Chronic effects of nicotine on catecholamine synthesizing enzymes in rats

Naquira, Daisy; E, Zunino; Arqueros, L.; Viveros, O. Humberto

doi:10.1016/0014-2999(78)90394-1

Cited by 15 publications

(6 citation statements)

References 9 publications

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“…1999), it may be surprising that no effect of oral nicotine was observed on TH protein levels in the NAc and VTA. However, this is consistent with previous reports showing no effect of subchronic nicotine injections on TH levels in the striatum (Naquira et al . 1978) or on TH activity in the VTA (Smith et al .…”

Section: Tyrosine Hydroxylasesupporting

confidence: 94%

In vivo nicotine treatment regulates mesocorticolimbic CREB and ERK signaling in C57Bl/6J mice

Brunzell¹,

Russell²,

Picciotto³

2003

Journal of Neurochemistry

169

153

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The extracellular regulated kinase (ERK) pathway was studied to determine its role in neuronal plasticity related to the development of nicotine dependence. Levels and phosphorylation state of ERK, cAMP response element binding protein (CREB) and proline-rich/Ca 2+ -activated tyrosine kinase (PYK2), and levels of tyrosine hydroxylase (TH), were determined using western blotting. C57Bl/6J mice received acute or chronic nicotine (200 lg/mL) in their drinking water or were withdrawn from nicotine for 24 h following chronic exposure. CREB phosphorylation was reduced in the nucleus accumbens following chronic nicotine, consistent with previous reports that decreased accumbens CREB activity increases drug reinforcement. In contrast, CREB phosphorylation was increased in the prefrontal cortex following chronic nicotine exposure and in the ventral tegmental area during nicotine withdrawal. In addition, total and phosphorylated ERK decreased in the amygdala following chronic nicotine exposure, but ERK phosphorylation increased in the prefrontal cortex. TH levels increased in both the amygdala and prefrontal cortex, supporting the hypothesis that increased catecholaminergic tone contributes to nicotine reinforcement. Overall, these results support a role for ERK and CREB activity in neural plasticity associated with nicotine dependence.

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Section: Tyrosine Hydroxylasesupporting

confidence: 94%

In vivo nicotine treatment regulates mesocorticolimbic CREB and ERK signaling in C57Bl/6J mice

Brunzell¹,

Russell²,

Picciotto³

2003

Journal of Neurochemistry

169

153

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“…We have recently reported that this potentiation at 28 days is accompanied by an increase in the activity of tyrosine hydroxylase (TH; tyrosine 3-monooxygenase; EC 1.14.16.2), the rate-limiting enzyme in catecholamine biosynthesis, selectively in the hippocampus. Earlier studies have noted increases in TH activity in the locus coeruleus 3 days after a single high dose of nicotine (Lewander et al, 1977) and in the hypothalamus after 14 days of multiple dosing (Naquira et al, 1978).…”

Section: I751mentioning

confidence: 92%

“…The cholinergic agonist nicotine has been shown to induce release of catecholamines from various preparations of several regions of rat brain in vitro (reviewed by Balfour, 1982). [3H]Noradrenaline release from slices of hypothalamus, hippocampus, cortex, and cerebellum and [3H]dopamine release from striatal slices are increased by nicotine (Westfall, 1974;Arqueros et al, 1978), as is noradrenaline release from hypothalamic synaptosomes (Yoshida et al, 1980). Increased catecholamine release is often accompanied by increased synthesis.…”

mentioning

confidence: 99%

Effects of Chronic and Subchronic Nicotine on Tyrosine Hydroxylase Activity in Noradrenergic and Dopaminergic Neurones in the Rat Brain

Smith

Mitchell

Joseph

1991

Journal of Neurochemistry

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Chronic nicotine (0.8 mg/kg by daily subcutaneous injection) over a 7 to 28-day period was found to increase the activity of tyrosine hydroxylase in predominantly noradrenergically innervated regions but not in dopaminergic projection areas. Increases in tyrosine hydroxylase activity were observed in dopaminergic cell body regions only after nicotine treatment for 3 to 5 days. The increase in tyrosine hydroxylase activity in noradrenergic neurones was evident first in the cell bodies in the locus coeruleus from 3 to 7 days, reaching 223% of control activities, and was followed by increases of up to 205% in the terminals up to 3 weeks later. It was then established that nicotine for 7 days was sufficient to increase the activity of the enzyme to the same extent in the terminals at 21 days even without further nicotine administration. This is consistent with axonal transport preceded by induction of the enzyme in noradrenergic cell bodies, whereas "delayed activation" might account for the transient effect seen in dopaminergic cell body regions. The response in the locus coeruleus to nicotine for 7 days was completely blocked by daily preinjection with mecamylamine but not with hexamethonium, which is consistent with the effect of nicotine on tyrosine hydroxylase being mediated by central nicotinic receptors.

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“…Nicotine-induced changes in brain CA chemistry are equally impressive. For example, rats given nicotine have neuroadaptive increases in tyrosine hydroxylase (TH), the rate-limiting step in catecholamine synthesis (Naquira et al 1978). Smith et al (1991) and Michell et al (1993) demonstrated that chronic or even acute nicotine causes significant increases in TH in rat ventral tegmental area (VTA) and locus coeruleus (LC).…”

Section: Introductionmentioning

confidence: 98%

Positron emission tomographic measure of brain dopamine dependence to nicotine as a model of drugs of abuse

Domino

Tsukada²,

Harada³

2009

Psychopharmacology

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Compared to a 0.9% NaCl control, acute i.v. nicotine as a bolus plus infusion for 30 min in similar doses to maintain a steady-state level for 30 min did not affect the utilization rate constant (k (3)) in dorsal or ventral striatum as measured by L-[beta-(11)C]DOPA. When monkeys were given nicotine bid repeatedly after overnight nicotine abstinence, CA utilization was reduced. A subsequent nicotine dose normalized utilization to slightly above control levels. Changes in ventral striatum were similar to those in dorsal striatum. The reduced rate of utilization demonstrated with L-[beta-(11)C]DOPA after overnight nicotine abstinence and its reversal by nicotine the next day provides an important PET measure of brain nicotine dependence and withdrawal. This method can be applied to other substances of abuse that release DA.

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Chronic effects of nicotine on catecholamine synthesizing enzymes in rats

Cited by 15 publications

References 9 publications

In vivo nicotine treatment regulates mesocorticolimbic CREB and ERK signaling in C57Bl/6J mice

In vivo nicotine treatment regulates mesocorticolimbic CREB and ERK signaling in C57Bl/6J mice

Effects of Chronic and Subchronic Nicotine on Tyrosine Hydroxylase Activity in Noradrenergic and Dopaminergic Neurones in the Rat Brain

Positron emission tomographic measure of brain dopamine dependence to nicotine as a model of drugs of abuse

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