Comparison of the Changes in Protein Kinase C Induced by Glutamate in Primary Cortical Neurons and by in Vivo Cerebral Ischaemia

1998 ◽  
Vol 10 (4) ◽  
pp. 291-295 ◽  
Author(s):  
Balu R Chakravarthy ◽  
Jian Wang ◽  
Roger Tremblay ◽  
Trevor G Atkinson ◽  
Fuhu Wang ◽  
...  
Keyword(s):  
Protein Kinase C ◽  
Protein Kinase ◽  
Cerebral Ischaemia ◽  
Cortical Neurons ◽  
Primary Cortical Neurons ◽  
Kinase C

Chronic treatment by the calcium channel blocker ± PN 200-110 in the rat counteracts the stimulations of pituitary weight, prolactin release and pituitary C-kinase activity induced by a chronic estradiol treatment, in vivo

1990 ◽  
Vol 122 (3) ◽  
pp. 403-408
Author(s):  
Ph. Touraine ◽  
P. Birman ◽  
F. Bai-Grenier ◽  
C. Dubray ◽  
F. Peillon ◽  
...  
Keyword(s):  
Protein Kinase C ◽  
Protein Kinase ◽  
Calcium Channel ◽  
Calcium Channel Blocker ◽  
Channel Blocker ◽  
Plasma Prolactin ◽  
Estradiol Treatment ◽  
Kinase C ◽  
Protein Kinase C Activity

Abstract In order to investigate whether a calcium channel blocker could modulate the protein kinase C activity in normal and estradiol pretreated rat pituitary, female Wistar rats were treated or not (controls) with ± PN 200-110 (3 mg · kg−1 · day−1, sc) for 8 days or with estradiol cervical implants for 8 or 15 days, alone or in combination with PN 200-110 the last 8 days. Estradiol treatment induced a significant increase in plasma prolactin levels and pituitary weight. PN 200-110 administered to normal rats did not modify these parameters, whereas it reduced the effects of the 15 days estradiol treatment on prolactin levels (53.1 ± 4.9 vs 95.0 ±9.1 μg/l, p<0.0001) and pituitary weight (19.9 ± 0.4 vs 23.0 ± 0.6 mg, p <0.001), to values statistically comparable to those measured after 8 days of estradiol treatment. PN 200-110 alone did not induce any change in protein kinase C activity as compared with controls. In contrast, PN 200-110 treatment significantly counteracted the large increase in soluble activity and the decrease in the particulate one induced by estradiol between day 8 and day 15. We conclude that PN 200-110 opposed the stimulatory effects of chronic in vivo estradiol treatment on plasma prolactin levels and pituitary weight and that this regulation was related to a concomitant modulation of the protein kinase C activity.

scholarly journals Regulation of protein kinase C by the anti-Parkinson drug, MAO-B inhibitor, rasagiline and its derivatives, in vivo

2004 ◽  
Vol 89 (5) ◽  
pp. 1119-1125 ◽  
Author(s):  
Orit Bar-Am ◽  
Merav Yogev-Falach ◽  
Tamar Amit ◽  
Yotam Sagi ◽  
Moussa B. H. Youdim
Keyword(s):  
Protein Kinase C ◽  
Protein Kinase ◽  
Mao B ◽  
Kinase C

scholarly journals Nuclear diacylglycerol is increased during cell proliferation in vivo

1993 ◽  
Vol 290 (3) ◽  
pp. 633-636 ◽  
Author(s):  
H Banfić ◽  
M Žižak ◽  
N Divecha ◽  
R F Irvine
Keyword(s):  
Cell Proliferation ◽  
Protein Kinase C ◽  
Protein Kinase ◽  
Nuclear Membrane ◽  
Cellular Proliferation ◽  
Detectable Change ◽  
Renal Growth ◽  
Kinase C ◽  
Stimulation Of

Highly purified nuclei were prepared from livers and kidneys of rats undergoing compensatory hepatic or renal growth, the former being predominantly by cellular proliferation, and the latter mostly by cellular enlargement. In liver, an increase in nuclear diacylglycerol (DAG) concentration occurred between 16 and 30 h, peaking at around 20 h. At the peak of nuclear DAG production a specific translocation of protein kinase C to the nucleus could be detected; no such changes occurred in kidney. There was no detectable change in whole-cell DAG levels in liver, and the increase in DAG was only measurable in nuclei freed of their nuclear membrane. Overall, these results suggest that there is a stimulation of intranuclear DAG production, possibly through the activation of an inositide cycle [Divecha, Banfić and Irvine (1991) EMBO J. 10, 3207-3214] during cell proliferation in vivo.

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