ResonanceCircuits · Illuminating neural microcircuitry underlying flicker resonance in the visual cortex
Horizon 2020 — Marie Skłodowska-Curie Actions
- Duration
- 2020-12-15 → 2022-12-14
- EU contribution
- €175,572
- Participants
- 1
- Scheme
- MSCA-IF
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Results in brief
Illuminating neural microcircuitry underlying flicker resonance in the visual cortex
Rhythmic sensory stimuli elicit oscillatory brain responses at the frequency identical or harmonically related to the stimulus. Aside from this frequency following response, increased amplitude (or resonance) responses are observed in response to ~10, ~20, and ~40 Hz in humans. Already one of the first studies using electroencephalography (EEG) in humans demonstrated that the amplitude of alpha brain rhythm (7-13 Hz) could be increased in amplitude when periodic light flashes were in synchrony with individual endogenous alpha rhythm (~10Hz; Adrian & Matthews, 1934). This study was the first to raise the possibility that light could noninvasively modulate brain rhythms. This posibility has been recently demonstrated (Iaccarino et al., 2016): Repetitive light therapy using 40 Hz visual stimulation has been shown to improve cognitive performance in Alzheimer disease mouse model by affecting synaptic transmission and synaptic plasticity, and as such, preserving neurons and synapses. Rhythmic sensory stimulation (flicker) has many applications: From human vision and cognitive neuroscience research to visual impairment diagnostics. Aberrant responses to flicker stimulation have also been used as diagnostic tools in clinical neuroscience (e.g. schizophrenia, mood disorders, epilepsy, migraine). Why do responses to alpha flicker predict effectiveness of medication? Why can alpha flicker trigger epileptiform dynamics? Answers to these questions require understanding the neural mechanisms underlying responses to rhythmic stimulation. Despite a long history and applications, the neural mechanisms by which rhythmic sensory stimuli interact with and modulate endogenous brain rhythms, are unknown. The objectives of this project were to: (1) measure the interactions between exogenous rhythms and endogenous brain oscillations at the level they are generated using high-density laminar probes that enable recording from hundreds of neurons across cortical laminae; (2) optogenetically identify and manipulate different classes of neurons. This fundamental research knowledge on interactions between exogenous and endogenous rhythms holds realistic promise in the clinical domain for diagnosis and therapeutic interventions of oscillopathies (neurodegenerative diseases hallmarked by aberrant endogenous brain rhythms).
Data: CORDIS, © European Union
Project objective
Almost 200 years ago, Jan Purkinje examined the visual illusions induced by flickering light. Since then, scientists, clinicians, and artists have been fascinated by the effects of flicker on brain rhythms. When entrained with rhythmic light of ~10, ~20, ~40 Hz, visual cortex responds more strongly, or resonates. In the visual and cognitive neurosciences, resonance flicker is used to study perception and attention; in clinical domain, aberrant resonance responses to flicker are used as a diagnostic tool and potential treatment. However, the neural mechanisms by which flicker engages resonant properties of local cortical circuits and entrains brain rhythms at the level they are generated remain unknown. Over the past decade, this level became accessible to neuroscientists due to the rapid development of new neurobiological tools such as cell-type-specific optical stimulation (optogenetics). In this project, using recordings that span multiple spatial scales (from neurons and local field potentials across cortical layers to EEG), I will characterize the neural mechanisms by which flicker stimuli engage resonant properties of brain rhythms. I will use optogenetic tools to identify and manipulate genetically targeted cell types, and will combine it with simultaneous EEG and high-density laminar recordings in primary visual cortex of awake mice. I will determine the laminar profile of neural activity underlying flicker resonance observed at the EEG level (Study 1). By recording from distinct GABAergic interneuron classes and optogenetically silencing them, I will test the novel hypothesis that distinct classes of interneurons mediate flicker resonance to low (theta, alpha) and high (beta, gamma) frequencies (Study 2). This research will allow me to uncover the neurophysiological basis of resonance responses to flicker in unprecedented detail, and provide means to exploit the untapped potential of flicker as a tool to study and modulate brain rhythms in a targeted way.
Original text from CORDIS.
Participants
- KONINKLIJKE NEDERLANDSE AKADEMIE VAN WETENSCHAPPEN - KNAW · AMSTERDAMCoordinatorNetherlands
Links
Data: CORDIS, © European Union