Staff Members - Benha University
PEPTIDERGIC AND NITRERGIC INHIBITORY NEUROTRANSMISSIONS IN THE HAMSTER JEJUNUM: REGULATION OF VASOACTIVE INTESTINAL PEPTIDE RELEASE BY NITRIC OXIDE
Neuroscience • 2002
Publication Information
Authors
H. MATSUYAMA, T. UNNO, A. M. EL-MAHMOUDY, S. KOMORI, H. KOBAYASHI,S. THAPALIYA and T. TAKEWAKI
Keywords
cyclic nucleotide, enteric nerve, guanylate cyclase, inhibitory junction potential, non-adrenergic non-cholinergic,
relaxation.
Journal
Neuroscience
Publisher
Pergamon
Volume
110
Issue
4
Pages
779-788
publication.type
International
Paper Link
Not Available
Supplementary Materials
Not Available
Abstract
jejunum. Electrical ¢eld stimulation and applied NO (3^100 WM) evoked biphasic hyperpolarizations consisting of an
initial transient hyperpolarizing component followed by a second more slowly developing component (late component).
The NO synthase inhibitor NG-nitro-L-arginine methyl ester (200 WM) abolished the biphasic inhibitory junction potential
evoked by electrical ¢eld stimulation. The NO scavenger oxyhemoglobin (50 WM) and the guanylate cyclase inhibitor 1H-
[1,2,4]oxadiazolo-[4,3-a]quinoxalin-1-one (ODQ; 10 WM) abolished both components of the inhibitory junction potentials
and the NO-induced hyperpolarizations. VIP(6^28) (1 WM), which abolished VIP (3 WM)-induced hyperpolarizations, also
inhibited the late components of the inhibitory junction potentials and the NO-induced hyperpolarizations. ODQ inhibited
VIP release and cAMP production by electrical ¢eld stimulation and NO application. N6-2,0-Dibutyryladenosine
3P,5P-cyclic monophosphate (0.1^3 mM) caused a membrane hyperpolarization.
These results suggest that NO may stimulate VIP release from enteric nerves in the hamster jejunum. In addition, we
propose that NO and NO-stimulated VIP contribute to the early and late components of the inhibitory junction
potentials, respectively, in the circular smooth muscle cells of the hamster jejunum.
initial transient hyperpolarizing component followed by a second more slowly developing component (late component).
The NO synthase inhibitor NG-nitro-L-arginine methyl ester (200 WM) abolished the biphasic inhibitory junction potential
evoked by electrical ¢eld stimulation. The NO scavenger oxyhemoglobin (50 WM) and the guanylate cyclase inhibitor 1H-
[1,2,4]oxadiazolo-[4,3-a]quinoxalin-1-one (ODQ; 10 WM) abolished both components of the inhibitory junction potentials
and the NO-induced hyperpolarizations. VIP(6^28) (1 WM), which abolished VIP (3 WM)-induced hyperpolarizations, also
inhibited the late components of the inhibitory junction potentials and the NO-induced hyperpolarizations. ODQ inhibited
VIP release and cAMP production by electrical ¢eld stimulation and NO application. N6-2,0-Dibutyryladenosine
3P,5P-cyclic monophosphate (0.1^3 mM) caused a membrane hyperpolarization.
These results suggest that NO may stimulate VIP release from enteric nerves in the hamster jejunum. In addition, we
propose that NO and NO-stimulated VIP contribute to the early and late components of the inhibitory junction
potentials, respectively, in the circular smooth muscle cells of the hamster jejunum.