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Monoamine oxidases (MAOs) are phylogenetically old enzymes which catalyze the deamination of monoamines. Interest in a relationship between MAO and aggressive behaviour derives from the report of a single family with a mutation which obliterates the activity of MAO A, as well as a long history of studies which substantiate a relationship between MAO activity and impulsive aggressive behaviour. The goals of this thesis were: (1) to examine the generalizability of the specific MAO mutation noted above; (2) to evaluate the relationship between platelet MAO activity and genetic polymorphisms in MAO genes, and (3) to extend knowledge regarding the developmental behavioural impact of MAO deficiency in mice treated pre- and perinatally with inhibitors of MAO. / In the first study we genotyped the C936T mutation in 100 subjects followed longitudinally and oversampled for aggressive behaviour. None of the subjects in our sample carried this mutation. / In the second study, we report the lack of association between platelet MAO activity and four intronic microsatellite polymorphisms of the MAO genes. / Studies of MAO knockout mice are at significant variance with clinical pharmacological experience using MAO inhibitors. Prompted by this and by other seminal basic experiments, we hypothesized that inhibition of MAO activity during the developmental period would have profound behavioural effects. MAO A and B inhibitors were administered, separately or in combination, to mice during gestation and lactation. Total prenatal MAO inhibition produced a severe pattern of behaviour, while MAO-B inhibited mice demonstrated a similar pattern with lower intensity. Aggression was elevated in MAO-A inhibited mice only after acute pharmacological challenges suggesting prenatal sensitization. Thus developmental inhibition of MAO activity engenders behavioural effects which parallel those observed in animals devoid functional MAO. These data underscore the importance of neurochemical changes during development and provide a possible model for uninhibited aggression, common in clinical populations.

Brain and behavioural disorders represent a leading cause of morbidity and suffering worldwide. The 'fierce' mouse has a spontaneous deletion of Nr2e1 that results in a complex phenotype that includes cortical hypoplasia and socially abnormal behaviours. Notably, functional protein and regulatory equivalency of mouse and human NR2E1 has been established. Furthermore, human studies implicate the genomic region containing NR2E1 in mental illness, although a role for NR2E1 in humans is currently unknown. Here, I integrate mouse models and human molecular genetics to understand the involvement of NR2E1 in human brain-behaviour development. First, we test the hypothesis that the spontaneous 'fierce' deletion involves onlyNr2el. It was demonstrated that the 'fierce' mutation results in the loss of all Nr2e1 exons without affecting neighbouring genes. Next, the hypothesis that some humans with cortical malformations will harbour NR2E1 mutations was tested by sequencing the coding, untranslated, splice-site, proximal promoter, and evolutionarily conserved regions of this gene in 60 subjects with microcephaly. Four candidate regulatory mutations were identified. To help interpret these findings, the genomic architecture and molecular evolution of NR2E1 were characterized in 94ethnically-diverse humans and 13 non-human primates, which indicated strong functional constraint. Finally, the hypothesis that some humans with behavioural and psychiatric disorders will harbour mutations in NR2E1 was tested by sequencing the regions outlined above in 126humans with impulsive-aggressive disorders, bipolar disorder, or schizophrenia. Eleven candidate regulatory mutations were identified. Taken together, the findings presented in this thesis are consistent with the proposal that non-coding regulatory mutations may be important to the pathogenesis of brain-behavioural disorders in some humans.

This study examined whether cortical changes underlying treatment for children with aggressive behaviour problems are related to changes in executive function (EF) performance. Fifty-five 8- to 12-year-old clinically-referred children were tested before and after a 14-week treatment intervention. Performance on four EF tasks varying in affective relevance was assessed at each session. EEG was also used to record peak amplitudes for the “inhibitory” N2, an event-related potential, while the children completed an emotion-induction Go/Nogo task. Results showed that changes in N2 amplitudes significantly predicted changes in performance only for the Iowa Gambling Task (IGT) – an affectively relevant task. Subsequent analysis revealed that only children who improved with treatment displayed significant decreases in N2 amplitudes and significant improvement in IGT performance from pre- to post-treatment. These findings suggest that cortical changes underlying successful treatment for children’s aggressive behaviour problems tap improvement in executive functions recruited for emotionally demanding events.

This study examined whether cortical changes underlying treatment for children with aggressive behaviour problems are related to changes in executive function (EF) performance. Fifty-five 8- to 12-year-old clinically-referred children were tested before and after a 14-week treatment intervention. Performance on four EF tasks varying in affective relevance was assessed at each session. EEG was also used to record peak amplitudes for the “inhibitory” N2, an event-related potential, while the children completed an emotion-induction Go/Nogo task. Results showed that changes in N2 amplitudes significantly predicted changes in performance only for the Iowa Gambling Task (IGT) – an affectively relevant task. Subsequent analysis revealed that only children who improved with treatment displayed significant decreases in N2 amplitudes and significant improvement in IGT performance from pre- to post-treatment. These findings suggest that cortical changes underlying successful treatment for children’s aggressive behaviour problems tap improvement in executive functions recruited for emotionally demanding events.

Sensory biology of animals is studied throughout the world for the insight it provides to understanding ecosystems and improving how we manage species. In this research, I designed experiments to investigate the sensory biology and behaviour of two Australian species of freshwater crayfish from the genus Cherax, the yabby (Cherax destructor) and redclaw crayfish (Cherax quadricarinatus). Experimental apparatus were constructed and tailored to test specific questions on physiology, tactile (touch) sensitivity, observation techniques, aggressive behaviour and responses to electrical fields. The outcomes were: / • abdominal muscle mass was positively correlated to the size of the electrical fields produced by swimming crayfish, / • behaviour changed in response to contact with different structures and textures of wall surfaces, / • computer analysis of underwater behaviour was similar to that scored by a human observer, / • the level of aggression in groups of crayfish changed as group size increased, and / • two species of crayfish responded to electrical fields in the water by decreasing their locomotory movement. / These results reveal a way in which physiology relates to behaviour, how crayfish and other crustaceans may sense the invisible and behave in aquaculture ponds, as well as documenting methodology to further investigate these areas in the future.

Thesis (M.S.)--Ohio University, August, 2007. / Title from PDF t.p. Includes bibliographical references.

Thesis (M.S.)--University of North Texas, Dec., 2007. / Title from title page display. Includes bibliographical references.

Thesis (B.A. (Hons.))-- University of Adelaide, Dept. of Psychology, 1972.