Activation of Beta-adrenergic Receptors Upregulates the Signal-to-Noise Ratio of Auditory Input in the Medial Prefrontal Cortex and Mediates Auditory Fear Conditioning

Norepinephrine (NE) is involved in auditory fear conditioning (AFC) in posttraumatic stress disorder (PTSD). However, it is still unclear how it acts on neurons. We aimed to investigate whether the activation of the β-adrenergic receptor (β-AR) improves AFC by sensitization of the prelimbic (PL) cor...

Full description

Saved in:
Bibliographic Details
Published inMolecular neurobiology Vol. 61; no. 3; pp. 1833 - 1844
Main Authors Xie, Haiting, Tian, Yueqin, Li, Zhongli, Wang, Kaitao, Li, Runtong, Yi, Shang, Chen, Aimin, Chen, Jian, Liu, Jun, Wei, Xuhong, Gao, Xiaoya
Format Journal Article
LanguageEnglish
Published New York Springer US 01.03.2024
Springer Nature B.V
Subjects
Online AccessGet full text

Cover

Loading…
More Information
Summary:Norepinephrine (NE) is involved in auditory fear conditioning (AFC) in posttraumatic stress disorder (PTSD). However, it is still unclear how it acts on neurons. We aimed to investigate whether the activation of the β-adrenergic receptor (β-AR) improves AFC by sensitization of the prelimbic (PL) cortex at the animal, cellular, and molecular levels. In vivo single-cell electrophysiological recording was used to characterize the changes in neurons in the PL cortex after AFC. Then, PL neurons were locally administrated by the β-AR agonist isoproterenol (ISO), the GABAaR agonist muscimol, or intervened by optogenetic method, respectively. Western blotting and immunohistochemistry were finally used to assess molecular changes. Noise and low-frequency tones induced similar AFC. The expression of β-ARs in PL cortex neurons was upregulated after fear conditioning. Microinjection of muscimol into the PL cortex blocked the conformation of AFC, whereas ISO injection facilitated AFC. Moreover, PL neurons can be distinguished into two types, with type I but not type II neurons responding to conditioned sound and being regulated by β-ARs. Our results showed that β-ARs in the PL cortex regulate conditional fear learning by activating type I PL neurons.
Bibliography:ObjectType-Article-1
SourceType-Scholarly Journals-1
ObjectType-Feature-2
content type line 14
content type line 23
ISSN:0893-7648
1559-1182
1559-1182
DOI:10.1007/s12035-023-03667-3