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

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...

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Published inFrontiers in behavioral neuroscience Vol. 13; p. 43
Main Authors Liu, Xiang-Hui, Zhu, Rong-Ting, Hao, Bo, Shi, Yan-Wei, Wang, Xiao-Guang, Xue, Li, Zhao, Hu
Format Journal Article
LanguageEnglish
Published Switzerland Frontiers Research Foundation 06.03.2019
Frontiers Media S.A
Subjects
Adrenergic receptors
AMPA
Amygdala
Arousal
basolateral amygdala
Ca2+/calmodulin-dependent protein kinase II
cAMP/PKA
Cyclic AMP
Drug dosages
fear conditioning
Forensic medicine
Glucocorticoids
Glutamic acid receptors (ionotropic)
Kinases
Laboratory animals
Memory
Neurobiology
Neuroscience
Norepinephrine
Phosphorylation
Post traumatic stress disorder
Propranolol
Protein kinase A
Protein kinase C
PTSD
Rodents
α-Amino-3-hydroxy-5-methyl-4-isoxazole propionic acid
α-Amino-3-hydroxy-5-methyl-4-isoxazole propionic acid receptors
China
PTSD
norepinephrine
AMPA
fear conditioning
cAMP/PKA
basolateral amygdala
CaMK II/PKC
Online AccessGet full text
ISSN1662-5153
1662-5153
DOI10.3389/fnbeh.2019.00043

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Abstract 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 regulation of the β-adrenoceptor receptor (β-AR)-3',5'-cyclic monophosphate (cAMP)/PKA and CaMK II/PKC signaling pathways.
AbstractList 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.
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 regulation of the β-adrenoceptor receptor (β-AR)-3',5'-cyclic monophosphate (cAMP)/PKA and CaMK II/PKC signaling pathways.
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.
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 PKA inhibitor or CaMK II inhibitor. These findings demonstrate that NE could induce PTSD-like memory impairments by inhibiting AMPA receptor phosphorylation via regulation of the β-adrenoceptor-cAMP/PKA and CaMK II/PKC signaling pathways.
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.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.
Author Hao, Bo
Shi, Yan-Wei
Zhao, Hu
Xue, Li
Liu, Xiang-Hui
Zhu, Rong-Ting
Wang, Xiao-Guang
AuthorAffiliation 2 Guangdong Province Key Laboratory of Brain Function and Disease, Zhongshan School of Medicine, Sun Yat-sen University , Guangzhou , China
3 Guangdong Province Translational Forensic Medicine Engineering Technology Research Center, Zhongshan School of Medicine, Sun Yat-sen University , Guangzhou , China
1 Faculty of Forensic Medicine, Zhongshan School of Medicine, Sun Yat-sen University , Guangzhou , China
AuthorAffiliation_xml – name: 2 Guangdong Province Key Laboratory of Brain Function and Disease, Zhongshan School of Medicine, Sun Yat-sen University , Guangzhou , China
– name: 3 Guangdong Province Translational Forensic Medicine Engineering Technology Research Center, Zhongshan School of Medicine, Sun Yat-sen University , Guangzhou , China
– name: 1 Faculty of Forensic Medicine, Zhongshan School of Medicine, Sun Yat-sen University , Guangzhou , China
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Keywords PTSD
norepinephrine
AMPA
fear conditioning
cAMP/PKA
basolateral amygdala
CaMK II/PKC
Language English
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These authors have contributed equally to this work
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Snippet Glucocorticoids (GCs) can modulate the memory enhancement process during stressful events, and this modulation requires arousal-induced norepinephrine (NE)...
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SubjectTerms Adrenergic receptors
AMPA
Amygdala
Arousal
basolateral amygdala
Ca2+/calmodulin-dependent protein kinase II
cAMP/PKA
Cyclic AMP
Drug dosages
fear conditioning
Forensic medicine
Glucocorticoids
Glutamic acid receptors (ionotropic)
Kinases
Laboratory animals
Memory
Neurobiology
Neuroscience
Norepinephrine
Phosphorylation
Post traumatic stress disorder
Propranolol
Protein kinase A
Protein kinase C
PTSD
Rodents
α-Amino-3-hydroxy-5-methyl-4-isoxazole propionic acid
α-Amino-3-hydroxy-5-methyl-4-isoxazole propionic acid receptors
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Title Norepinephrine Induces PTSD-Like Memory Impairments via Regulation of the β-Adrenoceptor-cAMP/PKA and CaMK II/PKC Systems in the Basolateral Amygdala
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