Role of L-type and N-type Voltage-dependent Calcium Channels (VDCCs) on Spontaneous Acetylcholine Release at the Mammalian Neuromuscular Junction

1998 ◽  
Vol 841 (1 MYASTHENIA GR) ◽  
pp. 636-645 ◽  
Author(s):  
ADRIANA LOSAVIO ◽  
SALOMON MUCHNIK
Keyword(s):  
Neuromuscular Junction ◽  
Calcium Channels ◽  
Acetylcholine Release ◽  
Voltage Dependent ◽  
Voltage Dependent Calcium Channels

The role of voltage-dependent calcium channels in angiotensin-stmulated glomerulosa cells

1996 ◽  
Vol 22 (4) ◽  
pp. 569-576 ◽  
Author(s):  
A. Spät ◽  
T. Rohács ◽  
A. Horváth ◽  
G Y. Szabadkai ◽  
P. Enyedi
Keyword(s):  
Calcium Channels ◽  
Voltage Dependent ◽  
Voltage Dependent Calcium Channels ◽  
Glomerulosa Cells

Ifenprodil reduces excitatory synaptic transmission by blocking presynaptic P/Q type calcium channels

2012 ◽  
Vol 107 (6) ◽  
pp. 1571-1575 ◽  
Author(s):  
Andrew J. Delaney ◽  
John M. Power ◽  
Pankaj Sah
Keyword(s):  
Calcium Channels ◽  
Synaptic Transmission ◽  
Nmda Receptors ◽  
Basolateral Amygdala ◽  
Excitatory Transmission ◽  
Voltage Dependent ◽  
Voltage Dependent Calcium Channels ◽  
P Type ◽  
Selective Blocker

Ifenprodil is a selective blocker of NMDA receptors that are heterodimers composed of GluN1/GluN2B subunits. This pharmacological profile has been extensively used to test the role of GluN2B-containing NMDA receptors in learning and memory formation. However, ifenprodil has also been reported to have actions at a number of other receptors, including high voltage-activated calcium channels. Here we show that, in the basolateral amygdala, ifenprodil dose dependently blocks excitatory transmission to principal neurons by a presynaptic mechanism. This action of ifenprodil has an IC50 of ∼10 μM and is fully occluded by the P/Q type calcium channel blocker ω-agatoxin. We conclude that ifenprodil reduces synaptic transmission in the basolateral amygdala by partially blocking P-type voltage-dependent calcium channels.

N-Type Voltage-Dependent Calcium Channels Mediate the Nicotinic Enhancement of GABA Release in Chick Brain

1999 ◽  
Vol 81 (2) ◽  
pp. 447-454 ◽  
Author(s):  
Trevor L. Tredway ◽  
Jian-Zhong Guo ◽  
Vincent A. Chiappinelli
Keyword(s):  
Calcium Channels ◽  
Channel Blocker ◽  
Brain Slices ◽  
Gaba Release ◽  
Channel Blockers ◽  
Chick Brain ◽  
Voltage Dependent ◽  
Voltage Dependent Calcium Channels ◽  
Whole Cell Recordings

N-type voltage-dependent calcium channels mediate the nicotinic enhancement of GABA release in chick brain. The role of voltage-dependent calcium channels (VDCCs) in the nicotinic acetylcholine receptor (nAChR)-mediated enhancement of spontaneous GABAergic inhibitory postsynaptic currents (IPSCs) was investigated in chick brain slices. Whole cell recordings of neurons in the lateral spiriform (SpL) and ventral lateral geniculate (LGNv) nuclei showed that cadmium chloride (CdCl2) blocked the carbachol-induced increase of spontaneous GABAergic IPSCs, indicating that VDCCs might be involved. To conclusively show a role for VDCCs, the presynaptic effect of carbachol on SpL and LGNv neurons was examined in the presence of selective blockers of VDCC subtypes. ω-Conotoxin GVIA, a selective antagonist of N-type channels, significantly reduced the nAChR-mediated enhancement of γ-aminobutyric acid (GABA) release in the SpL by 78% compared with control responses. Nifedipine, an L-type channel blocker, and ω-Agatoxin-TK, a P/Q-type channel blocker, did not inhibit the enhancement of GABAergic IPSCs. In the LGNv, ω-Conotoxin GVIA also significantly reduced the nAChR-mediated enhancement of GABA release by 71% from control values. Although ω-Agatoxin-TK did not block the nicotinic enhancement, L-type channel blockers showed complex effects on the nAChR-mediated enhancement. These results indicate that the nAChR-mediated enhancement of spontaneous GABAergic IPSCs requires activation of N-type channels in both the SpL and LGNv.

Role of calcium channels and adenylate cyclase in the PACAP-induced adrenal catecholamine secretion

2001 ◽  
Vol 281 (2) ◽  
pp. R495-R501 ◽  
Author(s):  
Yasuo Fukushima ◽  
Takahiro Nagayama ◽  
Hisako Kawashima ◽  
Hirohiko Hikichi ◽  
Makoto Yoshida ◽  
...  
Keyword(s):  
Adrenal Gland ◽  
Adenylate Cyclase ◽  
Calcium Channels ◽  
Catecholamine Secretion ◽  
Induced Responses ◽  
Free Solution ◽  
Pituitary Adenylate Cyclase ◽  
Voltage Dependent ◽  
Voltage Dependent Calcium Channels

We elucidated the functional contribution of voltage-dependent calcium channels (VDCCs) and adenylate cyclase to epinephrine (Epi) and norepinephrine (NE) secretion induced by pituitary adenylate cyclase-activating polypeptide (PACAP) in the isolated perfused rat adrenal gland. PACAP increased Epi and NE output, which was inhibited by perfusion with calcium-free solution or by nifedipine, an L-type VDCC blocker. However, the PACAP-induced responses were resistant to ω-conotoxin GVIA, an N-type VDCC blocker, or ω-conotoxin MVIIC, a P/Q-type VDCC blocker. MDL-12330A, an adenylate cyclase inhibitor, inhibited the PACAP-induced increase in Epi, but not NE, output. Treatment with nifedipine and MDL-12330A caused additive inhibition of the PACAP-induced catecholamine responses. These results suggest that opening of L-type VDCCs is responsible for adrenal catecholamine secretion induced by PACAP and that activation of adenylate cyclase is involved in the PACAP-induced Epi, but not NE, secretion. These pathways may act independently of each other.

The Role of L-Type Voltage-Dependent Calcium Channels in Anesthetic Depression of Contractility

1994 ◽  
pp. 207-214 ◽  
Author(s):  
Thomas J.J. Blanck ◽  
D.L. Lee ◽  
S. Yasukochi ◽  
C. Hollmann ◽  
J. Zhang
Keyword(s):  
Calcium Channels ◽  
Voltage Dependent ◽  
Voltage Dependent Calcium Channels
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