Preclinical and clinical studies have identified amygdala hyperactivity as well as impairment of cortical control mechanisms in pain states. The mPFC sends excitatory projections to GABAergic neurons in the intercalated cell mass (ITC) in the amygdala, which project to the laterocapsular division of the central nucleus of the amygdala (CeLC; output nucleus) and serve gating functions for amygdala output.
First-pass extracted concept
cortical control of amygdala output
Candidate: concept label1 source documents4 linked claims
Live refresh every 5sNext refresh in 5s
Evidence Snippets
Supporting Sources
Linked Claims
The review describes an mPFC-to-ITC-to-CeLC circuit in which mPFC excitation of GABAergic ITC neurons gates amygdala output.
Quoted textsource-backed
The mPFC sends excitatory projections to GABAergic neurons in the intercalated cell mass (ITC) in the amygdala, which project to the laterocapsular division of the central nucleus of the amygdala (CeLC; output nucleus) and serve gating functions for amygdala output.
The review describes hyperactivity of basolateral amygdala neurons as generating enhanced feedforward inhibition and deactivation of the medial prefrontal cortex, linked to pain-related cognitive deficits.
Quoted textsource-backed
Hyperactivity of basolateral amygdala (BLA) neurons generates enhanced feedforward inhibition and deactivation of the medial prefrontal cortex (mPFC), resulting in pain-related cognitive deficits.
The review states that impairment of cortical control mechanisms permits the development of amygdala pain plasticity.
Quoted textsource-backed
Impairment of these cortical control mechanisms allows the development of amygdala pain plasticity.
The review states that amygdala hyperactivity and impaired cortical control mechanisms are associated with pain states.
Quoted textsource-backed
Preclinical and clinical studies have identified amygdala hyperactivity as well as impairment of cortical control mechanisms in pain states.