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

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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

Content Provider	Springer Nature Link
Author	Marcantoni, A. Carabelli, V. Vandael, D. H. Comunanza, V. Carbone, E.
Copyright Year	2008
Abstract	We studied the effects of the cAMP-hydrolyzing enzyme phosphodiesterase type-4 (PDE4) on the L-type Ca2+ channels (LTCCs) and Ca2+-dependent secretion in mouse chromaffin cells (MCCs). The selective PDE4 inhibitor rolipram (3 μM) had a specific potentiating action on Ca2+ currents of MCCs (40% increase within 3 min). A similar effect was produced by the selective β1-AR agonist denopamine (1 μM) and by the unselective PDEs inhibitor IBMX (100 μM). Rolipram and denopamine actions were selective for LTCCs, and the Ca2+ 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 β1-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 μM), while nifedipine (3 μM) 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.
Starting Page	1093
Ending Page	1110
Page Count	18
File Format	PDF
ISSN	00316768
Journal	Pflügers Archiv
Volume Number	457
Issue Number	5
e-ISSN	14322013
Language	English
Publisher	Springer-Verlag
Publisher Date	2008-09-09
Publisher Place	Berlin, Heidelberg
Access Restriction	One Nation One Subscription (ONOS)
Subject Keyword	Calcium channel Chromaffin cells cAMP Capacitance Amperometry Human Physiology
Content Type	Text
Resource Type	Article
Subject	Physiology Physiology (medical) Clinical Biochemistry

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