Visually Induced Vasomotion Entrainment and Its Correlation with Cerebellar-Dependent Motor Learning

Core Concepts

Visually induced vasomotion can be entrained and frequency-locked to the temporal frequency of the visual stimulus, and this entrainment occurs globally across the brain surface and deep brain regions. The magnitude of visually induced vasomotion entrainment correlates with the performance gain in cerebellar-dependent motor learning.

Abstract

The content describes the presence of spontaneous vasomotion (oscillatory changes in blood vessel diameter) in the mouse brain and how this vasomotion can be entrained and frequency-locked to the temporal frequency of an oscillating visual stimulus. Key findings:

Spontaneous vasomotion was observed in the brain of awake, head-restrained mice through the intact skull using fluorescence imaging. The vasomotion occurred at low frequencies (around 0.1 Hz) distinct from the heartbeat.

Presenting horizontally oscillating visual stimuli at 0.25 Hz induced vasomotion that became entrained and frequency-locked to the visual stimulus over repeated training sessions. This entrainment was observed not only in the primary visual cortex but across the whole brain surface and in the deep cerebellar flocculus region.

The magnitude of the visually induced vasomotion entrainment, measured as the peak ratio at the stimulus frequency, increased with repeated training sessions. This increase correlated with the performance gain in the cerebellar-dependent horizontal optokinetic response (HOKR) eye movement.

The visually induced vasomotion was not simply a consequence of the eye movements, as the fluorescence fluctuations were not directly correlated with the amplitude of the eye movements.

Endogenous brain autofluorescence signals could be used to quantify the visually induced vasomotion dynamics, as the autofluorescence signals mirrored the blood vessel volume changes.

The results suggest an intimate relationship between the plasticity of visually induced vasomotion and the plasticity of neuronal circuits underlying cerebellar-dependent motor learning.

Stats

The temporal frequency of the visual stimulus was 0.25 Hz.
The spatial amplitude of the horizontal oscillation was 17 degrees in the visual angle of the mouse.
The horizontal spatial cycle of the vertical stripes was 6.4 degrees in the visual angle.

Quotes

"Visually induced vasomotion can be frequency-locked to the visual stimulus and can be entrained with repeated trials."
"The global entrainment could be realized through separate mechanisms from the local neurovascular coupling."
"The magnitude of the visually induced vasomotion entrainment, measured as the peak ratio at the stimulus frequency, increased with repeated training sessions. This increase correlated with the performance gain in the cerebellar-dependent horizontal optokinetic response (HOKR) eye movement."

Key Insights Distilled From

Plastic vasomotion entrainment

by Sasaki,D., I... at www.biorxiv.org 11-21-2023

https://www.biorxiv.org/content/10.1101/2023.11.20.567853v2

Deeper Inquiries

How might the plasticity of visually induced vasomotion be mechanistically linked to the plasticity of neuronal circuits underlying cerebellar-dependent motor learning?

The plasticity of visually induced vasomotion could be mechanistically linked to the plasticity of neuronal circuits underlying cerebellar-dependent motor learning through neurovascular coupling mechanisms. When the brain is engaged in a motor learning task such as the horizontal optokinetic response (HOKR), there is an increase in neuronal firing triggered by the visual stimuli. This neuronal activity leads to the release of vasodilator signals from neurons and astrocytes, resulting in vasodilation and vasoconstriction in the blood vessels. The synchronized oscillations of the vascular smooth muscle cells and pericytes contribute to the vasomotion observed in response to the visual stimulation.
In the context of cerebellar-dependent motor learning, the plasticity of vasomotion could play a crucial role in optimizing energy delivery to specific brain regions involved in motor coordination and learning. The entrainment of vasomotion to the frequency of the visual stimulus may enhance the efficiency of energy delivery to the cerebellar flocculus, where neuronal circuit plasticity essential for HOKR learning occurs. By ensuring adequate energy supply to the activated neuronal circuits, the plasticity of vasomotion may support and interact with the plastic changes in the cerebellar circuits, facilitating motor learning and memory consolidation.

How might the plasticity of visually induced vasomotion be mechanistically linked to the plasticity of neuronal circuits underlying cerebellar-dependent motor learning?

The global entrainment of visually induced vasomotion could support various cognitive and behavioral functions beyond the specific HOKR learning task examined in the study. One potential function is the regulation of cognitive processes such as attention, memory, and decision-making. The synchronized vasomotion across different brain regions could optimize energy delivery to areas involved in cognitive tasks, enhancing information processing and cognitive performance. Additionally, the entrainment of vasomotion may contribute to the coordination of neuronal activity during complex cognitive processes, leading to improved cognitive function.
Furthermore, the global entrainment of visually induced vasomotion could play a role in emotional regulation and stress response. By modulating blood flow and energy delivery to brain regions involved in emotion processing, vasomotion entrainment may influence emotional states and stress resilience. The coordinated vasomotion could facilitate the regulation of neurotransmitter release and neural activity in emotion-related circuits, impacting emotional well-being and stress coping mechanisms.
Overall, the global entrainment of visually induced vasomotion has the potential to support a wide range of cognitive and behavioral functions, contributing to brain function and adaptive behavior in various contexts.

Could the principles of visually induced vasomotion entrainment be leveraged to develop novel brain-computer interface or neurofeedback technologies?

The principles of visually induced vasomotion entrainment offer exciting possibilities for the development of novel brain-computer interface (BCI) or neurofeedback technologies. By harnessing the ability of the brain to entrain vasomotion to external visual stimuli, researchers could design innovative BCI systems that utilize changes in blood flow dynamics as a biomarker for cognitive states or mental processes. These systems could provide real-time feedback on brain activity and cognitive performance, enabling users to modulate their cognitive states or enhance their mental abilities.
In the field of neurofeedback, the principles of visually induced vasomotion entrainment could be applied to create biofeedback systems that help individuals regulate their brain activity and optimize cognitive function. By training individuals to modulate their vasomotion patterns through visual stimuli, neurofeedback technologies could promote cognitive enhancement, stress reduction, and emotional regulation. These systems could be used in various applications, such as cognitive training, mental health interventions, and performance optimization.
Overall, leveraging the principles of visually induced vasomotion entrainment in BCI and neurofeedback technologies holds great potential for advancing our understanding of brain function and developing innovative tools for enhancing cognitive abilities and well-being.