Differential regulation of levels of nicotinic receptor subunit transcripts in adult sympathetic neurons after axotomy

Zhou, Yuefang; Deneris, Evan S.; Zigmond, Richard E.

doi:10.1002/(sici)1097-4695(19980205)34:2<164::aid-neu6>3.0.co;2-0

Cited by 48 publications

(53 citation statements)

References 67 publications

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“…The transcript levels of ␣ 3 -, ␣ 5 -, ␣ 7 -and ␤ 4 -but not ␤ 2 -subunits in the SCG neurons have been shown to decrease in chronically denervated, but not decentralized, rat SCGs (11,48,51,52), suggesting that ␣ 3 ␤ 2 -nAChR and other subunits including ␣ 3 ␤ 4 -and ␣ 7 -nAChRs are located mainly on the postganglionic neurons of the SCGs. This finding allows a reasonable prediction that ␣ 3 ␤ 2 -nAChRs are present on the sympathetic nerve terminals on the arterial wall, mediating nicotine-induced cerebral neurogenic nitrergic vasodilation.…”

Section: Discussionmentioning

confidence: 98%

Sympathetic α₃β₂-nAChRs mediate cerebral neurogenic nitrergic vasodilation in the swine

Lee

Liu²,

Chen

et al. 2011

American Journal of Physiology-Heart and Circulatory Physiology

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Lee RH, Liu YQ, Chen PY, Liu CH, Chen MF, Lin HW, Kuo JS, Premkumar LS, Lee TJ. Sympathetic ␣3␤2-nAChRs mediate cerebral neurogenic nitrergic vasodilation in the swine. Am J Physiol Heart Circ Physiol 301: H344 -H354, 2011. First published May 2, 2011; doi:10.1152/ajpheart.00172.2011.-The ␣7-nicotinic ACh receptor (␣7-nAChR) on sympathetic neurons innervating basilar arteries of pigs crossed bred between Landrace and Yorkshire (LY) is known to mediate nicotine-induced, ␤-amyloid (A␤)-sensitive nitrergic neurogenic vasodilation. Preliminary studies, however, demonstrated that nicotine-induced cerebral vasodilation in pigs crossbred among Landrace, Yorkshire, and Duroc (LYD) was insensitive to A␤ and ␣-bungarotoxin (␣-BGTX). We investigated nAChR subtype on sympathetic neurons innervating LYD basilar arteries. Nicotine-induced relaxation of porcine isolated basilar arteries was examined by tissue bath myography, inward currents on nAChR-expressing oocytes by two-electrode voltage recording, and mRNA and protein expression in the superior cervical ganglion (SCG) and middle cervical ganglion (MCG) by reverse transcription PCR and Western blotting. Nicotine-induced basilar arterial relaxation was not affected by A␤, ␣-BGTX, and ␣-conotoxin IMI (␣7-nAChR antagonists), or ␣-conotoxin AuIB (␣3␤4-nAChR antagonist) but was inhibited by tropinone and tropane (␣3-containing nAChR antagonists) and ␣-conotoxin MII (selective ␣ 3␤2-nAChR antagonist). Nicotine-induced inward currents in ␣ 3␤2-nAChR-expressing oocytes were inhibited by ␣-conotoxin MII but not by ␣-BGTX, A␤, or ␣-conotoxin AuIB. mRNAs of ␣ 3-, ␣7-, ␤2-, and ␤4-subunits were expressed in both SCGs and MCGs with significantly higher mRNAs of ␣ 3-, ␤2-, and ␤ 4-subunits than that of ␣7-subunit. The A␤-insensitive sympathetic ␣ 3␤2-nAChR mediates nicotine-induced cerebral nitrergic neurogenic vasodilation in LYD pigs. The different finding from A␤-sensitive ␣ 7-nAChR in basilar arteries of LY pigs may offer a partial explanation for different sensitivities of individuals to A␤ in causing diminished cerebral nitrergic vasodilation in diseases involving A␤.␣ 3␤2-nicotinic ACh receptor; axo-axonal interaction; ␤-amyloid; cerebral perivascular sympathetic nerves; superior cervical ganglion IT IS WELL ESTABLISHED THAT cerebral arteries receive dense sympathetic innervation originating in the superior cervical ganglion (SCG) (24, 50) and that nicotinic ACh receptors (nAChRs) on the nerve terminals regulate norepinephrine (NE) release (50). In the pigs crossbred between Landrace and Yorkshire in the United States, activation by nicotinic agonists of the nAChRs on perivascular sympathetic nerves innervating cerebral arteries results in release of NE, which then causes release of nitric oxide (NO) from the nearby parasympathetic nitrergic nerves and dilation of the arteries (22, 39). This nicotinic agonist-induced axo-axonal interaction leading to nitrergic vasodilation is mediated by the ␣ 7 -nAChR subtype (39). The vasodilation is blocked by ␤-amyloid peptide (A␤) via inhib...

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Section: Discussionmentioning

confidence: 98%

Sympathetic α₃β₂-nAChRs mediate cerebral neurogenic nitrergic vasodilation in the swine

Lee

Liu²,

Chen

et al. 2011

American Journal of Physiology-Heart and Circulatory Physiology

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“…For example, denervation of neonatal rat superior cervical ganglion (SCG) neurons decreases all nAChR subunit mRNAs, but not ACh-induced current densities (Mandelzys et al, 1994). At later adult stages, however, the maintenance of mature nAChR subunit transcript levels may be less dependent on preganglionic tissue interactions (Fumagalli et al, 1978;Zhou et al, 1998). Studies of frog sympathetic and parasympathetic ganglia also show that whole-cell ACh-sensitivity is not altered by deafferentation (Dunn and Marshall, 1985;Streichert and Sargent, 1992).…”

Section: Maintenance Of Nachr Expression Requires Innervationmentioning

confidence: 99%

“…The large declines in AChinduced currents caused by axotomy are in sharp contrast to the lack of change after denervation. Similarly, postganglionic axotomy or nerve crush of the adult rodent SCG causes large reductions in synaptic transmission and expression of nAChR subunits (Purves, 1975;Fumagalli and De Renzis, 1980;Zhou et al, 1998Zhou et al, , 2001Yeh et al, 2001;Zaccaria et al, 2001).…”

Section: Maintenance Of Nachrs Also Requires Target Tissue Interactionsmentioning

confidence: 99%

Regulatory mechanisms that govern nicotinic synapse formation in neurons

et al. 2002

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Individual cholinoceptive neurons express high levels of different neuronal nicotinic acetylcholine receptor (nAChR) subtypes, and target them to the appropriate synaptic regions for proper function. This review focuses on the intercellular and intracellular processes that regulate nAChR expression in vertebrate peripheral nervous system (PNS) and central nervous system (CNS) neurons. Specifically, we discuss the cellular and molecular mechanisms that govern the induction and maintenance of nAChR expression-innervation, target tissue interactions, soluble factors, and activity. We define the regulatory principles of interneuronal nicotinic synapse differentiation that have emerged from these studies. We also discuss the molecular players that target nAChRs to the surface membrane and the interneuronal synapse.

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“…Postganglionic nerve transection of the adult rat SCG leads to a decrease in the transcript levels of ␤4 subunits in SCG neurons. In contrast, ␤2 transcripts remain almost at the control level and may even slightly increase 3 days after postganglionic axotomy (Zhou et al, 1998). ␤ subunits contribute to the nAChR channels and ACh-binding sites, which are believed to be at interfaces between ␣ and ␤ subunits.…”

mentioning

confidence: 97%

“…However, only 5 of the 12 nAChR subunits (␣3, ␣5, ␣7, ␤2, and ␤4) are known to exist in autonomic ganglia (Mandelzys et al, 1994;Zhou et al, 1998;Devay et al, 1999;Nelson and Lindstrom, 1999;Erkman et al, 2000), and they are not distributed homogenously (Covernton et al, 1994;Klimaschewski et al, 1994;Poth et al, 1997;Sivilotti et al, 1997). Different nAChR subunit combinations are spatially segregated from each other in discrete membrane microregions relative to synapses (Horch and Sargent, 1995;Poth et al, 1997;Shoop et al, 1999).…”

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confidence: 99%

Deficiency of Nicotinic Acetylcholine Receptor β4 Subunit Causes Autonomic Cardiac and Intestinal Dysfunction

et al. 2003

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Neuronal nicotinic acetylcholine receptors (nAChR) are composed of 12 subunits (␣2-␣10 and ␤2-␤4), which play the central role in autonomic transmission. ␤4 subunits are abundantly expressed in autonomic ganglia, forming acetylcholine binding sites and ion channels with ␣3 or ␣3 and ␣5 subunits as pentameric receptors. To investigate the physiological and pharmacological properties of ␤4 subunits in autonomic ganglia, we measured autonomic functions in knockout mice lacking nAChR subunit ␤4 (␤4 Ϫ/Ϫ ) and wild-type mice. ␤4 Ϫ/Ϫ mice had an attenuated bradycardiac response to high frequency (60 pulse/s) vagal stimulation, as well as an increased sensitivity to hexamethonium blockade at low dose (3 mg/kg) and a reduced ileal contractile response to the nicotinic agonists cytisine, dimethylphenylpiperazinium iodide, nicotine (10 mg/kg each), and epibatidine (0.1 mg/kg). The results suggest that ␤4 subunits are important components of nAChRs in autonomic ganglia. Deficiency of ␤4 subunits altered ion channel properties, conductance, and sensitivity and affinity of receptors to agonists and antagonists, affecting ganglionic transmission.

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Differential regulation of levels of nicotinic receptor subunit transcripts in adult sympathetic neurons after axotomy

Cited by 48 publications

References 67 publications

Sympathetic α₃β₂-nAChRs mediate cerebral neurogenic nitrergic vasodilation in the swine

Sympathetic α₃β₂-nAChRs mediate cerebral neurogenic nitrergic vasodilation in the swine

Regulatory mechanisms that govern nicotinic synapse formation in neurons

Deficiency of Nicotinic Acetylcholine Receptor β4 Subunit Causes Autonomic Cardiac and Intestinal Dysfunction

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Differential regulation of levels of nicotinic receptor subunit transcripts in adult sympathetic neurons after axotomy

Cited by 48 publications

References 67 publications

Sympathetic α3β2-nAChRs mediate cerebral neurogenic nitrergic vasodilation in the swine

Sympathetic α3β2-nAChRs mediate cerebral neurogenic nitrergic vasodilation in the swine

Regulatory mechanisms that govern nicotinic synapse formation in neurons

Deficiency of Nicotinic Acetylcholine Receptor β4 Subunit Causes Autonomic Cardiac and Intestinal Dysfunction

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Sympathetic α₃β₂-nAChRs mediate cerebral neurogenic nitrergic vasodilation in the swine

Sympathetic α₃β₂-nAChRs mediate cerebral neurogenic nitrergic vasodilation in the swine