Coexpression and Spatial Association of Nicotinic Acetylcholine Receptor Subunits α7 and α10 in Rat Sympathetic Neurons

Lips, Katrin Susanne; König, Peter; Schätzle, Katrin; Pfeil, Uwe; Krasteva, Gabriela; Spies, Markus; Haberberger, Rainer Viktor; Grando, Sergei A.; Kummer, Wolfgang

doi:10.1385/jmn:30:1:15

Cited by 26 publications

(29 citation statements)

References 7 publications

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“…In vitro, acetylcholine and other cholinergic agonists attenuate LPSinduced TNF in human and mouse macrophages and in mouse splenocytes through an ␣7-dependent mechanism (2, 4). The nicotinic acetylcholine receptor subunit ␣7 is expressed in autonomic ganglia (42), where it mediates fast synaptic transmission (43). It is possible that acetylcholine released by the vagus nerve acts on ␣7 expressed in the ganglia of the celiacsuperior mesenteric plexus to modulate splenic nerve function.…”

Section: Discussionmentioning

confidence: 99%

Splenic nerve is required for cholinergic antiinflammatory pathway control of TNF in endotoxemia

Rosas-Ballina¹,

Ochani²,

Parrish³

et al. 2008

Proc. Natl. Acad. Sci. U.S.A.

608

569

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The autonomic nervous system maintains homeostasis through its sympathetic and parasympathetic divisions. During infection, cells of the immune system release cytokines and other mediators that cause fever, hypotension, and tissue injury. Although the effect of cytokines on the nervous system has been known for decades, only recently has it become evident that the autonomic nervous system, in turn, regulates cytokine production through neural pathways. We have previously shown that efferent vagus nerve signals regulate cytokine production through the nicotinic acetylcholine receptor subunit ␣7, a mechanism termed ''the cholinergic antiinflammatory pathway.'' Here, we show that vagus nerve stimulation during endotoxemia specifically attenuates TNF production by spleen macrophages in the red pulp and the marginal zone. Administration of nicotine, a pharmacological agonist of ␣7, attenuated TNF immunoreactivity in these specific macrophage subpopulations. Synaptophysin-positive nerve endings were observed in close apposition to red pulp macrophages, but they do not express choline acetyltransferase or vesicular acetylcholine transporter. Surgical ablation of the splenic nerve and catecholamine depletion by reserpine indicate that these nerves are catecholaminergic and are required for functional inhibition of TNF production by vagus nerve stimulation. Thus, the cholinergic antiinflammatory pathway regulates TNF production in discrete macrophage populations via two serially connected neurons: one preganglionic, originating in the dorsal motor nucleus of the vagus nerve, and the second postganglionic, originating in the celiacsuperior mesenteric plexus, and projecting in the splenic nerve.brain ͉ cytokine ͉ innate ͉ spleen ͉ vagus T he autonomic nervous system is divided into two major branches based on anatomy and function. These divisions, sympathetic and parasympathetic, control organ function through a set of two serially connected neurons, the first of which is located in the CNS and the second in the peripheral ganglia. Typically, parasympathetic neurons originate in the brainstem medulla and sacral portion of the spinal cord, and the ganglia are located close to or within the innervated organ. Sympathetic neurons originate in the thoracic and lumbar portion of the spinal cord, and the ganglia are situated close to the spinal cord.

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Section: Discussionmentioning

confidence: 99%

Splenic nerve is required for cholinergic antiinflammatory pathway control of TNF in endotoxemia

Rosas-Ballina¹,

Ochani²,

Parrish³

et al. 2008

Proc. Natl. Acad. Sci. U.S.A.

608

569

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“…Whereas it seemed likely that functional expression of α7nAChR by macrophages and cytokine-producing cells accounted for the mechanism, it could not be ruled out that α7nAChR expressed in the brain and autonomic ganglia (23,24) was required to complete the cholinergic antiinflammatory circuit. For instance, vagus nerve stimulation in an intact animal elicits both efferent and afferent signals, and it would be conceivable that α7nAChRs in the central nervous system are involved in processing of afferent signals that ultimately result in efferent activity in the contralateral vagus or other nerves.…”

Section: Discussionmentioning

confidence: 99%

α7 Nicotinic Acetylcholine Receptor (α7nAChR) Expression in Bone Marrow-Derived Non-T Cells Is Required for the Inflammatory Reflex

Olofsson

Katz

Rosas-Ballina

et al. 2011

Mol Med

133

110

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“…Based on the blocking effects of ␣-RgIA and hexamethonium, ␣3 nAChRs appear to preferentially mediate sEPSCs in control rats, as previously reported (Barbara and Takeda, 1996), whereas ␣9-containing nAChRs predominantly mediate sEPSCs in cold-stressed rats. The contribution of ␣7 nAChRs needs further investigation, keeping in mind that ␣7 and ␣10 subunits can be spatially associated (Lips et al, 2006). The involvement of ␣7 nAChRs in adrenal synaptic transmission has been evidenced by the blocking effect of ␣-bungarotoxin (␣-Bgt) on sEPSCs (Martin et al, 2003).…”

Section: Discussionmentioning

confidence: 99%

Functional Characterization of α9-Containing Cholinergic Nicotinic Receptors in the Rat Adrenal Medulla: Implication in Stress-Induced Functional Plasticity

Colomer

Olivos-Oré²,

Vincent³

et al. 2010

J. Neurosci.

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An increase in circulating adrenal catecholamine levels constitutes one of the mechanisms whereby organisms cope with stress. Accordingly, stimulus-secretion coupling within the stressed adrenal medullary tissue undergoes persistent remodeling. In particular, cholinergic synaptic neurotransmission between splanchnic nerve terminals and chromaffin cells is upregulated in stressed rats. Since synaptic transmission is mainly supported by activation of postsynaptic neuronal acetylcholine nicotinic receptors (nAChRs), we focused our study on the role of ␣9-containing nAChRs, which have been recently described in chromaffin cells. Taking advantage of their specific blockade by the ␣-conotoxin RgIA (␣-RgIA), we unveil novel functional roles for these receptors in the stimulus-secretion coupling of the medulla. First, we show that in rat acute adrenal slices, ␣9-containing nAChRs codistribute with synaptophysin and significantly contribute to EPSCs. Second, we show that these receptors are involved in the tonic inhibitory control exerted by cholinergic activity on gap junctional coupling between chromaffin cells, as evidenced by an increased Lucifer yellow diffusion within the medulla in ␣-RgIA-treated slices. Third, we unexpectedly found that ␣9-containing nAChRs dominantly (Ͼ70%) contribute to acetylcholine-induced current in cold-stressed rats, whereas ␣3 nAChRs are the main contributing channels in unstressed animals. Consistently, expression levels of ␣9 nAChR transcript and protein are overexpressed in cold-stressed rats. As a functional relevance, we propose that upregulation of ␣9-containing nAChR channels and ensuing dominant contribution in cholinergic signaling may be one of the mechanisms whereby adrenal medullary tissue appropriately adapts to increased splanchnic nerve electrical discharges occurring in stressful situations.

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Coexpression and Spatial Association of Nicotinic Acetylcholine Receptor Subunits α7 and α10 in Rat Sympathetic Neurons

Cited by 26 publications

References 7 publications

Splenic nerve is required for cholinergic antiinflammatory pathway control of TNF in endotoxemia

Splenic nerve is required for cholinergic antiinflammatory pathway control of TNF in endotoxemia

α7 Nicotinic Acetylcholine Receptor (α7nAChR) Expression in Bone Marrow-Derived Non-T Cells Is Required for the Inflammatory Reflex

Functional Characterization of α9-Containing Cholinergic Nicotinic Receptors in the Rat Adrenal Medulla: Implication in Stress-Induced Functional Plasticity

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