Cholinoceptor regulation of cyclic AMP levels in bovine adrenal medullary cells

Anderson, Karen E.; Robinson, Phillip J.; Marley, Philip D.

doi:10.1111/j.1476-5381.1992.tb14341.x

Cited by 27 publications

(20 citation statements)

References 43 publications

(60 reference statements)

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“…A second important finding is that LTCCs act as pace-maker channels and control AP generation in resting MCCs. This has a direct consequence on the action of PDE4 or of any other compound controlling intracellular cAMP, such as nicotine [1], histamine [37], PACAP [51], VIP [63], and β 1 -AR agonists (Fig. 2).…”

Section: Discussionmentioning

confidence: 98%

“…In BCCs, intracellular cAMP and catecholamine secretion can be effectively raised by either applying neurotransmitters, such as nicotine [1], PACAP [51], histamine [37], and VIP [63] or by inhibiting cAMP degradation mediated by cyclic nucleotide phosphodiesterares (PDEs) [33,36]. Inhibition of PDEs is very effective in elevating the basal levels of cAMP, suggesting high PDE enzymatic activity in chromaffin cells.…”

Section: Introductionmentioning

confidence: 99%

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PDE type-4 inhibition increases L-type Ca2+ currents, action potential firing, and quantal size of exocytosis in mouse chromaffin cells

Marcantoni

Carabelli

Vandael

et al. 2008

Pflugers Arch - Eur J Physiol

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We studied the effects of the cAMP-hydrolyzing enzyme phosphodiesterase type-4 (PDE4) on the L-type Ca(2+) channels (LTCCs) and Ca(2+)-dependent secretion in mouse chromaffin cells (MCCs). The selective PDE4 inhibitor rolipram (3 microM) had a specific potentiating action on Ca(2+) currents of MCCs (40% increase within 3 min). A similar effect was produced by the selective beta(1)-AR agonist denopamine (1 microM) and by the unselective PDEs inhibitor IBMX (100 microM). Rolipram and denopamine actions were selective for LTCCs, and the Ca(2+) current increase remained unchanged if the two compounds were applied simultaneously. This suggests that at rest, LTCCs in MCCs are down-regulated by the low levels of cAMP determined by PDE4 activity and that LTCCs can be up-regulated by either inhibiting PDE4 or activating beta(1)-AR. No other PDEs are likely involved in this specific action. PDE4 inhibition had also a marked effect on the spontaneous firing of resting MCCs and catecholamine secretion. Rolipram up-regulated the LTCCs contributing to the "pace-maker" current underlying action potential (AP) discharges and accelerated the firing rate, with no significant effects on AP waveform. Acceleration of AP firing was also induced by the LTCC-agonist Bay K (1 microM), while nifedipine (3 microM) reduced the firing frequency, suggesting that LTCCs and intracellular cAMP play a key role in setting the pace-maker current regulating MCCs excitability. Rolipram increased also the size of the ready-releasable pool and the quantal content of secretory vesicles without affecting their probability of release. Thus, rolipram acts on MCCs by up-regulating both exocytosis and AP firings. These two processes are effectively down-regulated by PDE4 at rest and can dramatically increase the quantity of released catecholamines when PDE4 is inhibited and/or cAMP is raised.

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Section: Discussionmentioning

confidence: 98%

Section: Introductionmentioning

confidence: 99%

PDE type-4 inhibition increases L-type Ca2+ currents, action potential firing, and quantal size of exocytosis in mouse chromaffin cells

Marcantoni

Carabelli

Vandael

et al. 2008

Pflugers Arch - Eur J Physiol

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“…Previous reports have suggested that nAChR may control some of its cellular functions through cAMP and PKA activation. In particular, nicotine has been shown to increase cAMP levels in PC12 cells (Anderson et al . 1992; Gueorguiev et al .…”

Section: Discussionmentioning

confidence: 99%

Nicotine activates the extracellular signal‐regulated kinase 1/2 via the α7 nicotinic acetylcholine receptor and protein kinase A, in SH‐SY5Y cells and hippocampal neurones

Dajas-Bailador¹,

Soliakov²,

Wonnacott³

2002

Journal of Neurochemistry

178

138

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Neuronal nicotinic acetylcholine receptors (nAChR) can modulate many cellular mechanisms, such as cell survival and memory processing, which are also in¯uenced by the serine/ threonine protein kinases ERK1/2. In SH-SY5Y cells and hippocampal neurones, nicotine (100 lM) increased the activity of ERK1/2. This effect was Ca 2+ dependent, and prevented by the a7 nAChR antagonist a-bungarotoxin (a-Bgt) and an inhibitor (PD98059) of the upstream kinase MEK. To determine the intervening steps linking Ca 2+ entry to MEK-ERK1/2 activation, inhibitors of Ca 2+ -dependent kinases were deployed. In SH-SY5Y cells, selective blockers for PKC (Ro 31±8220), CaM kinase II (KN-62) or PI3 kinase (LY 294002) failed to inhibit the nicotine-evoked increase in ERK1/2 activity. In contrast, two structurally different inhibitors of PKA (KT 5720 and H-89) completely prevented the nicotinedependent increase in ERK1/2 activity. Inhibition of the nicotine-evoked increase in ERK1/2 activity by H-89 was also observed in hippocampal cultures. Down stream of PKA, the activity of B-Raf was signi®cantly decreased by nicotine in SH-SY5Y cells, as determined by direct measurement of MEK1 phosphorylation or in vitro kinase assays, whereas the modulation of MEK1 phosphorylation by Raf-1 tended to increase. Thus, this study provides evidence for a novel signalling route coupling the stimulation of a7 nAChR to the activation of ERK1/2, in a Ca 2+ and PKA dependent manner. Neuronal nicotinic acetylcholine receptors (nAChR) are ligand gated cation channels permeable to Na + and Ca 2+ and therefore capable of increasing intracellular Ca 2+ concentrations per se and by activation of voltage-operated Ca 2+ channels (VOCC). As a result, they have the capacity to in¯uence a variety of neuronal activities, such as neurotransmitter release (Wonnacott 1997), cell survival (Donnelly Roberts and Brioni 1999), synaptic plasticity (Ji et al. 2001) and memory processing (Levin and Simon 1998). Numerous subtypes of nAChR occur in the brain, including the two major subtypes comprised of a7 and a4b2 subunits, respectively. The a7 nAChR, in particular, has been implicated in several cellular processes, including long-term potentiation (Mansvelder and McGehee 2000;Matsuyama et al. 2000), neuroprotection (Donnelly Roberts et al. 1996;Dajas-Bailador et al. 2000;Kihara et al. 2001) and learning and memory (Levin et al. 1999). Although the Ca 2+ dependence of some of these a7 nAChR-mediated actions has been demonstrated, the downstream mechanisms that follow nAChR activation, and those attributed to a7 in particular, have not been fully elucidated.One candidate implicated in many of the cellular processes also modulated by nAChR stimulation is the mitogen activated/extracellular signal-regulated protein kinase Abbreviations used: a-Bgt, a-bungarotoxin; CaM, kinase II, Ca 2+ calmodulin dependent kinase II; CREB, cyclic AMP response element binding protein; DMEM, Dulbecco's modi®ed Eagle's medium; ECL, electrochemiluminescence; ERK1/2, extracellular-signal regulated pro...

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“…It has been shown that nicotinic receptor stimulation per se increases cAMP levels in adrenal medullary cells, and suggested that cAMP plays a role in nicotinic receptor-mediated CA release (Wilson, 1988;Keogh and Marley, 1991;Anderson et al, 1992). Accordingly, NKH477 may elevate cAMP levels further during nicotinic receptor stimulation.…”

Section: Discussionmentioning

confidence: 99%

Effects of NKH477, a forskolin derivative, and dibutyryl‐cyclic AMP on adrenal catecholamine release in response to splanchnic nerve stimulation, acetylcholine, DMPP and muscarine in anesthetized dogs

Koshika

Nagayama

Iizuka

et al. 1997

Fundamemntal Clinical Pharma

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The effects of NKH477, a water-soluble forskolin derivative, and dibutyryl-cyclic adenosine monophosphate (dbcAMP) on the release of adrenal catecholamines (CAs) in response to splanchnic nerve stimulation (SNS), acetylcholine (ACh), the nicotinic receptor stimulant 1,1-dimethyl-4-phenyl-piperazinium iodide (DMPP) and muscarine were examined in anesthetized dogs. NKH477, dbcAMP and the cholinergic agonists were infused and injected, respectively, into the adrenal gland intra-arterially. SNS (3 Hz) or injections of ACh (3 micrograms), DMPP (2 micrograms) and muscarine (2 micrograms) produced increases in CA output determined from adrenal venous blood. Both NKH477 infusion (0.3, 1 and 3 micrograms/min) and dbcAMP infusion (0.1, 0.3 and 1 mg/min) caused dose-dependent enhancement of the SNS-, ACh- and DMPP-induced increases in CA output, whereas they failed to affect the muscarine-induced increases in CA output. Neither NKH477 nor dbcAMP affected basal CA output. Cyclic AMP (cAMP) overflow determined from adrenal venous blood increased during NKH477 infusion. These results indicate that NKH477 and dbcAMP have facilitatory effects on adrenal CA release mediated by nicotinic receptors, but not by muscarinic receptors in the dog, and suggest the selective action of cAMP on nicotinic mechanism.

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Cholinoceptor regulation of cyclic AMP levels in bovine adrenal medullary cells

Cited by 27 publications

References 43 publications

PDE type-4 inhibition increases L-type Ca2+ currents, action potential firing, and quantal size of exocytosis in mouse chromaffin cells

PDE type-4 inhibition increases L-type Ca2+ currents, action potential firing, and quantal size of exocytosis in mouse chromaffin cells

Nicotine activates the extracellular signal‐regulated kinase 1/2 via the α7 nicotinic acetylcholine receptor and protein kinase A, in SH‐SY5Y cells and hippocampal neurones

Effects of NKH477, a forskolin derivative, and dibutyryl‐cyclic AMP on adrenal catecholamine release in response to splanchnic nerve stimulation, acetylcholine, DMPP and muscarine in anesthetized dogs

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