Dopamine D1 Receptor in the Nucleus Accumbens Modulates the Emergence from Propofol Anesthesia in Rat

It has been reported that systemic activation of D1 receptors promotes emergence from isoflurane-induced unconsciousness, suggesting that the central dopaminergic system is involved in the process of recovering from general anesthesia. The nucleus accumbens (NAc) contains abundant GABAergic medium s...

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Vydané v:Neurochemical research Ročník 46; číslo 6; s. 1435 - 1446
Hlavní autori: Zhang, Yi, Gui, Huan, Duan, Zikun, Yu, Tian, Zhang, Jie, Liang, Xiaoli, Liu, Chengxi
Médium: Journal Article
Jazyk:English
Vydavateľské údaje: New York Springer US 01.06.2021
Springer Nature B.V
Predmet:
Agonists
Anesthesia
Anesthetics, Intravenous - pharmacology
Animals
Arousal - physiology
Biochemistry
Biomedical and Life Sciences
Biomedicine
Cell Biology
Dopamine
Dopamine D1 receptors
EEG
GABAergic Neurons - drug effects
GABAergic Neurons - metabolism
General anesthesia
Inhibitory postsynaptic potentials
Inhibitory Postsynaptic Potentials - physiology
Isoflurane
Male
Microinjection
Modulation
Neurochemistry
Neurology
Neurosciences
Nuclei (cytology)
Nucleus accumbens
Nucleus Accumbens - cytology
Nucleus Accumbens - drug effects
Nucleus Accumbens - metabolism
Original Paper
Photometry
Propofol
Propofol - pharmacology
Rats
Rats, Sprague-Dawley
Receptors
Receptors, Dopamine D1 - metabolism
Sleep and wakefulness
Spiny neurons
Unconsciousness
γ-Aminobutyric acid
Nucleus accumbens
General anesthesia
Propofol
Dopamine D1 receptor
Patch-clamp
ISSN:0364-3190, 1573-6903, 1573-6903
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Shrnutí:It has been reported that systemic activation of D1 receptors promotes emergence from isoflurane-induced unconsciousness, suggesting that the central dopaminergic system is involved in the process of recovering from general anesthesia. The nucleus accumbens (NAc) contains abundant GABAergic medium spiny neurons (MSNs) expressing the D1 receptor (D1R), which plays a key role in sleep–wake behavior. However, the role of NAc D1 receptors in the process of emergence from general anesthesia has not been identified. Here, using real-time in vivo fiber photometry, we found that neuronal activity in the NAc was markedly disinhibited during recovery from propofol anesthesia. Subsequently, microinjection of a D1R selective agonist (chloro-APB hydrobromide) into the NAc notably reduced the time to emerge from propofol anesthesia with a decrease in δ-band power and an increase in β-band power evident in the cortical electroencephalogram. These effects were prevented by pretreatment with a D1R antagonist (SCH-23390). Whole-cell patch clamp recordings were performed to further explore the cellular mechanism underlying the modulation of D1 receptors on MSNs under propofol anesthesia. Our data primarily demonstrated that propofol increased the frequency and prolonged the decay time of spontaneous inhibitory postsynaptic currents (sIPSCs) and miniature IPSCs (mIPSCs) of MSNs expressing D1 receptors. A D1R agonist attenuated the effect of propofol on the frequency of sIPSCs and mIPSCs, and the effects of the agonist were eliminated by preapplication of SCH-23390. Collectively, these results indicate that modulation of the D1 receptor on the activity of NAc MSNs is vital for emergence from propofol-induced unconsciousness.
Bibliografia:ObjectType-Article-1
SourceType-Scholarly Journals-1
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ISSN:0364-3190
1573-6903
1573-6903
DOI:10.1007/s11064-021-03284-3