Ethanol inhibits histaminergic neurons in mouse tuberomammillary nucleus slices via potentiating GABAergic transmission onto the neurons at both pre- and postsynaptic sites

Sun, Yu; Jiang, Shiyu; Ni, Jian; Luo, Yan-Jia; Chen, Chang-Rui; Zhao, Hong; Yanagawa, Yuchio; Qu, Wei‐Min; Wang, Lu; Huang, Zhi‐Li

doi:10.1038/aps.2016.66

Cited by 6 publications

(3 citation statements)

References 46 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…In this study, we found that ethanol significantly increased the frequency and the amplitude of sIPSCs and mIPSCs in LPB neurons. This finding was consistent with other studies demonstrating ethanol-mediated presynaptic enhancement of action potential-dependent sIPSCs and action potential-independent mIPSCs, such as tuberomammillary nucleus [12], the hippocampus [8,17], and the central amygdala, as well as in the ventral tegmental area [18]. And these nuclei are involved in the regulation of hypnosis, memory loss, anxiety or drug addiction, which correspond to the possible symptoms of acute and chronic drinkers.…”

Section: Discussionsupporting

confidence: 93%

“…The inhibitory effect of ethanol on the firing rate of LPB neurons is similar to that of commonly used anesthetics in clinical practice [9,12,13]. It is accepted that GABA A -Rs are the ligand-gated Cl - channels widely distributed throughout the CNS, have long been appreciated as potential targets of general anesthetics [14–16].…”

Section: Discussionmentioning

confidence: 93%

“…And these nuclei are involved in the regulation of hypnosis, memory loss, anxiety or drug addiction, which correspond to the possible symptoms of acute and chronic drinkers. A change in the frequency of mIPSCs implies an altered probability of transmitter release at the presynaptic site and that a change in the amplitude of mIPSCs reflects alterations in the sensitivity of postsynaptic receptors [8,12]. Therefore, these results suggested that ethanol acts on LPB neurons via potentiating GABAergic transmission onto the neurons at both presynaptic site and postsynaptic site.…”

Section: Discussionmentioning

confidence: 99%

See 2 more Smart Citations

Ethanol depresses neurons in the lateral parabrachial nucleus by potentiating pre- and postsynaptic GABAA receptors

et al. 2023

View full text Add to dashboard Cite

As a psychoactive substance, ethanol is widely used in people’s life. However, the neuronal mechanisms underlying its sedative effect remain unclear. In this study, we investigated the effects of ethanol on the lateral parabrachial nucleus (LPB), which is a novel component related to sedation. Coronal brain slices (280 μm thick) containing the LPB were prepared from C57BL/6J mice. The spontaneous firing and membrane potential of LPB neurons, and GABAergic transmission onto these neurons were recorded using whole-cell patch-clamp recordings. Drugs were applied through superfusion. The LPB neurons exhibited a regular spontaneous discharge at a rate of 1.5–3 Hz without burst firing. Brief superfusion of ethanol (30, 60, and 120 mM) concentration-dependently and reversibly suppressed the spontaneous firing of the neurons in LPB. In addition, when synaptic transmission was blocked by tetrodotoxin (TTX) (1 μM), ethanol (120 mM) caused hyperpolarization of the membrane potential. Furthermore, superfusion of ethanol markedly increased the frequency and amplitude of spontaneous and miniature inhibitory postsynaptic currents, which were abolished in the presence of the GABAA receptor (GABAA-R) antagonist picrotoxin (100 μM). In addition, the inhibitory effect of ethanol on the firing rate of LPB neurons was completely abolished by picrotoxin. Ethanol inhibits the excitability of LPB neurons in mouse slices, possibly via potentiating GABAergic transmission onto the neurons at pre- and postsynaptic sites.

show abstract