Nicotine elicits changes in expression of adrenal catecholamine biosynthetic enzymes, neuropeptide Y and immediate early genes by injection but not continuous administration

Hiremagalur, Bhargava; Sabban, Esther L.

doi:10.1016/0169-328x(95)00068-4

Cited by 61 publications

(39 citation statements)

References 25 publications

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“…However, recent studies have indicated that a single injection of nicotine does induce adrenal TH mRNA (Hiremagalur and Sabban, 1995;Serova et al, 1999), although in these reports it was not determined whether a single nicotine injection induces TH protein or enzymatic activity. The studies in this article were undertaken to investigate these discrepancies and to test the hypothesis that chronic nicotine treatment results in sustained stimulation of the TH gene leading to the observed changes in TH expression.…”

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confidence: 77%

“…An early report showed that nicotine, when it is administered twice daily for 14 days, induces adrenal TH activity (Seidler and Slotkin, 1976). More recently, it has been shown that nicotine induces adrenal TH mRNA, when it is injected subcutaneously once or twice daily for 3 to 5 days, but not when it is administered by continuous infusion for up to 27 days (Stachowiak et al, 1988;Hiremagalur and Sabban, 1995;Serova et al, 1999). This latter result suggests that the induction of adrenal TH is dependent on intermittent, repetitive exposure to nicotine.…”

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confidence: 99%

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Chronic Nicotine Treatment Leads to Sustained Stimulation of Tyrosine Hydroxylase Gene Transcription Rate in Rat Adrenal Medulla

Sun

Sterling²,

Tank³

2003

J Pharmacol Exp Ther

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Nicotine is a powerful stimulant of the sympathoadrenal system, causing the release of peripheral catecholamines and activation of catecholamine biosynthesis. In previous reports, we have studied the mechanisms by which short-term nicotine treatment regulates tyrosine hydroxylase (TH) in adrenal medulla. In this report, we study the effects of chronic nicotine treatment on adrenal TH gene expression. Rats were injected with either saline or nicotine twice per day for up to 14 days. Chronic nicotine treatment elicited long-lasting, dose-dependent increases in the levels of adrenal TH mRNA, TH protein, and TH activity. In contrast, a single injection of nicotine elicited only a small increase in adrenal TH mRNA levels, which was transient and did not result in the induction of TH enzyme.Chronic nicotine administration also elicited a sustained increase in adrenal TH gene transcription rate, which persisted for up to 7 days after the final nicotine injection. This sustained transcriptional response correlated with a modest sustained increase in adrenal TH AP1 binding, but not in the levels of Fra-2 or other fos or jun proteins. These results demonstrate that repeated nicotine injections administered chronically over 1 to 2 weeks lead to sustained stimulation of the TH gene and consequent induction of TH gene expression in rat adrenal medulla. These studies support the hypothesis that chronic nicotine administration produces long-lasting cellular changes in adrenal medulla that lead to sustained transcriptional responses.

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confidence: 77%

mentioning

confidence: 99%

Chronic Nicotine Treatment Leads to Sustained Stimulation of Tyrosine Hydroxylase Gene Transcription Rate in Rat Adrenal Medulla

Sun

Sterling²,

Tank³

2003

J Pharmacol Exp Ther

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“…Tyrosine hydroxylase (TH) is induced in the adrenal medulla following several different stimuli, including prolonged stress (Kvetnansky et al, 1970;Thoenen, 1970;Kvetnansky and Sabban, 1993), treatment with catecholamine-depleting drugs, like reserpine Thoenen et al, 1969), chronic electroconvulsive shock (Masserano et al, 1981), and treatment with nicotine (Fossom et al, 1991a;Hiremagalur and Sabban, 1995;Jahng et al, 1997). The increases in adrenal TH protein elicited by these stimuli are usually preceded by induction of TH mRNA and stimulation of TH gene transcription rate (Tank et al, 1985;Faucon Biguet et al, 1986;Fossom et al, 1991a;Osterhout et al, 1997).…”

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confidence: 99%

Regulation of Tyrosine Hydroxylase Gene Expression by Muscarinic Agonists in Rat Adrenal Medulla

1999

Journal of Neurochemistry

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Tyrosine hydroxylase (TH) gene expression in the adrenal medulla is regulated by numerous stimuli via transsynaptic mechanisms. The adrenal chromaffin cell receptors that mediate this transsynaptic response remain unidentified. In this report we demonstrate that the muscarinic acetylcholine receptor agonist bethanechol stimulates the TH gene transcription rate in both innervated and denervated adrenal glands. Hence, this muscarinic response is not dependent on transsynaptic influences, suggesting that agonist occupation of adrenal chromaffin cell muscarinic receptors is sufficient to activate intracellular signaling pathways that stimulate the TH gene. When bethanechol is administered repeatedly over a 3-h interval (four injections spaced 1 h apart), TH mRNA levels are increased two-to threefold at 6 and 12 h after the initial injection of drug. It is surprising that this induction of TH mRNA does not lead to increases in TH activity or TH protein level. These results are consistent with the hypothesis that both transcriptional and posttranscriptional mechanisms must be regulated to induce TH protein and that muscarinic agonists activate only a subset of these mechanisms.

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“…Enkephalins (64) and catecholamine biosynthetic enzymes (tyrosine hydroxylase, dopamine ␤-hydroxylase, and phenylethanolamine-N-methyltransferase) are up-regulated in response to nicotinic cholinergic stimulation (7,29,66,67). Nicotine can also function centrally to activate tyrosine hydroxylase in the adrenal medulla, both transcriptionally and posttranslationally (67).…”

Section: Stimulus-transcription Coupling In Vivo and The Role Of Nicomentioning

confidence: 99%

“…Besides stimulation of neurotransmitter release, nicotine triggers expression of genes encoding enzymes involved in neurotransmitter synthesis such as tyrosine hydroxylase (26), neurotransmitter transporters such as the vesicular acetylcholine transporter (27), neuropeptides such as neuropeptide Y (28), and transcription factors such as c-Fos and the cAMP-response element-binding protein (29). FIG.…”

Section: Stimulus-transcription Coupling In Brain After Direct Nicotimentioning

confidence: 99%

Catecholamine Secretory Vesicle Stimulus-Transcription Coupling in Vivo

Mahata¹,

Mahapatra²,

Mahata³

et al. 2003

Journal of Biological Chemistry

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Stimulation of the splanchnic (efferent, preganglionic sympathetic) nerves innervating the adrenal medulla and sympathetic postganglionic axons releases multiple neurotransmitters, including acetylcholine (acting on neuronal nicotinic cholinergic receptors), ATP, and chromogranin A, precursor of the catecholamine release inhibitory peptide "catestatin" (bovine chromogranin A 344 -364 ) (1).Chromogranin A, the major soluble protein in the core of amine and peptide hormone and neurotransmitter secretory vesicles (2, 3), plays both intracellular and extracellular roles. Within the catecholamine storage vesicle, chromogranin A plays a necessary role in vesiculogenesis and the ability to conduct regulated catecholamine secretion (4). Its extracellular roles derive from its biologically active proteolytic cleavage fragments (3): the catecholamine release-inhibitory fragment catestatin (bovine chromogranin A 344 -364 ) (1), the vasodilator vasostatin (bovine chromogranin A 1-76 ) (5), and the dysglycemic peptide pancreastatin (porcine chromogranin A 240 -288 ) (6).When secretory stimuli (such as acetylcholine interacting with nicotinic cholinergic receptors) trigger transmitter release from chromaffin cells or sympathetic axons, is the resynthesis of just released transmitters also initiated by the secretory stimulus? We have characterized this process (sometimes called "stimulus-secretion-synthesis coupling" or "stimulustranscription coupling") in chromaffin cells in vitro (7-9) and established transcriptional activation of chromogranin A by nicotinic cholinergic (physiologic pathway) stimulation. The process occurs at the level of transcript initiation (7), requires particular elements in cis in the proximal promoter (7), and has well defined signal transduction pathways in trans (8, 9). However, whether this nicotinic cholinergic stimulation of chromogranin A occurs in vivo is uncertain.We therefore set out to explore whether chromaffin cell stimulus-transcription coupling (specifically nicotinic cholinergic transcriptional stimulation of chromogranin A) occurs in vivo. To test this possibility, we employed a transgenic strain in which a mouse chromogranin A 4.8-kbp proximal promoter drives the expression of firefly luciferase, an extraordinarily sensitive reporter of gene expression (10 -12). In the in vivo experiments reported here, we used nicotine (mimicking the autonomic ganglionic transmitter acetylcholine) and reserpine (indirect stimulation by vesicular depletion) to evoke cate-

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Nicotine elicits changes in expression of adrenal catecholamine biosynthetic enzymes, neuropeptide Y and immediate early genes by injection but not continuous administration

Cited by 61 publications

References 25 publications

Chronic Nicotine Treatment Leads to Sustained Stimulation of Tyrosine Hydroxylase Gene Transcription Rate in Rat Adrenal Medulla

Chronic Nicotine Treatment Leads to Sustained Stimulation of Tyrosine Hydroxylase Gene Transcription Rate in Rat Adrenal Medulla

Regulation of Tyrosine Hydroxylase Gene Expression by Muscarinic Agonists in Rat Adrenal Medulla

Catecholamine Secretory Vesicle Stimulus-Transcription Coupling in Vivo

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