Tyrosine hydroxylase regulation in neurotransmission and neuroplasticity

Icard-Liepkalns, Christine; Berrard, Sylvie; Biguet, Nicole Faucon; Lebourdelles, B; Ravassard, Philippe; Robert, J; Mallet, Jacques

doi:10.1016/0928-4257(93)90026-p

Cited by 10 publications

(7 citation statements)

References 13 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Nicotinic stimulus transcription coupling in chromaffin cells has also been examined for responsible promoter regions in the catecholamine biosynthetic enzymes tyrosine hydroxylase (3,4,57,58), dopamine ␤-hydroxylase (59), and phenylethanolamine N-methyltransferase (60), as well as the secretory peptide proenkephalin A (61). Such previous studies suggest that two promoter domains may be crucial in nicotinic responses: the cAMP response element (3,4) and the AP1 site (62).…”

Section: Discussionmentioning

confidence: 99%

Stimulus coupling to transcription versus secretion in pheochromocytoma cells. Convergent and divergent signal transduction pathways and the crucial roles for route of cytosolic calcium entry and protein kinase C.

Tang

Wu²,

Mahata³

et al. 1997

J. Clin. Invest.

View full text Add to dashboard Cite

How do chromaffin cell secretory stimuli program resynthesis of secreted peptides and amines? We previously showed that the physiologic nicotinic cholinergic signal for secretion also activates the biosynthesis of chromogranin A, the major protein released with catecholamines. Here, we examine signal transduction pathways whereby secretory stimuli influence exocytotic secretion versus chromogranin A transcription. Both secretion and transcription depended on initial nicotinic-triggered sodium entry into the cytosol, followed by calcium entry through L -type voltage-gated channels. When calcium entered through L -type channels, activation of secretion paralleled activation of transcription ( r ϭ 0.897, P ϭ 0.002). Calcium entry from intracellular stores or through calcium ionophore channels activated secretion, though not transcription. Nicotinic-stimulated transcription depended upon protein kinase C activation; nicotine caused translocation of protein kinase C to the cell membrane fraction, and inhibition of protein kinase C blocked activation of transcription, while activation of protein kinase C mimicked nicotine effects. Transcriptional responses to both nicotine and protein kinase C mapped principally onto the chromogranin A promoter's cAMP response element (TGACGTAA; CRE box). KCREB, a dominant negative mutant of the CREbinding protein CREB, blunted activation of chromogranin A transcription by nicotine, phorbol ester, or membrane depolarization. We conclude that activation of chromogranin A transcription by secretory stimulation in chromaffin cells is highly dependent upon precise route of calcium entry into the cytosol; transcription occurred after entry of calcium through L -type channels on the cell surface, and was mediated by protein kinase C activation. The trans -acting factor CREB ultimately relays the secretory signal to the chromogranin A promoter's CRE box in cis. ( J. Clin. Invest.

show abstract

Section: Discussionmentioning

confidence: 99%

Stimulus coupling to transcription versus secretion in pheochromocytoma cells. Convergent and divergent signal transduction pathways and the crucial roles for route of cytosolic calcium entry and protein kinase C.

Tang

Wu²,

Mahata³

et al. 1997

J. Clin. Invest.

View full text Add to dashboard Cite

show abstract

“…Biosynthesis is another important step in the metabolic pathway of catecholamines. TH is a specific marker of catecholaminergic neurons and the enzymatic key in the biosynthesis of catecholamines (Icard-Liepkalns et al, 1993;Kumer and Vrana, 1996). This enzyme regulates the conversion of L-tyrosine to L-dopa.…”

Section: Discussionmentioning

confidence: 99%

Untitled

Rodriguez-Campos

Kadarian

Rodano

et al. 2000

Cellular and Molecular Neurobiology

View full text Add to dashboard Cite

1. We previously reported that angiotensin III modulates noradrenergic neurotransmission in the hypothalamus of the rat. In the present work we studied the effects of angiotensin III on norepinephrine release and tyrosine hydroxylase activity. We also investigated the receptors and intracellular pathways involved in angiotensin III modulation of noradrenergic transmission. 2. In rat hypothalamic tissue labeled with [3H]norepinephrine 1, 10, and 100 nM and 1 microM losartan (AT1 receptor antagonist) had no effect on basal neuronal norepinephrine release, whereas 10 and 100 nM and 1 microM losartan partially diminished norepinephrine secretion evoked by 25 mM KCl. The AT2 receptor antagonist PD 123319 showed no effect either on basal or evoked norepinephrine release. The increase in both basal and evoked norepinephrine output induced by 1 microM angiotensin III was blocked by 1 microM losartan, but not by 1 microM PD 123319. 3. The phospholipase C inhibitor 5 microM neomicin inhibited the increase in basal and evoked norepinephrine release produced by 1 microM angiotensin III. 4. Tyrosine hydroxylase activity was increased by 1 microM angiotensin III and this effect was blocked by 1 microM LST and 5 microM neomicin, but not by PD 123319. On the other hand, 1 microM angiotensin III enhanced phosphatidyl inositol hydrolysis that was blocked by 1 microM losartan and 5 microM neomicin. PD 123319 (1 microM) did not affect ANG III-induced phosphatidyl inositol hydrolysis enhancement. 5. Our results confirm that angiotensin III acts as a modulator of noradrenergic transmission at the hypothalamic level through the AT1-phospholipase C pathway. This enhancement of hypothalamic noradrenergic activity suggests that angiotensin III may act as a central modulator of several biological processes regulated at this level by catecholamines, such as cardiovascular, endocrine, and autonomic functions as well as water and saline homeostasis.

show abstract

“…Several detailed descriptions of dopamine synthesis have been published previously and a summary is provided in Figure 1 (Elsworth and Roth, 1997; Fernstrom, 1983; Icard-Liepkalns et al, 1993; Milner and Wurtman, 1986; Misu and Goshima, 1993). Dopamine has several receptors to which it binds (e.g.…”

Section: Dopaminementioning

confidence: 99%

Catecholaminergic based therapies for functional recovery after TBI

Osier

Dixon

2016

Brain Research

View full text Add to dashboard Cite

Among the many pathophysiologic consequences of traumatic brain injury are changes in catecholamines, including dopamine, epinephrine, and norepinephrine. In the context of TBI, dopamine is the one most extensively studied, though some research exploring epinephrine and norepinephrine have also been published. The purpose of this review is to summarize the evidence surrounding use of drugs that target the catecholaminergic system on pathophysiological and functional outcomes of TBI using published evidence from pre-clinical and clinical brain injury studies. Evidence of the effects of specific drugs that target catecholamines as agonists or antagonists will be discussed. Taken together, available evidence suggests that therapies targeting the catecholaminergic system may attenuate functional deficits after TBI. Notably, it is fairly common for TBI patients to be treated with catecholamine agonists for either physiological symptoms of TBI (e.g. altered cerebral perfusion pressures) or a co-occuring condition (e.g. shock), or cognitive symptoms (e.g. attentional and arousal deficits). Previous clinical trials are limited by methodological limitations, failure to replicate findings, challenges translating therapies to clinical practice, the complexity or lack of specificity of catecholamine receptors, as well as potentially counfounding effects of personal and genetic factors. Overall, there is a need for additional research evidence, along with a need for systematic dissemination of important study details and results as outlined in the common data elements published by the National Institute of Neurological Diseases and Stroke. Ultimately, a better understanding of catecholamines in the context of TBI may lead to therapeutic advancements.

show abstract

Tyrosine hydroxylase regulation in neurotransmission and neuroplasticity

Cited by 10 publications

References 13 publications

Stimulus coupling to transcription versus secretion in pheochromocytoma cells. Convergent and divergent signal transduction pathways and the crucial roles for route of cytosolic calcium entry and protein kinase C.

Stimulus coupling to transcription versus secretion in pheochromocytoma cells. Convergent and divergent signal transduction pathways and the crucial roles for route of cytosolic calcium entry and protein kinase C.

Untitled

Catecholaminergic based therapies for functional recovery after TBI

Contact Info

Product

Resources

About