Effect of Cold Storage on the Sensitivity of and Calcium Influx into Rat, Rabbit and Guinea Pig Portal Veins

1978 ◽  
Vol 15 (4) ◽  
pp. 217-230 ◽  
Author(s):  
M. Kaiman ◽  
S. Shibata
Keyword(s):  
Guinea Pig ◽  
Cold Storage ◽  
Calcium Influx ◽  
Portal Veins

Calcium influx and spontaneous phasic contractions of portal veins after treatment with reserpine, 6-hydroxydopamine, and cocaine

1978 ◽  
Vol 56 (2) ◽  
pp. 199-201 ◽  
Author(s):  
M. Kaiman ◽  
S. Shibata
Keyword(s):  
Guinea Pig ◽  
Portal Vein ◽  
Calcium Influx ◽  
Phasic Contraction ◽  
Reserpine Treatment ◽  
Portal Veins ◽  
6 Hydroxydopamine ◽  
Induced Changes

Reserpine treatment increased the amplitude of the spontaneous phasic contraction (SPC) of portal veins obtained from rabbit and guinea pig but did not alter that of rat. The amplitude of the SPC of portal veins from these animals was increased after 6-hydroxydopamine (6-OHDA) but was not changed after cocaine treatment. Reserpine-and 6-OHDA-induced changes in portal vein SPC amplitude were accompanied by an increase in 45Ca influx.These results indicate that the elevation in SPC amplitude is accompanied by an increase in calcium influx.

scholarly journals Mechanism of Calcium Influx in Cortical Synaptosomes of the Guinea Pig Fetus. 257

1996 ◽  
Vol 40 (3) ◽  
pp. 558-558
Author(s):  
S. Zanelli ◽  
Y. Numagami ◽  
O. P. Mishra ◽  
M. Delivoria-Papadopoulos
Keyword(s):  
Guinea Pig ◽  
Calcium Influx ◽  
Guinea Pig Fetus

scholarly journals 8 Effect of Dexamethasone on Neuronal Nuclear Calcium Influx in the Developing Fetal Guinea Pig

2005 ◽  
Vol 58 (2) ◽  
pp. 355-355
Author(s):  
E K Anday ◽  
S J Handley ◽  
Q M Ashraf ◽  
O P Mishra
Keyword(s):  
Guinea Pig ◽  
Calcium Influx ◽  
Nuclear Calcium

scholarly journals Nickel suppresses the PACAP-induced increase in guinea pig cardiac neuron excitability

2015 ◽  
Vol 308 (11) ◽  
pp. C857-C866 ◽  
Author(s):  
John D. Tompkins ◽  
Laura A. Merriam ◽  
Beatrice M. Girard ◽  
Victor May ◽  
Rodney L. Parsons
Keyword(s):  
Guinea Pig ◽  
Neuronal Excitability ◽  
Low Voltage ◽  
Calcium Influx ◽  
Quantitative Polymerase Chain Reaction ◽  
Intercellular Signaling ◽  
Neuron Excitability ◽  
Unique System ◽  
Cell Recording ◽  
Recording Conditions

Pituitary adenylate cyclase-activating polypeptide (PACAP) is a potent intercellular signaling molecule involved in multiple homeostatic functions. PACAP/PAC1 receptor signaling increases excitability of neurons within the guinea pig cardiac ganglia, making them a unique system to establish mechanisms underlying PACAP modulation of neuronal function. Calcium influx is required for the PACAP-increased cardiac neuron excitability, although the pathway is unknown. This study tested whether PACAP enhancement of calcium influx through either T-type or R-type channels contributed to the modulation of excitability. Real-time quantitative polymerase chain reaction analyses indicated transcripts for Cav3.1, Cav3.2, and Cav3.3 T-type isoforms and R-type Cav2.3 in cardiac neurons. These neurons often exhibit a hyperpolarization-induced rebound depolarization that remains when cesium is present to block hyperpolarization-activated nonselective cationic currents ( Ih). The T-type calcium channel inhibitors, nickel (Ni2+) or mibefradil, suppressed the rebound depolarization, and treatment with both drugs hyperpolarized cardiac neurons by 2–4 mV. Together, these results are consistent with the presence of functional T-type channels, potentially along with R-type channels, in these cardiac neurons. Fifty micromolar Ni2+, a concentration that suppresses currents in both T-type and R-type channels, blunted the PACAP-initiated increase in excitability. Ni2+ also blunted PACAP enhancement of the hyperpolarization-induced rebound depolarization and reversed the PACAP-mediated increase in excitability, after being initiated, in a subset of cells. Lastly, low voltage-activated currents, measured under perforated patch whole cell recording conditions and potentially flowing through T-type or R-type channels, were enhanced by PACAP. Together, our results suggest that a PACAP-enhanced, Ni2+-sensitive current contributes to PACAP-induced modulation of neuronal excitability.

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