Effects of acetylcholine and GABA on neurons in the area postrema of Suncus murinus brainstem slices

Strominger, Norman L.; Hori, Nobuaki; Carpenter, David O.; Tan, Yi; Folger, Walter

doi:10.1016/s0304-3940(01)02049-3

Cited by 8 publications

(3 citation statements)

References 17 publications

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“…These findings have been extended to show increased ACh release in the cerebral cortex of rats exposed for 1 h with 75% N 2 O [63]. The area postrema is one of the major centres involved in emesis and can be stimulated by acetylcholine [64]. This increased cholinergic output has been postulated to underlie the increased nausea and vomiting often accompanying N 2 O administration.…”

Section: Mechanisms Of Neurotoxicitymentioning

confidence: 99%

The Neurotoxicity of Nitrous Oxide: The Facts and “Putative” Mechanisms

Savage

2014

Brain Sciences

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Nitrous oxide is a widely used analgesic agent, used also in combination with anaesthetics during surgery. Recent research has raised concerns about possible neurotoxicity of nitrous oxide, particularly in the developing brain. Nitrous oxide is an N-methyl-d-aspartate (NMDA)-antagonist drug, similar in nature to ketamine, another anaesthetic agent. It has been linked to post-operative cardiovascular problems in clinical studies. It is also widely known that exposure to nitrous oxide during surgery results in elevated homocysteine levels in many patients, but very little work has investigated the long term effect of these increased homocysteine levels. Now research in rodent models has found that homocysteine can be linked to neuronal death and possibly even cognitive deficits. This review aims to examine the current knowledge of mechanisms of action of nitrous oxide, and to describe some pathways by which it may have neurotoxic effects.

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Section: Mechanisms Of Neurotoxicitymentioning

confidence: 99%

The Neurotoxicity of Nitrous Oxide: The Facts and “Putative” Mechanisms

Savage

2014

Brain Sciences

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“…Ionophoretic pulses of ACh, NMDA, AMPA or GABA were delivered for 1 s through an independent multi-barrelled micropipette placed in proximity to the recording neuron (Strominger et al, 2001). Intracellular membrane potentials were also recorded with microelectrodes from DMV neurons in response to electrical field stimulation (EFS) applied to the AP area.…”

Section: Electrical Measurementsmentioning

confidence: 99%

“…excitation of AP neurons, we used single neurons isolated from AP and applied conventional whole-cell patch clamp recording. Since it is known that AP neurons do not possess mAChR (Strominger et al, 2001), we used nicotine in the following experiments. As shown in Fig.…”

Section: Effects Of Z-338 On the Actions Of Nicotine Ka Nmda And Atmentioning

confidence: 99%

Effects of Z-338, a novel gastroprokinetic agent, on the actions of excitatory and inhibitory neurotransmitters on neurons in area postrema

Akaike

Jang

Hori

et al. 2010

J. Smooth Muscle Res.

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We investigated the effects of the novel gastroprokinetic agent Z-338 on the actions of excitatory and inhibitory neurotransmitters on neurons in area postrema (AP). Iontophoretic applications of acetylcholine (ACh), AMPA and NMDA increased, while GABA suppressed the firing rates of AP neurons recorded by extracellular electrodes. Z-338 (10 µM) suppressed the ACh-induced acceleratory and GABA-induced inhibitory actions without affecting the excitatory actions of AMPA and NMDA. Under voltageclamp conditions, nicotine, NMDA, kainic acid (KA) and ATP evoked inward currents in dissociated single AP neurons recorded by whole-cell patch clamp technique, and GABA produced outward currents, at holding potentials (VH) of -60 or 0 mV. Z-338 (>3 µM) specifically suppressed the nicotine-and GABA-induced currents without affecting the currents induced by NMDA, KA and ATP. In addition, we found that Z-338 (30 µM) suppressed the spontaneous inhibitory postsynaptic currents (sIPSCs) recorded from AP neurons in slice preparations. Experiments with microelectrode and histochemical methods revealed the presence of direct excitatory and di-synaptic inhibitory neural connections from AP to dorsal motor nucleus of the vagus (DMV). In some AP neurons, Z-338 (10 µM) enhanced the spontaneous firing rates recorded by extracellular electrode.The excitatory or inhibitory effects of Z-338 on the firing rates or actions of nicotine and GABA on AP neurons observed in the present study may explain the postmeal relaxation induced by Z-338 in patients with functional dyspepsia.

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Nicotinic modulation of area postrema neuronal excitability in rat brain slices

Funahashi¹,

Mitoh²,

Matsuo³

2004

Brain Research

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We investigated the functions of nicotinic receptor activation on area postrema neurons by making whole-cell recordings in rat brainstem slices. Excitatory responses to nicotine application were found in approximately 78% (35/45) of all cells tested. Responsive cells included both the cells that display the hyperpolarization-activated cation current (I(h)) and cells that do not display I(h). An inhibitory effect of nicotine was never seen. Current-clamp recordings showed the nicotine-induced depolarization of a cell's membrane potential that could be sufficient to cause spontaneous firing. In voltage-clamp recordings, many cells showed nicotine-induced inward currents (18.3+/-3.2 pA, n=6) that persisted during pharmacological blockade of synaptic transmission (e.g., zero [Ca(2+)](out) and 5 mM [Mg(2+)](out), n=6/8). Other two cells, however, showed increases in the frequency of excitatory postsynaptic currents (EPSCs), which were blocked by CNQX (n=2/8). We analyzed miniature EPSCs (mEPSCs) recorded from cells that showed no inward currents but marked increases in the frequency of mEPSCs (0.8+/-0.2 to 4.8+/-1.7 Hz, n=4) during nicotine application. Nicotine augmented mEPSC amplitude (n=4); however, amplitude distribution was not significantly changed in two of four cells tested. We conclude that nicotinic receptors in the rat area postrema can excite cells via (1) a direct post- and/or extrasynaptic mechanism; and (2) an indirect enhancement of glutamate release.

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Effects of acetylcholine and GABA on neurons in the area postrema of Suncus murinus brainstem slices

Cited by 8 publications

References 17 publications

The Neurotoxicity of Nitrous Oxide: The Facts and “Putative” Mechanisms

The Neurotoxicity of Nitrous Oxide: The Facts and “Putative” Mechanisms

Effects of Z-338, a novel gastroprokinetic agent, on the actions of excitatory and inhibitory neurotransmitters on neurons in area postrema

Nicotinic modulation of area postrema neuronal excitability in rat brain slices

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