activation of the mutant receptors with clozapine-n-oxide (CNO) was used to measure how amygdala neural changes affect the acoustic startle reflex (ASR). Excitation of amygdala PV+ neurons potentiated the ASR. Activation of basolateral amygdalar CCK+ neurons potentiated the ASR and caused seizures, possibly by activating glutamate CCK+ neurons. The CCK+ subset of GAD neurons were targeted with a new triple transgenic mouse line (Dlx5-flpe/CCK-Cre/FrePe) to show that most CCK+ neurons were GAD negative. These findings are compared with optogenetic approaches to target specific neuronal populations.

Parvalbumin (PV) and cholecystokinin (CCK) proteins are found in the basolateral amygdala nuclei, particularly in gamma-aminobutyric acid (GABA) interneurons. PV+ neurons were localized to the basolateral amygdala and they expressed the GABA neuron marker glutamic acid decarboxylase (GAD). Here, we used Cre recombinase mouse lines to induce expression of mutant muscarinic inhibitory (hM4D) and excitatory (hM3D) receptors on PV+ or CCK+ neurons. Activation of the mutant receptors with clozapine-n-oxide (CNO) was used to measure how amygdala neural changes affect the acoustic startle reflex (ASR). Excitation of amygdala PV+ neurons potentiated the ASR. Activation of basolateral amygdalar CCK+ neurons potentiated the ASR and caused seizures, possibly by activating glutamate CCK+ neurons. The CCK+ subset of GAD neurons were targeted with a new triple transgenic mouse line (Dlx5-flpe/CCK-Cre/FrePe) to show that most CCK+ neurons were GAD negative. These findings are compared with optogenetic approaches to target specific neuronal populations.

Lifespan theories of emotion suggest that the ability to regulate emotion improves with age. The supporting evidence, however, is indirect: older adults pay less attention to negative events, remember less negative information, and report fewer experiences of negative emotion. Few studies directly measure emotion regulation by explicitly instructing older adults to modulate their feelings while exposed to emotion-evoking stimuli. The purpose of this thesis was to directly compare younger and older adults in their ability to modulate feelings to investigate whether aging results in decline, stability, or improvement in emotion regulation and also to examine potential mechanisms underlying regulation skills. The study employed a startle modulation paradigm to measure both emotional reactivity and regulation. Two experimental tasks (Stroop colour-word interference, reversal learning) were also administered to explore the relationship between emotion regulation and two theoretically-relevant processes: (a) cognitive control and (b) modification of learned emotional associations. There were three main findings: (1) emotional reactivity was preserved in older adults. Both age groups showed emotion-modulated startle (negative > neutral) during the pre-regulation viewing period; (2) age-related decline in emotion regulation was evident on an objective measure of emotion regulation (startle eyeblink reflex) but not on a subjective measure (self-ratings). Specifically, for older adults, startle eyeblink was not enhanced or attenuated following increase and decrease instructions, respectively. In contrast, both groups showed similar modulation of valence and arousal ratings by regulation instruction (increase > look > decrease); (3) for older adults, reversal learning performance correlated positively with the degree of reappraisal-related startle attenuation in the decrease condition, suggesting a possible mechanism for impaired down-regulation. These findings suggest that even when emotional reactivity is similar, older adults are less effective at modulating their physiological responses.

Thesis (Ph.D.)--University of Western Australia, 2004.

Thesis (Ph. D.)--University of Wisconsin--Madison, 1973. / Typescript. Vita. eContent provider-neutral record in process. Description based on print version record. Includes bibliographical references.

Thesis (Ph.D) - University of Queensland, 2006. / Includes bibliography.

Startle modification is a robust phenomenon that has been used as a tool in the research of emotion and motivation. In a picture viewing paradigm, valence of affective pictures modulates startle magnitude. There is a debate on whether emotional or attentional processes are the mechanism of startle modification. The present study sought to address this question by investigating the individual differences related to startle modification and explore the relationship of the trait-like physiological variables and startle modification. The study creatively calculated standardized startle scores and treated personality variables as continuous variable. The results showed that specific contents of the affective pictures had different effects of startle modification. Personality variables influence the startle modification in emotion conditions differently. Cardiac activities were related to raw startle magnitude but not to startle modification. The results have suggested that there are the influences of individual differences in attention and effortful control on startle modification and attention and that emotion and attention interact with each other in startle modification. The study filled gaps in the research on startle modification and personality and guided future studies of this topic. / Master of Science

Syftet var att undersöka om exponering inför emotionella röster påverkar muskelanspänning och hjärtats slagfrekvens samt om det finns en samvariation mellan storlek eller längd på muskelanspänning vid aversiv emotionell input och grad av alexitymi. 24 studenter lyssnade på arga, glada och neutrala röster samtidigt som muskelanspänning mättes med EMG och hjärtats slagfrekvens med EKG. Grad av alexitymi mättes med Toronto Alexithymia Scale 20. Resultaten visade att arg eller glad röststimuli gav större muskelanspänningen än neutralröststimuli. Ingen skillnad i muskelanspänning fanns mellan arg eller glad röst. Det fanns inget samband mellan storlek eller längd på muskelanspänning och grad av alexitymi. / The object was to investigate whether exposure to emotionally valid voices, affect muscle tension and heart rate, and if there is a correlation between size or length of muscle tension during aversive emotional input and degree of Alexithymia. 24 students listened to angry, happy and neutral voices while muscle tension was measured by EMG and heart rate by EKG. Degree of Alexithymia was measured by Toronto Alexithymia Scale 20. The results showed that angry or happy voice stimuli caused higher muscle tension than neutral voice stimuli. No difference in muscle tension was shown between angry and happy voice. There was no correlation between size or length of muscle tension and degree of Alexithymia.

Thesis (M.S.)--University of Michigan, 2000. / Includes bibliographical references.

Thesis (M.S.)--University of Michigan, [2000] / Includes bibliographical references.