MEMBRANE EXCITABILITY AND SECRETION FROM NERVE ENDINGS
Project Number3R37NS030016-10S1
Former Number2R01NS030016-10
Contact PI/Project LeaderJACKSON, MEYER B.
Awardee OrganizationUNIVERSITY OF WISCONSIN-MADISON
Description
Abstract Text
DESCRIPTION: The posterior pituitary is formed by nerve terminals emanating
from the hypothalamus. The posterior pituitary releases two peptide hormones,
vasopressin, which regulates blood circulation and renal function, and
oxytocin, which regulates various reproductive functions. The nerve terminals
of the posterior pituitary are unusually large, making them ideal for
experimentation with patch clamp and imaging techniques. This provides a unique
opportunity to investigate basic mechanisms underlying the regulation of
neurosecretion. The present plan continues an investigation of membrane
excitability in the posterior pituitary, emphasizing two recently discovered
aspects of ion channel modulation. The first of these involves the labile
gaseous signaling molecule nitric oxide (NO), which modulates ion channels in
the posterior pituitary. Experiments will explore how NO and the NO signaling
cascade modulate ion channels. The second involves sigma receptors, which
modulate posterior pituitary ion channels in response to a number of ligands,
including antipsychotic and psychotomimetic drugs. NO and sigma receptors
employ novel mechanisms in the modulation of ion channels, and represent
important additions to the repertoire of signaling pathways that affect
electrical excitability. These mechanisms of ion channel modulation take on
added significance in the context of the posterior pituitary, because they
contribute to the regulation of neurosecretion. This study will examine how
alterations in channel function influence action potential shape, calcium
entry, and the propagation of electrical impulses through the complex terminal
arborizations of the posterior pituitary. These factors influence release in
profoundly different ways. Thus, this project will test basic hypotheses about
how chemical signaling controls neurosecretion. Since axons generally extend
over considerable distances, exhibit complex geometries, and have very large
numbers of secretory specializations, these studies of the relationship between
axonal geometry and ion channel modulation will have broad implications for the
role of axon terminals in neural circuit function.
National Institute of Neurological Disorders and Stroke
CFDA Code
853
DUNS Number
161202122
UEI
LCLSJAGTNZQ7
Project Start Date
01-January-1992
Project End Date
30-November-2004
Budget Start Date
06-February-2001
Budget End Date
30-November-2001
Project Funding Information for 2001
Total Funding
$17,904
Direct Costs
$15,276
Indirect Costs
$2,628
Year
Funding IC
FY Total Cost by IC
2001
National Institute of Neurological Disorders and Stroke
$17,904
Year
Funding IC
FY Total Cost by IC
Sub Projects
No Sub Projects information available for 3R37NS030016-10S1
Publications
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No Publications available for 3R37NS030016-10S1
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Outcomes
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No Outcomes available for 3R37NS030016-10S1
Clinical Studies
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History
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