Inhibitory Effect of L-Type Voltage-Dependent Calcium Channel Blocker on Response of Urinary Bladder with Acute Ethanol Intoxication

2010 ◽  
Vol 85 (3) ◽  
pp. 341-346 ◽  
Author(s):  
Mi Mi Oh ◽  
Jae Hyun Bae ◽  
Je Jong Kim ◽  
Hyung Jee Kim ◽  
Du Geon Moon ◽  
...  
Keyword(s):  
Urinary Bladder ◽  
Calcium Channel ◽  
Calcium Channel Blocker ◽  
Channel Blocker ◽  
Inhibitory Effect ◽  
Ethanol Intoxication ◽  
Voltage Dependent Calcium Channel ◽  
Voltage Dependent ◽  
Acute Ethanol ◽  
Acute Ethanol Intoxication

L-Type Voltage-Dependent Calcium Channel Blocker Nifedipine Enhances Memory Retention When Infused into the Hippocampus

1998 ◽  
Vol 69 (3) ◽  
pp. 320-325 ◽  
Author(s):  
João Quevedo ◽  
Mônica Vianna ◽  
Doriana Daroit ◽  
Antônio G. Born ◽  
Carlos R. Kuyven ◽  
...  
Keyword(s):  
Calcium Channel ◽  
Calcium Channel Blocker ◽  
Channel Blocker ◽  
Memory Retention ◽  
Voltage Dependent Calcium Channel ◽  
Voltage Dependent

scholarly journals Agatoxin-IVA-Sensitive Calcium Channels Mediate the Presynaptic and Postsynaptic Nicotinic Activation of Cardiac Vagal Neurons

2001 ◽  
Vol 85 (1) ◽  
pp. 164-168 ◽  
Author(s):  
Jijiang Wang ◽  
Mustapha Irnaten ◽  
David Mendelowitz
Keyword(s):  
Calcium Channels ◽  
Calcium Channel ◽  
Calcium Channel Blocker ◽  
Channel Blocker ◽  
Patch Clamp Technique ◽  
Current Increase ◽  
Inward Current ◽  
Voltage Dependent Calcium Channel ◽  
Voltage Dependent ◽  
Voltage Dependent Calcium Channels

Whole cell currents and miniature glutamatergic synaptic events (minis) were recorded in vitro from cardiac vagal neurons in the nucleus ambiguus using the patch-clamp technique. We examined whether voltage-dependent calcium channels were involved in the nicotinic excitation of cardiac vagal neurons. Nicotine evoked an inward current, increase in mini amplitude, and increase in mini frequency in cardiac vagal neurons. These responses were inhibited by the nonselective voltage-dependent calcium channel blocker Cd (100 μM). The P-type voltage-dependent calcium channel blocker agatoxin IVA (100 nM) abolished the nicotine-evoked responses. Nimodipine (2 μM), an antagonist of L-type calcium channels, inhibited the increase in mini amplitude and frequency but did not block the ligand gated inward current. The N- and Q-type voltage-dependent calcium channel antagonists conotoxin GVIA (1 μM) and conotoxin MVIIC (5 μM) had no effect. We conclude that the presynaptic and postsynaptic facilitation of glutamatergic neurotransmission to cardiac vagal neurons by nicotine involves activation of agatoxin-IVA-sensitive and possibly L-type voltage-dependent calcium channels. The postsynaptic inward current elicited by nicotine is dependent on activation of agatoxin-IVA-sensitive voltage-dependent calcium channels.

Spinal Antinociceptive Action of an N-Type Voltage-dependent Calcium Channel Blocker and the Synergistic Interaction with Morphine

1996 ◽  
Vol 84 (3) ◽  
pp. 636-643 ◽  
Author(s):  
Keiichi Omote ◽  
Mikito Kawamata ◽  
Osamu Satoh ◽  
Hiroshi Iwasaki ◽  
Akiyoshi Namiki
Keyword(s):  
Spinal Cord ◽  
Calcium Channels ◽  
Calcium Channel ◽  
Calcium Channel Blocker ◽  
Channel Blocker ◽  
Intrathecal Morphine ◽  
Tail Flick ◽  
Dependent Manner ◽  
Antinociceptive Effects ◽  
Voltage Dependent

Background Four different voltage-dependent calcium channels (L-, N-, T-, and P-types) are distinguished in the central nervous system. Both L- and N-type calcium channels have been implicated in the release of neurotransmitters from sensory neurons in the spinal cord. It has been demonstrated that intrathecal L-type calcium channel blockers, which alone do not exhibit any antinociceptive effects, potentiate the antinociceptive effect of intrathecal morphine. The current study was designed to investigate the antinociceptive effects of the intrathecally administered N-type calcium channel blocker, omega-conotoxin GVIA (omega-CgTx). The interaction between morphine and omega-CgTx at the level of the spinal cord also was examined. Methods In male Sprague-Dawley rats, lumbar intrathecal catheters were chronically implanted. Tail flick and mechanical paw pressure tests were used to assess thermal and mechanical nociceptive thresholds, respectively. Morphine, omega-CgTx, or a combination of morphine and omega-CgTx was administered intrathecally, and the nociceptive thresholds were determined. Isobolographic analyses were used to define the nature of the functional interactions between morphine and omega-CgTx. Results Intrathecal omega-CgTx produced antinociception in a dose- and time-dependent manner. Isobolographic analyses revealed that intrathecal omega-CgTx and morphine interacted synergistically in both nociceptive tests. Conclusions This study indicates the importance of the N-type calcium channel in the spinal cord on nociception and suggests the functional interaction between the N-type calcium channel blocker and opioid at the level of the spinal cord.

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