IFIBIO HOUSSAY   25014
INSTITUTO DE FISIOLOGIA Y BIOFISICA BERNARDO HOUSSAY
Unidad Ejecutora - UE
congresos y reuniones científicas
Título:
Network dynamics of pain processing in the anterior cingulate cortex
Autor/es:
MARIO ACUÑA; FERNANDO KASANETZ; THOMAS NEVIAN
Lugar:
Berlin
Reunión:
Congreso; 11th FENS Forum of Neuroscience; 2018
Institución organizadora:
FENS
Resumen:
Chronic pain affects to 20% of the European population; therefore, understanding the processes underlying pain chronification is imperative. Accumulating evidence indicates that abnormal neuronal plasticity and a resulting hyperactivity of the anterior cingulate cortex (ACC) contributes to the manifestation of the emotional distress that characterizes the chronic pain conditions. However, how the functional organization of ACC neuronal microcircuits is affected in chronic pain is poorly understood. Moreover, apart from its involvement in pain processing, the ACC is engaged in a variety of other cognitive and emotional tasks. Therefore, we addressed the question whether the ACC possesses specialized neuronal circuits that process nociceptive information and how this putative network changes its dynamics in chronic 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. Additionally, to monitor the activity of the same network of neurons with single cell resolution on subsequent days during the transition to chronic pain, we took advantage of in vivo two-photon calcium imaging of neuronal populations in the mouse ACC. Our results show that nociceptive inputs are encoded 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 neuronal over-representation of noxious events.