Network dynamics of nociceptive and aversive processing in the ACC during the transition to chronic pain

FERNANDO KASANETZ; THOMAS NEVIAN

Wengen

Simposio; BENESCO (Bern Network Epilepsy Sleep Consciosness) 5th Winter Research Meeting; 2017

BENESCO

The Anterior Cingulate Cortex (ACC) plays a central role in the evaluation of the affective and emotional aspects of pain. Accumulating evidence indicates that abnormal neuronal plasticity and a resulting hyperactivity of the ACC is the cause for the manifestation of the emotional distress that characterizes chronic pain conditions. However, little is known on how the functional organization of ACC microcircuits is affected in chronic pain.Apart from its involvement in pain perception, the ACC is engaged in a variety of other cognitive and emotional processes such as working memory, inhibitory control, conflict monitoring, fear, attention, salience and reward expectancy. How neuronal populations in the ACC can be involved in such a diversity of functions is a matter of debate. One intriguing hypothesis would be that the ACC is composed of multiple sub-circuits mediating separate aspects of behavior.Here we addressed whether the ACC possesses specialized neurons that process nociceptive information and how this putative microcircuit organization is affected in chronic neuropathic pain.Using in vivo recording of spiking activity in the mouse ACC, we have identified a subpopulation of neurons that are activated in response to nociceptive stimulation. Interestingly, this ?nociceptive neurons? showed a preferential increase in spontaneous activity during chronic pain, suggesting that ACC hyperactivity might be restricted to a sub-network of pain-related cells.In order to gain insight into the organization and plasticity of the ACC, we are using in vivo two-photon calcium imaging to monitor the activity of the same network of neurons with single cell resolution on subsequent days during the transition to chronic pain. Our preliminary results show that nociceptive inputs are codified by the activity of a discrete and partially stable assembly of ACC neurons. This fine-tuned representation is degraded after peripheral nerve injury resulting in a wide-spread neuronal representation of noxious events.