Amygdala nuclei play important roles in emotional responses, fear,
depression, and pain processing. However, the identity of the
amygdala neuronal subtypes involved in the pain signal is not
completely understood. The lateral subdivision of amygdala central
nucleus (CEl) contains two major subpopulations of GABAergic
neurons which express somatostatin (SOM+) and protein kinase Cδ
(PKCδ+). It has been demonstrated that ERK was activated in
amygdala central nucleus (CEL) in different pain models. In this
study, we showed most of the ERK positive neurons were colocolized
with PKC δ+ neurons in different pain models in mice. Optogenetic
activation of PKC δ+ neurons was sufficient to induce hyperalgesia
without changing the anxiety behaviors in naïve mice. And also,
chemogenetic inhibition of the PKC δ+ neurons showed significantly
reduce the acute pain response induced by 5% formalin injection.
Conversely, activation of SOM+ neurons changed the anxiety
behaviors but did not affect the pain behavior. Taken together, our
data suggest that CEl PKCδ+ neurons play an important role in
mediating the pain signals.

DIFFERENTIAL REGULATION OF PAIN AND ANXIETY BEHAVIORS BY CEA NEURONS