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Handb Exp Pharmacol. 2015;227:261-84. doi: 10.1007/978-3-662-46450-2_13.

Amygdala pain mechanisms.

Author information

1
Department of Pharmacology and Neuroscience, Center for Translational Neuroscience and Therapeutics, Texas Tech University Health Sciences Center, 3601 4th Street, Lubbock, TX, 79430-6592, USA, volker.neugebauer@ttuhsc.edu.

Abstract

A limbic brain area, the amygdala plays a key role in emotional responses and affective states and disorders such as learned fear, anxiety, and depression. The amygdala has also emerged as an important brain center for the emotional-affective dimension of pain and for pain modulation. Hyperactivity in the laterocapsular division of the central nucleus of the amygdala (CeLC, also termed the "nociceptive amygdala") accounts for pain-related emotional responses and anxiety-like behavior. Abnormally enhanced output from the CeLC is the consequence of an imbalance between excitatory and inhibitory mechanisms. Impaired inhibitory control mediated by a cluster of GABAergic interneurons in the intercalated cell masses (ITC) allows the development of glutamate- and neuropeptide-driven synaptic plasticity of excitatory inputs from the brainstem (parabrachial area) and from the lateral-basolateral amygdala network (LA-BLA, site of integration of polymodal sensory information). BLA hyperactivity also generates abnormally enhanced feedforward inhibition of principal cells in the medial prefrontal cortex (mPFC), a limbic cortical area that is strongly interconnected with the amygdala. Pain-related mPFC deactivation results in cognitive deficits and failure to engage cortically driven ITC-mediated inhibitory control of amygdala processing. Impaired cortical control allows the uncontrolled persistence of amygdala pain mechanisms.

PMID:
25846623
PMCID:
PMC4701385
DOI:
10.1007/978-3-662-46450-2_13
[Indexed for MEDLINE]
Free PMC Article

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