This paper provides a personal history of work starting with the discovery that anxiolytic drugs reduce hippocampal theta frequency. It includes parallel work on septal elicitation of theta carried out in Jeffrey Gray's laboratory in Oxford; a statement of my original scientific perspective on the work; and a description of later work in my laboratory in New Zealand confirming the function of theta rhythmicity per se and its mediation of the effects of anxiolytic drugs on behavior. I finish with comments on risk management with such experiments and their use in larger scale theory development.
View Article and Find Full Text PDFPurpose: Anxiety disorders are a major global issue. Diagnosis via symptoms, not biological causes, delivers poor treatment outcomes. Our frontal EEG biomarker, Goal Conflict Specific Rhythmicity (GCSR; 4-12 Hz), developed from our long-standing detailed neuropsychological theory of anxiety processes, is reduced by all chemical types of selective anxiolytic and is high in cases across a range of currently diagnosed anxiety disorders.
View Article and Find Full Text PDFThe supramammillary nucleus (SuM) in the hypothalamus, in conjunction with the hippocampus (HPC), has been implicated through theta oscillations in various brain functions ranging from locomotion to learning and memory. While the indispensable role of the SuM in HPC theta generation in anesthetized animals is well-characterized, the SuM is not always necessary for HPC theta in awake animals. This raises questions on the precise behavioral relevance of SuM theta activity and its interaction with HPC theta activity.
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