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.

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

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.

scholarly journals Voltage-Dependent Calcium Channel CaV1.3 Subunits Regulate the Light Peak of the Electroretinogram

2007 ◽  
Vol 97 (5) ◽  
pp. 3731-3735 ◽  
Author(s):  
Jiang Wu ◽  
Alan D. Marmorstein ◽  
Jörg Striessnig ◽  
Neal S. Peachey
Keyword(s):  
Calcium Channel ◽  
Pigment Epithelium ◽  
Retinal Pigment ◽  
Rod Photoreceptor ◽  
Wild Type ◽  
Fast Oscillation ◽  
Light Peak ◽  
Voltage Dependent Calcium Channel ◽  
Voltage Dependent ◽  
Voltage Dependent Calcium Channels

In response to light, the mouse retinal pigment epithelium (RPE) generates a series of slow changes in potential that are referred to as the c-wave, fast oscillation (FO), and light peak (LP) of the electroretinogram (ERG). The LP is generated by a depolarization of the basolateral RPE plasma membrane by the activation of a calcium-sensitive chloride conductance. We have previously shown that the LP is reduced in both mice and rats by nimodipine, which blocks voltage-dependent calcium channels (VDCCs) and is abnormal in lethargic mice, carrying a null mutation in the calcium channel β4 subunit. To define the α1 subunit involved in this process, we examined mice lacking CaV1.3. In comparison with wild-type (WT) control littermates, LPs were reduced in CaV1.3−/− mice. This pattern matched closely with that previously noted in lethargic mice, confirming a role for VDCCs in regulating the signaling pathway that culminates in LP generation. These abnormalities do not reflect a defect in rod photoreceptor activity, which provides the input to the RPE to generate the c-wave, FO, and LP, because ERG a-waves were comparable in WT and CaV1.3−/− littermates. Our results identify CaV1.3 as the principal pore-forming subunit of VDCCs involved in stimulating the ERG LP.

Depolarization-stimulated cholecystokinin secretion is mediated by L-type calcium channels in STC-1 cells

1996 ◽  
Vol 270 (2) ◽  
pp. G287-G290 ◽  
Author(s):  
A. W. Mangel ◽  
L. Scott ◽  
R. A. Liddle
Keyword(s):  
Calcium Channels ◽  
Calcium Channel ◽  
Calcium Channel Blocker ◽  
Channel Blocker ◽  
Single Channel ◽  
Bay K 8644 ◽  
Ic50 Value ◽  
Single Channel Currents ◽  
Dose Dependent ◽  
Cck Release

To examine the role of calcium channels in depolarization-activated cholecystokinin (CCK) release, studies were performed in an intestinal CCK-secreting cell line, STC-1. Blockade of potassium channels with barium chloride (5 mM) increased the release of CCK by 374.6 +/- 46.6% of control levels. Barium-induced secretion was inhibited by the L-type calcium-channel blocker, nicardipine. Nicardipine (10(-9)-10(-5) M) produced a dose-dependent inhibition in barium-stimulated secretion with a half-maximal inhibition (IC50) value of 0.1 microM. A second L-type calcium-channel blocker, diltiazem (10(-9)-10(-4) M), also inhibited barium-induced CCK secretion with an IC50 value of 5.1 microM. By contrast, the T-type calcium-channel blocker, nickel chloride (10(-7)-10(-8) M), failed to significantly inhibit barium-induced CCK secretion. To further evaluate a role for L-type calcium channels in the secretion of CCK, the effects of the L-type calcium channel opener, BAY K 8644, were examined. BAY K 8644 (10(-8)-10(-4) M) produced a dose-dependent stimulation in CCK release with a mean effective concentration value of 0.2 microM. Recordings of single-channel currents from inside-out membrane patches showed activation of calcium channels by BAY K 8644 (1 microM), with a primary channel conductance of 26.0 +/- 1.2 pS. It is concluded that inhibition of potassium channel activity depolarizes the plasma membrane, thereby activating L-type, but not T-type, calcium channels. The corresponding influx of calcium serves to trigger secretion of CCK.

Voltage-dependent calcium channels in ventricular cells of rainbow trout: effect of temperature changes in vitro

2000 ◽  
Vol 278 (6) ◽  
pp. R1524-R1534 ◽  
Author(s):  
Catherine S. Kim ◽  
Mary D. Coyne ◽  
Judith K. Gwathmey
Keyword(s):  
Rainbow Trout ◽  
Calcium Channels ◽  
Temperature Sensitivity ◽  
Calcium Currents ◽  
Temperature Dependency ◽  
Patch Clamp Technique ◽  
Ventricular Cells ◽  
Voltage Dependent ◽  
Voltage Dependent Calcium Channels

Voltage-dependent calcium channels (VDCC) in ventricular myocytes from rainbow trout ( Oncorhynchus mykiss) were investigated in vitro using the perforated patch-clamp technique, which maintains the integrity of the intracellular milieu. First, we characterized the current using barium as the charge carrier and established the doses of various pharmacological agents to use these agents in additional studies. Second, we examined the current at several physiological temperatures to determine temperature dependency. The calcium currents at 10°C (acclimation temperature) were identified as l-type calcium currents based on their kinetic behavior and response to various calcium channel agonists and antagonists. Myocytes were chilled (4°C) and warmed (18 and 22°C), and the response of VDCC to varying temperatures was observed. There was no significant dependency of the current amplitude and kinetics on temperature. Amplitude decreased 25–36% at 4°C (Q10 ∼1.89) and increased 18% at 18°C (Q10 ∼1.23) in control, Bay K8644 (Bay K)-, and forskolin-enhanced currents. The inactivation rates (τi) did not demonstrate a temperature sensitivity for the VDCC (Q10 1.23–1.92); Bay K treatment, however, increased temperature sensitivity of τi between 10 and 18°C (Q10 3.98). The low Q10 values for VDCC are consistent with a minimal temperature sensitivity of trout myocytes between 4 and 22°C. This low-temperature dependency may provide an important role for sarcolemmal calcium channels in adaptation to varying environmental temperatures in trout.

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