Cognitive Impairment in Pain through Amygdala-Driven Prefrontal Cortical Deactivation

• DOI: 10.1523/jneurosci.0225-10.2010
• Publication Date: 2010-04-14T16:40:34Z
• Authors: Guangchen Ji; Hao Sun; Yu Fu; Zhen Li; Miguel Pais-Vieira; Vasco Galhardo; Volker Neugebauer
• Keywords: Basolateral amygdala

Cognitive deficits such as impaired decision-making can be a consequence of persistent pain. Normal functions the intact amygdala and prefrontal cortex are required for emotion-based that relies on ability to assess risk, attribute value, identify advantageous strategies. We tested hypothesis pain-related cognitive result from amygdala-driven impairment medial cortical (mPFC) function. To do this, we used electrophysiological single-unit recordings in vivo , patch clamp brain slices, various behavioral assays show increased neuronal activity an animal model arthritis pain was accompanied by decreased mPFC activation decision-making. Furthermore, pharmacologic inhibition (with corticotropin-releasing factor 1 receptor antagonist) hyperactivity basolateral (BLA), but not central (CeA), reversed deactivation pyramidal cells improved deficits. Pain-related resulted shift balance between inhibitory excitatory synaptic transmission. Direct transmission did change model, whereas polysynaptic increased. GABAergic reduced non-NMDA antagonists, suggesting glutamate driven. The results consistent with BLA-driven feedforward neurons. In contrast differential effects BLA versus CeA cortical-cognitive functions, both nuclei modulate emotional-affective behavior. Thus, this study shows contributes only also novel amygdalo-cortical mechanism has important implications our understanding interactions.