Nicotinic and muscarinic cholinergic receptors are recruited by acetylcholine-mediated neurotransmission within the locus coeruleus during the organisation of post-ictal antinociception

Oliveira, Reinaldo Cunha de; Oliveira, Ricardo de; Biagioni, Audrey Franceschi; Falconi‐Sobrinho, Luiz Luciano; Anjos‐Garcia, Tayllon dos; Coimbra, Norberto Cysne

doi:10.1016/j.brainresbull.2016.08.011

Cited by 6 publications

(2 citation statements)

References 42 publications

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“…Activation of M1/M3 mAChRs (m 1/3 AChRs) on these neurons increases their firing activity (Berridge & Abercrombie, 1999) and induces an inward cationic current that results in membrane depolarization (Li et al, 2016). Furthermore, local infusion of mAChR agonists into the LC has several effects on brain function and behaviour, including that mAChR activation in vivo increases an animal's arousal level as indicated by a change in electroencephalogram activity (Berridge & Foote, 1991), disengages an animal from its current task (Aston‐Jones et al, 1998; Aston‐Jones & Cohen, 2005; Usher et al, 1999), decreases pre‐pulse inhibition of auditory startle response (Alsene & Bakshi, 2011) and decreases post‐ictal antinociception (de Oliveira et al, 2016). Nevertheless, the exact underlying mechanisms are not well understood at the cellular and local circuitry levels.…”

Section: Introductionmentioning

confidence: 99%

Carbachol increases locus coeruleus activation by targeting noradrenergic neurons, inhibitory interneurons and inhibitory synaptic transmission

Kuo

Chan

Hung

et al. 2022

Eur J of Neuroscience

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The locus coeruleus (LC) consists of noradrenergic (NA) neurons and plays an important role in controlling behaviours. Although much of the knowledge regarding LC functions comes from studying behavioural outcomes upon administration of muscarinic acetylcholine receptor (mAChR) agonists into the nucleus, the exact mechanisms remain unclear. Here, we report that the application of carbachol (CCh), an mAChR agonist, increased the spontaneous action potentials (sAPs) of both LC‐NA neurons and local inhibitory interneurons (LC I‐INs) in acute brain slices by activating M1/M3 mAChRs (m1/3AChRs). Optogenetic activation of LC I‐INs evoked inhibitory postsynaptic currents (IPSCs) in LC‐NA neurons that were mediated by γ‐aminobutyric acid type A (GABAA) and glycine receptors, and CCh application decreased the IPSC amplitude through a presynaptic mechanism by activating M4 mAChRs (m4AChRs). LC‐NA neurons also exhibited spontaneous phasic‐like activity (sPLA); CCh application increased the incidence of this activity. This effect of CCh application was not observed with blockade of GABAA and glycine receptors, suggesting that the sPLA enhancement occurred likely because of the decreased synaptic transmission of LC I‐INs onto LC‐NA neurons by the m4AChR activation and/or increased spiking rate of LC I‐INs by the m1/3AChR activation, which could lead to fatigue of the synaptic transmission. In conclusion, we report that CCh application, while inhibiting their synaptic transmission, increases sAP rates of LC‐NA neurons and LC I‐INs. Collectively, these effects provide insight into the cellular mechanisms underlying the behaviour modulations following the administration of muscarinic receptor agonists into the LC reported by the previous studies.

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Section: Introductionmentioning

confidence: 99%

Carbachol increases locus coeruleus activation by targeting noradrenergic neurons, inhibitory interneurons and inhibitory synaptic transmission

Kuo

Chan

Hung

et al. 2022

Eur J of Neuroscience

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“…In particular, we focus on NE nuclei located within the lateral column of the bulbo-pontine RF and a mixed neuronal population within the dorsal raphe/periaqueductal gray (PAG), which contains a subset of NE and DA neurons (Battenberg and Bloom, 1975; Saavedra et al, 1976; Steinbusch et al, 1981; Nieuwenhuys et al, 1988; Baker et al, 1990, 1991; Lu et al, 2006; Li et al, 2016; Bucci et al, 2017; Cho et al, 2017). We also overview cholinergic cells placed in the lateral column of the pontine RF, which extend up to the lateral wings of the dorsal raphe (Satoh et al, 1983; Nieuwenhuys et al, 2007; Vasudeva and Waterhouse, 2014; de Oliveira et al, 2016). In detail, the dorsal raphe contains 5-HT neurons in all nuclear regions, while catecholamine and acetylcholine cells are placed in the most rostral extent of the dorsal raphe both in rodents and humans (Saavedra et al, 1976; Steinbusch et al, 1981; Baker et al, 1990, 1991; Nieuwenhuys et al, 2007; Mai and Paxinos, 2012; Li et al, 2016; Cho et al, 2017).…”

Section: Introductionmentioning

confidence: 99%

The Effects of Amphetamine and Methamphetamine on the Release of Norepinephrine, Dopamine and Acetylcholine From the Brainstem Reticular Formation

et al. 2019

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Amphetamine (AMPH) and methamphetamine (METH) are widely abused psychostimulants, which produce a variety of psychomotor, autonomic and neurotoxic effects. The behavioral and neurotoxic effects of both compounds (from now on defined as AMPHs) stem from a fair molecular and anatomical specificity for catecholamine-containing neurons, which are placed in the brainstem reticular formation (RF). In fact, the structural cross-affinity joined with the presence of shared molecular targets between AMPHs and catecholamine provides the basis for a quite selective recruitment of brainstem catecholamine neurons following AMPHs administration. A great amount of investigations, commentary manuscripts and books reported a pivotal role of mesencephalic dopamine (DA)-containing neurons in producing behavioral and neurotoxic effects of AMPHs. Instead, the present review article focuses on catecholamine reticular neurons of the low brainstem. In fact, these nuclei add on DA mesencephalic cells to mediate the effects of AMPHs. Among these, we also include two pontine cholinergic nuclei. Finally, we discuss the conundrum of a mixed neuronal population, which extends from the pons to the periaqueductal gray (PAG). In this way, a number of reticular nuclei beyond classic DA mesencephalic cells are considered to extend the scenario underlying the neurobiology of AMPHs abuse. The mechanistic approach followed here to describe the action of AMPHs within the RF is rooted on the fine anatomy of this region of the brainstem. This is exemplified by a few medullary catecholamine neurons, which play a pivotal role compared with the bulk of peripheral sympathetic neurons in sustaining most of the cardiovascular effects induced by AMPHs.

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The μ1-opioid receptor and 5-HT2A- and 5HT2C-serotonergic receptors of the locus coeruleus are critical in elaborating hypoalgesia induced by tonic and tonic–clonic seizures

et al. 2016

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Nicotinic and muscarinic cholinergic receptors are recruited by acetylcholine-mediated neurotransmission within the locus coeruleus during the organisation of post-ictal antinociception

Cited by 6 publications

References 42 publications

Carbachol increases locus coeruleus activation by targeting noradrenergic neurons, inhibitory interneurons and inhibitory synaptic transmission

Carbachol increases locus coeruleus activation by targeting noradrenergic neurons, inhibitory interneurons and inhibitory synaptic transmission

The Effects of Amphetamine and Methamphetamine on the Release of Norepinephrine, Dopamine and Acetylcholine From the Brainstem Reticular Formation

The μ1-opioid receptor and 5-HT2A- and 5HT2C-serotonergic receptors of the locus coeruleus are critical in elaborating hypoalgesia induced by tonic and tonic–clonic seizures

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