Ian Kirk

The University of Auckland, Psychology, Faculty Member

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Cognitive Neuroscientist. Uses EEG and diffusion imaging to study memory networks. Includes a connectomics approach in research (e.g. graph theory). Also investigates in using imaging tools for earlier diagnosis of Alzheimer's.
Address: Auckland, Auckland, New Zealand

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Daniel D. Hutto

University of Wollongong

Steven Pinker

Harvard University

Matthew Broome

University of Oxford

Marc Champagne

Kwantlen Polytechnic University

Shaun Gallagher

University of Memphis

John Johnson

Pennsylvania State University

Richard Cook

Birkbeck College, University of London

Tore Nielsen

Université de Montréal

Caroline Catmur

King's College London

Tarik N. Mohamed

Sohag University

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Papers by Ian Kirk

Acute exercise as a modifier of neocortical plasticity and aperiodic activity in the visual cortex

Scientific Reports, May 9, 2023

Long-term potentiation (LTP) is a form of neuroplasticity commonly implicated in mechanistic mode... more Long-term potentiation (LTP) is a form of neuroplasticity commonly implicated in mechanistic models of learning and memory. Acute exercise can boost LTP in the motor cortex, and is associated with a shift in excitation/inhibition (E:I) balance, but whether this extends to other regions such as the visual cortex is unknown. We investigated the effect of a preceding bout of exercise on LTP induction and the E:I balance in the visual cortex using electroencephalography (EEG). Young adults (N = 20, mean age = 24.20) engaged in 20 min of high-intensity interval training (HIIT) exercise and rest across two counterbalanced sessions. LTP was induced using a high frequency presentation of a visual stimulus; a "visual tetanus". Established EEG markers of visual LTP, the N1b and P2 component of the visual evoked potential, and an EEG-derived measure of the E:I balance, the aperiodic exponent, were measured before and after the visual tetanus. As expected, there was a potentiation of the N1b following the visual tetanus, with specificity to the tetanised stimulus, and a non-specific potentiation of the P2. These effects were not sensitive to a preceding bout of exercise. However, the E:I balance showed a late shift towards inhibition following the visual tetanus. A preceding bout of exercise resulted in specificity of this E:I balance shift to the tetanised stimulus, that was not seen following rest. This novel finding suggests a possible exercise-induced tuning of the visual cortex to stimulus details following LTP induction. Cardiorespiratory exercise is a modifiable lifestyle factor with the capacity to influence neural processes underlying cognition. One line of investigation suggests that exercise can augment long-term potentiation (LTP), a form of neuroplasticity thought to be important for the encoding and storage of information in the brain 1,2. LTP is a long-lasting increase in the strength of synaptic communication between neurons, induced experimentally by repeated, high frequency activation of an afferent neural pathway 1. Although LTP is commonly associated with hippocampal function and memory in animal models, it is a crucial brain-wide process 3-5. Exercise is known to have diffuse effects throughout the brain that are likely to support the LTP process, such as increased concentrations of brain-derived neurotrophic factor (BDNF) 6 , glutamate and gamma-aminobutyric acid 7 , and an increase in cerebral lactate uptake 8. Thus, exercise is thought to create an environment that is conducive for LTP. Advances over the last two decades have seen the emergence of non-invasive paradigms that allow the indirect measurement of LTP in humans (as reviewed by Refs. 9,10). Using these methods, it has been demonstrated that an acute bout of high-intensity interval training (HIIT) exercise can augment LTP-like potentiation in an unexercised area of the motor cortex 11,12. Further investigation into the mechanisms that might underlie this exercise-related augmentation of LTP using transcranial magnetic stimulation (TMS) found that there was decrease in short intracortical inhibition and an increase in intracortical facilitation 13-16 , indicating a shift in the cortical excitation-inhibition (E:I) balance towards excitation 13. Although these results demonstrate the potential

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