Nerve growth factor treatment enhances nicotine-stimulated dopamine release and increases in cyclic adenosine 3':5'-monophosphate levels in PC12 cell cultures

Baizer, Lawrence; Weiner, N.

doi:10.1523/jneurosci.05-05-01176.1985

Cited by 32 publications

(19 citation statements)

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“…without involvement of transcription factors such as CREB. These data do not fully agree with previously published results showing increase in cAMP levels and activation of protein kinase C by nicotinic stimulation [29][30][31][32], Several reasons could be evoked to explain apparent discrepancies. The second messenger pathways induced by nicotinic receptor activation could differ firstly according to the cell types studied as PC 12 rat pheochromocytoma cells [29], NG 108-15 mouse neuroblastoma x rat glioma hybrid cells [32] or bovine adrenal chromaffin cells [30], and secondly according to the mode of nicotine treatment (long-term vs. acute administration) and experimental protocol.…”

Section: Effects O F Metyrapone and Nicotinic Preganglionic Blockadecontrasting

confidence: 96%

Effect of Cholinergic Blockade on Glucocorticoid Regulation of NPY and Catecholamines in the Rat Adrenal Gland

et al. 1997

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Catecholamines and neuropeptide Y (NPY) levels were determined in the adrenals of rats treated for 2.5 days with chlorisondamine (6 mg/day), a nicotinic ganglionic blocking agent, metyrapone (66 mg/day), an inhibitor of the 11 β-hydroxylase activity or both metyrapone and chlorisondamine. Chlorisondamine induced a significant increase in adrenal weight (31%) without significant rise in hypothalamic CRH content, plasma ACTH level and plasma corticosterone concentration. This drug was unable to affect significantly dopamine (DA), norepinephrine (NE) and epinephrine (E) content of the adrenals; in contrast, it induced a significant decrease (90%) of plasma NE and E levels. Chlorisondamine induced no change in adrenal NPY content as well as NPY mRNA level determined by Northern blot but significantly increased NPY plasma level. Metyrapone-treatment induced a significant drop of plasma corticosterone level and elicited a significant reduction of hypothalamic CRH content, a rise (460%) of the plasma ACTH concentration associated with a significant increase (18%) of the adrenal weight. A marked increase of DA (240%) and significant decrease of E (22%) in the adrenal gland were observed in response to metyrapone treatment. In addition, metyrapone induced a drop (23%) in plasma E level. In both the adrenals and the plasma, the ratio E/NE was significantly reduced by metyrapone treatment. Metyrapone elicited a significant increase of adrenal NPY content (88%) as well as of NPY mRNA revealed by Northern blot analysis but was unable to significantly affect NPY plasma level. The effects of chlorisondamine, given in combination with metyrapone on both hypothalamic CRH content and plasma ACTH level, were similar to those induced by metyrapone given alone. Chlorisondamine-mediated pharmacological ganglionic blockade increased metyrapone-induced adrenal hypertrophy and adrenal DA storage but prevented metyrapone-induced depletion of adrenal E as well as increase of the adrenal NPY mRNA level and NPY content. Chlorisondamine-induced elevation of plasma NPY level was not observed under metyrapone treatment. Present data suggest that the increase in adrenal NPY synthesis in response to metyrapone treatment is mediated by transsynaptic cholinergic activation and implies nicotinic receptors. On the other hand, adrenal TH may be regulated by additional or different mechanisms, which possibly involve nonnicotinic transmission. Present work also suggests that the suppression of the glucocorticoid feedback inhibition of hypothalamic CRH neurons could stimulate sympathoneuronal outflow and consequently elicit transsynaptic cholinergic activation of adrenal neuropeptide Y gene expression.

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Section: Effects O F Metyrapone and Nicotinic Preganglionic Blockadecontrasting

confidence: 96%

Effect of Cholinergic Blockade on Glucocorticoid Regulation of NPY and Catecholamines in the Rat Adrenal Gland

et al. 1997

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“…These data, together with the data from the binding studies (Fig. 5B) (Greene and Rein, 1977;Baizer and Weiner, 1985). This assay provides a measurement of nAChR function that, although downstream from the receptor itself, might be more sensitive than the 86 Rb ϩ efflux assay for certain nAChR subtypes.…”

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confidence: 71%

“…One of these is the PC12 cell line, which was developed from a transplantable rat adrenal pheochromocytoma by Greene and Tischler (1976). These cells exhibit several key physiological features of adrenal chromaffin cells and sympathetic neurons, such as synthesis, storage, and release of catecholamines (Greene and Tischler, 1976;Greene and Reine, 1977;Baizer and Weiner, 1985) and depolarization in response to acetylcholine (Dichter et al, 1977). Moreover, like sympathetic neurons, these cells express receptors for nerve growth factor (NGF), and in response to this neurotrophin they cease cell division and differentiate into sympathetic-like neurons, with a flattened cell body and extension of neurites (Greene and Tischler, 1976).…”

mentioning

confidence: 99%

“…NGF treatment of PC12 cells increases nicotine-stimulated responses, including catecholamine release (Greene and Reine, 1977;Baizer and Weiner, 1985), ion flux (Amy and Bennett, 1983;Whiting et al, 1987), and whole cell currents (Ifune and Steinbach, 1990;Henderson et al, 1994). Furthermore, NGF has also been reported to increase Henderson et al, 1994;Hu et al, 1994;Takahashi et al, 1999;Nakayama et al, 2000) as well as decrease mRNA encoding certain nAChR subunits in PC12 cells.…”

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confidence: 99%

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Differential Regulation of Nicotinic Acetylcholine Receptors in PC12 Cells by Nicotine and Nerve Growth Factor

Avila

Dávila‐García²,

Ascarrunz³

et al. 2003

Mol Pharmacol

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ABSTRACT3 H]epibatidine were found: one that was increased about 4-fold in cells grown for 2 to 4 days in the presence of nicotine and one that was increased 5-fold in cells grown for 2 to 4 days in the presence of nerve growth factor (NGF). The actions of the two treatments were superadditive, resulting in approximately a 13-fold increase in binding sites in cells grown in the combination of the two treatments. The pharmacology of the binding sites in the nicotine-and NGF-treated cells was compared with the pharmacology of defined ␣3␤2 and ␣3␤4 nicotinic acetylcholine receptor (nAChR) subtypes heterologously expressed in human embryonic kidney 293 cells. Nicotine treatment predominantly increased a receptor with characteristics of an ␣3␤2 subtype, whereas the NGF treatment exclusively increased a receptor with characteristics of an ␣3␤4 subtype. Nicotinic receptormediated function measured with the 86 Rb ϩ efflux assay was evident only in the NGF-treated cells, and it had a pharmacological profile that was, again, nearly identical to that of the heterologously expressed ␣3␤4 receptor subtype. Receptor function measured with the [ 3 H]norepinephrine release assay was measurable in both nicotine-treated and NGF-treated cells; however, cytisine-stimulated [ 3 H]norepinephrine release indicated that nicotine treatment increased an nAChR containing ␤2 subunits, whereas NGF increased a receptor containing ␤4 subunits. NGF treatment increased mRNA only for ␤4 subunits in these cells, whereas nicotine treatment did not affect mRNA for any of the subunits measured. After withdrawal of the treatments, the receptors increased by nicotine were much less stable than those increased by NGF.Neuronal nicotinic acetylcholine receptors (nAChRs) are found throughout the central nervous system as well as in autonomic ganglia and the adrenal gland, where they mediate cholinergic neurotransmission critical to the functions of the autonomic nervous system. These receptors are composed of two types of subunits, ␣ and ␤. To date, nine neuronal ␣ subunit genes (␣2-␣10) and three ␤ subunit genes (␤2-␤4) have been found in vertebrate tissues. Different combinations of subunits compose subtypes of nicotinic receptors, all of which are ligand-gated cation channels that conduct Na ϩ , K ϩ , and Ca 2ϩ when activated by the endogenous neurotransmitter acetylcholine or by nicotine or other nicotinic agonists. However, the different receptor subtypes have distinguishing biophysical and/or pharmacological properties, including channel conductances, rates of desensitization and recovery, and sensitivity to drugs (for reviews, see Sargent, 1993;Colquhoun and Patrick, 1997;Lukas, 1998).Certain subtypes of nAChRs are strongly regulated by nicotine. Previous studies have shown that chronic administration of nicotine increases nicotinic receptor binding sites in rat and mouse brain (Schwartz and Kellar, 1983;Marks et al., 1983; for review, see Gentry and Lukas, 2002), and a similar increase is found in human brains from people who smoked tobacco (Benwe...

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“…Some forms of adenylyl cyclase are stimulated by calcium to generate cAMP (Mons et al, 1998;Gueorguiev et al, 1999) and cAMP is a known regulator of cAMP-dependent protein kinase A (Exton et al, 1981). In PC-12 cells, nicotine increases intracellular cAMP by a Ca 2ϩ -dependent mechanism that is blocked by d-tubocurarine (Baizer and Weiner, 1985). When hepatocytes were incubated in buffer containing nicotine and H-89, oxygen uptake was not stimulated (Table 2).…”

Section: Downloaded Frommentioning

confidence: 99%

Nicotine Increases Hepatic Oxygen Uptake in the Isolated Perfused Rat Liver by Inhibiting Glycolysis

Dewar

Bradford²,

Thurman³

2002

J Pharmacol Exp Ther

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Nicotine influences energy metabolism, yet mechanisms remain unclear. Since the liver is one of the largest organs and performs many metabolic functions, the goal of this study was to determine whether nicotine would affect respiration and other metabolic functions in the isolated perfused liver. Infusion of 85 M nicotine caused a rapid 10% increase in oxygen uptake over basal values of 105 Ϯ 5 mol/g/h in perfused livers from fed rats, and an increase of 27% was observed with 850 M nicotine. Concomitantly, rates of glycolysis of 105 Ϯ 8 mol/g/h were decreased to 52 Ϯ 9 mol/g/h with nicotine, whereas ketone body production was unaffected. Nicotine had no effect on oxygen uptake in glycogen-depleted livers from 24-h fasted rats. Furthermore, addition of glucose to perfused livers from fasted rats partially restored the stimulatory effect of nicotine. Infusion of atractyloside, potassium cyanide, or glucagon blocked the nicotine-induced increase in respiration. Intracellular calcium was increased in isolated hepatocytes by nicotine, a phenomenon prevented by incubation of cells with d-tubocurarine, a nicotinic acetylcholine receptor antagonist. Respiration was also increased ϳ30% in hepatocytes isolated from fed rats by nicotine, whereas hepatocytes isolated from fasted rats showed little response. In the presence of N- [2-(pbromocinnamylamino)ethyl]-5-isoquinolinesulfonamide (H-89), an inhibitor of cyclic AMP-dependent protein kinase A, nicotine failed to stimulate respiration. These data support the hypothesis that inhibition of glycolysis by nicotine increases oxygen uptake due to an ADP-dependent increase in mitochondrial respiration.

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Nerve growth factor treatment enhances nicotine-stimulated dopamine release and increases in cyclic adenosine 3':5'-monophosphate levels in PC12 cell cultures

Cited by 32 publications

References 0 publications

Effect of Cholinergic Blockade on Glucocorticoid Regulation of NPY and Catecholamines in the Rat Adrenal Gland

Effect of Cholinergic Blockade on Glucocorticoid Regulation of NPY and Catecholamines in the Rat Adrenal Gland

Differential Regulation of Nicotinic Acetylcholine Receptors in PC12 Cells by Nicotine and Nerve Growth Factor

Nicotine Increases Hepatic Oxygen Uptake in the Isolated Perfused Rat Liver by Inhibiting Glycolysis

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