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Synaptic gating of viscerosensory signals

We aim to discover the neural pathways that modulate the reflexes that allow optimum organ performance in different circumstances. 

Aims

Modulation of autonomic reflexes is thought to be mediated in the brain stem via hypothalamic and limbic inputs, including those to the solitary tract nucleus. Our hypothesis is that modulation of viscerosensory signals at the level of the solitary tract nucleus underlies autonomic reflex flexibility. To address this, we are combining electrophysiology, a method to record signalling between neurons and across neural networks, with optogenetic tools, which allow selective activation of neurons with light.

The brain receives sensory signals from internal organs that initiate automatic reflexes to adjust their function. We aim to discover the neural pathways that modulate these reflexes that allow optimum organ performance in different circumstances. Defining the fundamental synaptic mechanisms that underlie this information processing by the brain is critical to our understanding of the pathophysiology of cardiovascular and neurological diseases ranging from hypertension through to depression.

Sensory information enables organisms to respond appropriately to changes in environmental and internal conditions. Sensory information is subject to integration and modulation within the brain to enable assignment of salience and relevance. As a consequence, internal organ function can be rapidly reconfigured with a change in behavioral goals – such as during a fight or flight response. Viscerosensory signals, which are the subject of this application, enable the brain to control and coordinate internal organ function via autonomic reflexes. A vital characteristic of autonomic reflexes is that they remain flexible to allow for optimal organ performance under different circumstances. For example, the baroreceptor reflex governs short term blood pressure and operates under different rules at rest as compared to during exercise, stress or disease. How this is achieved is critical to our understanding of the pathophysiology of cardiovascular and neurological diseases.

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