Rate My Professor Emmet Power

Dr. Emmet Power serves as a Research Fellow in the Department of Physiology, Faculty of Biomedical Sciences, Health Sciences Division, at the University of Otago. He is affiliated with the Centre for Neuroendocrinology and works in Dr. Karl Iremonger's laboratory. His current research centers on sex differences in neural circuits that control stress responses, particularly focusing on corticotropin-releasing hormone (CRH) neurons in the paraventricular nucleus (PVN) of the hypothalamus. This includes studies on ultradian rhythms of CRH^PVN neuron activity, associated behaviors, and corticosterone secretion; direct modulation of CRH nerve terminal function by noradrenaline and corticosterone; and plasticity of intrinsic excitability across the estrous cycle in hypothalamic CRH neurons.

Emmet Power completed his MSc in Neuroscience and PhD at the University of Otago, with the latter awarded in 2016 for his thesis titled 'Altered metabotropic glutamate receptor activity in the early stages of spinocerebellar ataxia type 1.' His doctoral research, supported by a University of Otago PhD Scholarship, investigated synaptic mechanisms in motor systems and cerebellar ataxia, earning him a prize from the Otago Medical School Research Society. Power's publication record spans neuroendocrinology and motor neuroscience. Notable works include 'The paraventricular nucleus of the hypothalamus: a key node in the control of behavioural states' (Journal of Physiology, 2025); 'Ultradian rhythms of CRH^PVN neuron activity, behavior, and corticosterone secretion' (2025); 'Direct modulation of CRH nerve terminal function by noradrenaline and corticosterone' (2024); 'Plasticity of intrinsic excitability across the estrous cycle in hypothalamic CRH neurons' (2021); 'Motor and cerebellar architectural abnormalities during the early progression of ataxia in a mouse model of SCA1' (Frontiers in Cellular Neuroscience, 2017); 'Are Type 1 metabotropic glutamate receptors a viable therapeutic target for the treatment of cerebellar ataxia?' (Journal of Physiology, 2016); 'Prolonged type 1 metabotropic glutamate receptor dependent synaptic signaling contributes to spino-cerebellar ataxia type 1' (Journal of Neuroscience, 2016); 'Functional contributions of glutamate transporters at the parallel fibre to Purkinje neuron synapse' (Cerebellum & Ataxias, 2014); and 'Transient reversal of the sodium/calcium exchanger boosts presynaptic calcium and synaptic transmission at a cerebellar synapse' (Journal of Neurophysiology, 2013). His contributions advance understanding of stress hormone regulation and potential therapeutic targets for ataxia.