scholarly journals The effect of Cyclin-dependent kinase 5 on voltage-dependent calcium channels in PC12 cells varies according to channel type and cell differentiation state

2014 ◽  
Vol 130 (4) ◽  
pp. 498-506 ◽  
Author(s):  
Kotaro Furusawa ◽  
Akiko Asada ◽  
Taro Saito ◽  
Shin-ichi Hisanaga
Keyword(s):  
Cell Differentiation ◽  
Calcium Channels ◽  
Pc12 Cells ◽  
Cyclin Dependent Kinase ◽  
Voltage Dependent ◽  
Voltage Dependent Calcium Channels ◽  
Cyclin Dependent Kinase 5 ◽  
Channel Type

Ketamine induced cell death can be mediated by voltage dependent calcium channels in PC12 cells

2019 ◽  
Vol 111 ◽  
pp. 104318 ◽  
Author(s):  
Juanita Bustamante ◽  
Lucas Acosta ◽  
Analía G. Karadayian ◽  
Silvia Lores-Arnaiz
Keyword(s):  
Cell Death ◽  
Calcium Channels ◽  
Pc12 Cells ◽  
Voltage Dependent ◽  
Voltage Dependent Calcium Channels

Atrial natriuretic peptide differentially modulates T- and L-type calcium channels

1990 ◽  
Vol 258 (3) ◽  
pp. F473-F478 ◽  
Author(s):  
R. T. McCarthy ◽  
C. M. Isales ◽  
W. B. Bollag ◽  
H. Rasmussen ◽  
P. Q. Barrett
Keyword(s):  
Calcium Channels ◽  
Atrial Natriuretic Peptide ◽  
Natriuretic Peptide ◽  
Calcium Influx ◽  
Patch Clamp Technique ◽  
Voltage Dependent ◽  
Voltage Dependent Calcium Channels ◽  
Glomerulosa Cells ◽  
Channel Type ◽  
Atrial Natriuretic

Atrial natriuretic peptide (ANP) inhibits the secretion of aldosterone stimulated by any of these major physiological agonists: angiotensin II, adrenocorticotropic hormone, or K+. The stimulatory actions of each of these agonists depend on calcium influx through voltage-dependent calcium channels. Because two types of calcium channels have been previously described in bovine glomerulosa cells (T- and L-type), the patch-clamp technique was used to evaluate the effect of ANP on each voltage-dependent calcium channel type. ANP was found to differentially modulate these two channel types, stimulating L-current while inhibiting T-current. Inhibition of T-current resulted from a shift in the voltage dependence of inactivation to more negative potentials within the physiological range. These results indicate that the ANP-induced inhibition of aldosterone secretion may be partially mediated via a reduction of the calcium current through T-type channels.

Effects of N- and L-type calcium channel antagonists on the responses of nociceptive spinal cord neurons to mechanical stimulation of the normal and the inflamed knee joint

1996 ◽  
Vol 76 (6) ◽  
pp. 3740-3749 ◽  
Author(s):  
V. Neugebauer ◽  
H. Vanegas ◽  
J. Nebe ◽  
P. Rumenapp ◽  
H. G. Schaible
Keyword(s):  
Spinal Cord ◽  
Knee Joint ◽  
Calcium Channels ◽  
Mechanical Stimulation ◽  
Topical Administration ◽  
Knee Joints ◽  
Spinal Cord Neurons ◽  
Inflammatory Conditions ◽  
Voltage Dependent ◽  
Voltage Dependent Calcium Channels

1. The present study addresses the involvement of voltage-dependent calcium channels of the N and L type in the spinal processing of innocuous and noxious input from the knee joint, both under normal conditions and under inflammatory conditions in which spinal cord neurons become hyperexcitable. In 30 anesthetized rats, extracellular recordings were performed from single dorsal horn neurons in segments 1–4 of the lumbar spinal cord. All neurons had receptive fields in the ipsilateral knee joint. In 22 rats, an inflammation was induced in the ipsilateral knee joint by kaolin and carrageenan 4–16 h before the recordings. The antagonist at N-type calcium channels, omega-conotoxin GVIA (omega-CTx GVIA), was administered topically in solution to the dorsal surface of the spinal cord at the appropriate spinal segments in 6 rats with normal joints and in 12 rats with inflamed knee joints. The antagonist at L-type channels, nimodipine, was administered topically in 5 rats with normal joints and in 11 rats with inflamed knee joints. In another five rats with inflamed joints, antagonists at L-type calcium channels (diltiazem and nimodipine) and omega-CTx GVIA were administered ionophoretically with multibarrel electrodes close to the neurons recorded. 2. The topical administration of omega-CTx GVIA to the spinal cord reduced the responses to both innocuous and noxious pressure applied to the knee joint in a sample of 11 neurons with input from the normal joint and in a sample of 16 neurons with input from the inflamed joint (hyperexcitable neurons). The responses were decreased to approximately 65% of the predrug values within administration times of 30 min. A similar reduction of the responses to innocuous and noxious pressure was observed when omega-CTx GVIA was administered ionophoretically to nine hyperexcitable neurons. In neurons with input from the normal or the inflamed knee joint, the administration of omega-CTx GVIA led also to a reduction of the responses to innocuous and noxious pressure applied to the noninflamed ankle joint. 3. The topical administration of nimodipine decreased the responses to innocuous and noxious pressure applied to the knee in a sample of 9 neurons with input from the normal joint and in a sample of 16 neurons with input from the inflamed knee joint (hyperexcitable neurons). Within administration times of 30 min, the responses were reduced to approximately 70% of the predrug values. In hyperexcitable neurons, the responses to innocuous and noxious pressure applied to the knee were also decreased during ionophoretic administration of nimodipine (6 neurons) and diltiazem (9 neurons). When the noninflamed ankle was stimulated, the responses to innocuous pressure were reduced neither in neurons with input from the normal knee nor in neurons with input from the inflamed knee, but the responses of hyperexcitable neurons to noxious pressure onto the ankle were reduced. The ionophoretic administration of the agonist at the L-type calcium channel, S(-)-Bay K 8644, enhanced the responses to mechanical stimulation of the knee joint in all 14 hyperexcitable neurons tested. The effect of S(-)-Bay K 8644 was counteracted by both diltiazem (in 6 of 6 neurons) and nimodipine (in 5 of 5 neurons). 4. These data show that antagonists at both the N- and the L-type voltage-dependent calcium channels influence the spinal processing of input from the knee joint. The data suggest, therefore, that voltage-dependent calcium calcium channels of both the N and the L type are important for the sensory functions of the spinal cord. They are involved in the spinal processing of nonnociceptive as well as nociceptive mechanosensory input from the joint, both under normal and inflammatory conditions. The present results show in particular that N- and L-type channels are likely to be involved in the generation of pain evoked by noxious mechanical stimulation in normal tissue as well as in the mechanical hyperalgesia that is usually pres

Sign in / Sign up

Export Citation Format

Share Document