Norepinephrine Induces PTSD-Like Memory Impairments via Regulation of the β-Adrenoceptor-cAMP/PKA and CaMK II/PKC Systems in the Basolateral Amygdala

• Main Authors: Xiang-Hui Liu, Rong-Ting Zhu, Bo Hao, Yan-Wei Shi, Xiao-Guang Wang, Li Xue, Hu Zhao
• Format: Article
• Language: English
• Published: Frontiers Media S.A. 2019-03-01
• Series: Frontiers in Behavioral Neuroscience
• Subjects: PTSD; fear conditioning; basolateral amygdala; norepinephrine; AMPA; cAMP/PKA
• Online Access: https://www.frontiersin.org/article/10.3389/fnbeh.2019.00043/full

Glucocorticoids (GCs) can modulate the memory enhancement process during stressful events, and this modulation requires arousal-induced norepinephrine (NE) activation in the basolateral amygdale (BLA). Our previous study found that an intrahippocampal infusion of propranolol dose-dependently induced post-traumatic stress disorder (PTSD)-like memory impairments. To explore the role of the noradrenergic system of the BLA in PTSD-like memory impairment, we injected various doses of NE into the BLA. We found that only a specific quantity of NE (0.3 μg) could induce PTSD-like memory impairments, accompanied by a reduction in phosphorylation of GluR1 at Ser845 and Ser831. Moreover, this phenomenon could be blocked by a protein kinase A (PKA) inhibitor or calcium/calmodulin-dependent protein kinase II (CaMK II) inhibitor. These findings demonstrate that NE could induce PTSD-like memory impairments via regulation of the β-adrenoceptor receptor (β-AR)-3′,5′-cyclic monophosphate (cAMP)/PKA and CaMK II/PKC signaling pathways.