Elevation of RNA Coding for Tyrosine Hydroxylase in Rat Adrenal Gland by Reserpine Treatment and Exposure to Cold

Aw, Tank; Ej, Lewis; Chikaraishi, DM; Weiner, Norman

doi:10.1111/j.1471-4159.1985.tb05519.x

Cited by 112 publications

(61 citation statements)

References 16 publications

(18 reference statements)

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“…However, nicotine also induces TH protein and TH activity two-to threefold 24 h after the initial injection of the drug (Fossom et al, 1991a). Similarly, reserpine administration induces adrenal TH mRNA and TH activity two-to threefold 12 h and 2-3 days, respectively, after drug administration (Tank et al, 1985;Faucon Biguet et al, 1986). Hence, based on these previous studies, we expected that the initial induction of TH mRNA observed after repeated bethanechol administration would lead to induction of TH protein/activity at later time points (24 or 48 h after the initial injection).…”

Section: Figmentioning

confidence: 99%

“…For instance, paradigms such as cold stress or reserpine administration elicit sustained increases in TH mRNA levels for 24 -48 h (Tank et al, 1985;Faucon Biguet et al, 1986), resulting in TH induction at these time points. According to this model, bethanechol administration does not induce TH protein, because TH mRNA is only induced for a transient (6 -12-h) interval.…”

Section: Figmentioning

confidence: 99%

“…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). These responses are also usually dependent on presynaptic innervation of the adrenal medulla and hence are mediated by transsynaptic mechanisms Kvetnansky et al, 1971;Fluharty et al, 1983;Stachowiak et al, 1985Stachowiak et al, , 1986.…”

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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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Section: Figmentioning

confidence: 99%

Section: Figmentioning

confidence: 99%

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confidence: 99%

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

1999

Journal of Neurochemistry

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“…Long term increases of TH activity are induced by various physiological stimuli including cyclic AMP (cAMP), epidermal growth factor, glucocorticoids, nerve growth factor, transsynaptic neuronal activity, and depolarization. These inducers have been shown to increase TH mRNA levels, and several studies indicate that they increase mRNA levels by inducing transcription: cAMP (Lewis et al, 1983Tank et al, 1986Tank et al, , 1990Fader and Lewis, 1990;Carroll et al, 1991;Fossom et al, 1992;Fung et al, 1992;Kim et al, 1993a), epidermal growth factor , glucocorticoids (Lewis et al, 1983Tank et al, 1986Tank et al, , 1990, nerve growth factor (Gizang-Ginsberg and Ziff, 1990), and transsynaptic neuronal activity and depolarization (Hefti et al, 1982;Black et al, 1985;Tank et al, 1985;Faucon-Biquet et al, 1989;Erlich et al, 1990;Sabban 1990, 1992;Banerjee et al, 1992). Investigation of the DNA regulatory elements that direct basal and induced TH transcription has been of interest because of the role TH has in the long term regulation of catecholamine biosynthesis.…”

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The Cyclic AMP Response Element Directs Tyrosine Hydroxylase Expression in Catecholaminergic Central and Peripheral Nervous System Cell Lines from Transgenic Mice

Lazaroff

Patankar

Yoon

et al. 1995

Journal of Biological Chemistry

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Enhancer elements regulating the neuronal gene, tyrosine hydroxylase (TH), were identified in TH-expressing peripheral nervous system PATH and central nervous system CATH cell lines. Mutational analysis in which rat TH 5-flanking sequences directed chloramphenicol acetyltransferase (CAT) reporter gene expression demonstrated that mutating the cyclic AMP response element (CRE) at ؊45 base pair reduced expression by 80 -90%. A CRE linked to an enhancerless TH promoter fully supported expression. Cotransfection of a dominant-negative CREB protein reduced expression 50 -60%, suggesting that the CRE is bound by CREB or a CREB dimerization partner. Although mutating the AP1/dyad (AD) element at ؊205 base pair only modestly reduced CAT levels, AD minimal enhancer constructs gave 45-80% of wild type expression when positioned at ؊91 or ؊95. However, in its native context at ؊205, the AD could not support expression. In contrast, a CRE, moved from its normal position at ؊45 to ؊206, gave full activity. These results indicate that the CRE is critical for TH transcription in central nervous system CATH and peripheral nervous system PATH cells, whereas the AD is less important and its enhancer activity is contextand/or position-dependent. These results represent the first attempts to map regulatory elements directing TH expression in central nervous system cell lines. Tyrosine hydroxylase (TH)1 converts L-tyrosine to 3,4-dihydroxy-L-phenylalanine and is the first and rate-limiting enzyme in catecholamine synthesis (Nagatsu et al., 1964;Levitt et al., 1965). TH is expressed in specific cell types in the peripheral and central nervous systems. Sympathetic ganglia and chromaffin cells of the adrenal medulla are major sites of peripheral TH expression. In the central nervous system, TH-expressing neurons are located in the diencephalon, midbrain, brainstem, olfactory bulb, and retina (Bjorklund and Lindvall, 1984).TH activity is regulated at the protein level and the RNA level. Activation at the protein level is short term with a time course of less than 1 h and mainly occurs via phosphorylation of preexisting protein molecules, which increases TH activity (reviewed by Zigmond et al. (1989)). Induction of TH at the mRNA level is long term, resulting in increased mRNA levels for hours to days. Long term increases of TH activity are induced by various physiological stimuli including cyclic AMP (cAMP), epidermal growth factor, glucocorticoids, nerve growth factor, transsynaptic neuronal activity, and depolarization. These inducers have been shown to increase TH mRNA levels, and several studies indicate that they increase mRNA levels by inducing transcription: cAMP (Lewis et al

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“…4). The increase in adrenal TH activity after repeated and chronic stress involves increased TH mRNA levels (5)(6)(7)(8). Recently, activation ofTH gene expression was found with a single immobilization stress (7,8).…”

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Induction of tyrosine hydroxylase gene expression by a nonneuronal nonpituitary-mediated mechanism in immobilization stress.

Nankova

Květňanský

McMahon

et al. 1994

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

110

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Elevation of RNA Coding for Tyrosine Hydroxylase in Rat Adrenal Gland by Reserpine Treatment and Exposure to Cold

Cited by 112 publications

References 16 publications

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

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

The Cyclic AMP Response Element Directs Tyrosine Hydroxylase Expression in Catecholaminergic Central and Peripheral Nervous System Cell Lines from Transgenic Mice

Induction of tyrosine hydroxylase gene expression by a nonneuronal nonpituitary-mediated mechanism in immobilization stress.

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