Dopamine D1-like receptors modulate synchronized oscillations in the hippocampal–prefrontal–amygdala circuit in contextual fear

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Název: Dopamine D1-like receptors modulate synchronized oscillations in the hippocampal–prefrontal–amygdala circuit in contextual fear
Autoři: Christine Stubbendorff, Ed Hale, Tobias Bast, Helen J Cassaday, Stephen J Martin, Sopapun Suwansawang, David M Halliday, Carl W Stevenson
Zdroj: Sci Rep
Scientific Reports, Vol 13, Iss 1, Pp 1-18 (2023)
Informace o vydavateli: Springer Science and Business Media LLC, 2023.
Rok vydání: 2023
Témata: Science, Dopamine, Receptors, Dopamine D1, Prefrontal Cortex, Fear, Amygdala, Hippocampus, Article, Rats, Fear/physiology, name=General, Prefrontal Cortex/physiology, Dopamine D1, Receptors, Amygdala/physiology, Medicine, Animals, Hippocampus/physiology, Dopamine/pharmacology
Popis: Contextual fear conditioning (CFC) is mediated by a neural circuit that includes the hippocampus, prefrontal cortex, and amygdala, but the neurophysiological mechanisms underlying the regulation of CFC by neuromodulators remain unclear. Dopamine D1-like receptors (D1Rs) in this circuit regulate CFC and local synaptic plasticity, which is facilitated by synchronized oscillations between these areas. In rats, we determined the effects of systemic D1R blockade on CFC and oscillatory synchrony between dorsal hippocampus (DH), prelimbic (PL) cortex, basolateral amygdala (BLA), and ventral hippocampus (VH), which sends hippocampal projections to PL and BLA. D1R blockade altered DH–VH and reduced VH–PL and VH–BLA synchrony during CFC, as inferred from theta and gamma coherence and theta-gamma coupling. D1R blockade also impaired CFC, as indicated by decreased freezing at retrieval, which was characterized by altered DH–VH and reduced VH–PL, VH–BLA, and PL–BLA synchrony. This reduction in VH–PL–BLA synchrony was not fully accounted for by non-specific locomotor effects, as revealed by comparing between epochs of movement and freezing in the controls. These results suggest that D1Rs regulate CFC by modulating synchronized oscillations within the hippocampus–prefrontal–amygdala circuit. They also add to growing evidence indicating that this circuit synchrony at retrieval reflects a neural signature of learned fear.
Druh dokumentu: Article
Other literature type
Popis souboru: application/pdf
Jazyk: English
ISSN: 2045-2322
DOI: 10.1038/s41598-023-44772-6
DOI: 10.1101/2023.06.15.545080
Přístupová URL adresa: https://pubmed.ncbi.nlm.nih.gov/37848657
https://doaj.org/article/eae002c208e64f068bd882f77cb856c9
Rights: CC BY
Přístupové číslo: edsair.doi.dedup.....6714b7dcdd28ce10677587353e5f5b7b
Databáze: OpenAIRE
Popis
Abstrakt:Contextual fear conditioning (CFC) is mediated by a neural circuit that includes the hippocampus, prefrontal cortex, and amygdala, but the neurophysiological mechanisms underlying the regulation of CFC by neuromodulators remain unclear. Dopamine D1-like receptors (D1Rs) in this circuit regulate CFC and local synaptic plasticity, which is facilitated by synchronized oscillations between these areas. In rats, we determined the effects of systemic D1R blockade on CFC and oscillatory synchrony between dorsal hippocampus (DH), prelimbic (PL) cortex, basolateral amygdala (BLA), and ventral hippocampus (VH), which sends hippocampal projections to PL and BLA. D1R blockade altered DH–VH and reduced VH–PL and VH–BLA synchrony during CFC, as inferred from theta and gamma coherence and theta-gamma coupling. D1R blockade also impaired CFC, as indicated by decreased freezing at retrieval, which was characterized by altered DH–VH and reduced VH–PL, VH–BLA, and PL–BLA synchrony. This reduction in VH–PL–BLA synchrony was not fully accounted for by non-specific locomotor effects, as revealed by comparing between epochs of movement and freezing in the controls. These results suggest that D1Rs regulate CFC by modulating synchronized oscillations within the hippocampus–prefrontal–amygdala circuit. They also add to growing evidence indicating that this circuit synchrony at retrieval reflects a neural signature of learned fear.
ISSN:20452322
DOI:10.1038/s41598-023-44772-6