Endopeptidase-24.15 Is the Primary Enzyme that Degrades Luteinizing Hormone Releasing Hormone Both In Vitro and In Vivo

1988 ◽  
Vol 51 (2) ◽  
pp. 624-633 ◽  
Author(s):  
Christopher J. Molineaux ◽  
Abraham Lasdun ◽  
Charlene Michaud ◽  
Marian Orlowski
1994 ◽  
Vol 37 (5) ◽  
pp. 701-705 ◽  
Author(s):  
Fortuna Haviv ◽  
Timothy D. Fitzpatrick ◽  
Charles J. Nichols ◽  
Eugene N. Bush ◽  
Gilbert Diaz ◽  
...  

1993 ◽  
Vol 90 (21) ◽  
pp. 10130-10134 ◽  
Author(s):  
V. Rettori ◽  
N. Belova ◽  
W. L. Dees ◽  
C. L. Nyberg ◽  
M. Gimeno ◽  
...  

1976 ◽  
Vol 5 (s1) ◽  
pp. s279-s289 ◽  
Author(s):  
L. FERLAND ◽  
F. LABRIE ◽  
M. SAVARY ◽  
M. BEAULIEU ◽  
D.H. COY ◽  
...  

2000 ◽  
Vol 78 (8) ◽  
pp. 636-644 ◽  
Author(s):  
Christopher P Ford ◽  
Alexander Y Ivanoff ◽  
Peter A Smith

A 2 min sample of an intracellular recording of in vivo synaptic activity from a vasomotor C-neuron in a bullfrog sympathetic ganglion was converted to a series of stimulus pulses. This physiologically derived activity was used to stimulate preganglionic C-fibres of similar ganglia studied in vitro. Intracellular recordings were made from exocrine B-cells within the ganglia. Although they do not receive fast, nicotinic synaptic input from preganglionic C-fibres, B-cell excitability was profoundly increased by stimulation of C-fibres with physiologically derived activity. Also, subthreshold depolarizing current pulses that failed to generate action potentials in B-cells under control conditions almost always generated action potentials whilst C-fibres were activated. These effects were attenuated or prevented by the luteinizing hormone releasing hormone antagonist, [D-pyro-Glu1,D-Phe2,D-Trp3,6]-LHRH (70 µM). The physiological release of luteinizing hormone releasing hormone from C-fibres therefore causes an interaction between vasomotor and exocrine outflow within a paravertebral sympathetic ganglion.Key words: ganglionic transmission, hypertension, autonomic nerve, m-current, neuropeptide.


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