Spinal modulation of duodenal and colonic motility and arterial pressure by neuropeptide Y, neuropeptide Y fragment 13–36, peptide YY, and pancreatic polypeptide in rats: involvement of the cholinergic nervous system

1993 ◽  
Vol 71 (2) ◽  
pp. 112-119 ◽  
Author(s):  
S. A. Wager-Pagé ◽  
E. Raizada ◽  
W. L. Veale ◽  
J. S. Davison
Keyword(s):  
Spinal Cord ◽  
Arterial Pressure ◽  
Neuropeptide Y ◽  
Pancreatic Polypeptide ◽  
Peptide Yy ◽  
Colonic Motility ◽  
Intraluminal Pressure ◽  
Thoracic Spinal Cord ◽  
Fold Family ◽  
Thoracic Spinal

The pancreatic polypeptide-fold (PP-fold) peptides, peptide YY (PYY) and pancreatic polypeptide (PP) (200 pmol), increased duodenal intraluminal pressure following intrathecal (IT) administration into the thoracic (T8–T10) spinal cord of urethane-anesthetized rats. Neuropeptide Y (NPY), PPY, and PP (IT) increased colonic intraluminal pressure of rats. The excitatory effects of the PP-fold peptides, NPY and PYY, were accompanied by increases in mean arterial pressure (MAP) during the same time period followed by a decrease to hypotensive levels. There were no further alterations of duodenal or colonic pressure in rats during the hypotensive period. The effect of PP (IT) on MAP was characterized by a pattern of hypotension frequently followed by a hypertensive period. The modulation of duodenal and colonic pressure does not differ between the members of the PP-fold family of peptides; however, the effects of the different members of the PP-fold family of peptides on MAP were varied. The Y2 receptor ligand, NPY (13–36) (200 pmol) (IT), did not alter duodenal and colonic pressure or MAP in rats. Therefore, the effects of PYY and NPY in the thoracic spinal cord on duodenal and colonic motility may be mediated via Y1 (postjunctional) receptors. Atropine, a muscarinic antagonist, attenuated NPY's (IT) excitatory effect on colonic pressure but did not alter the MAP response to this peptide. Atropine did not modify PYY's (IT) regulation of duodenal and colonic intraluminal pressure. However, atropine did attenuate PPY's inhibitory effect on MAP. The modulatory effects of PP (IT) on colonic pressure and MAP were attenuated by atropine, suggesting that the cholinergic system may be mediating the effects of this peptide. These observations provide further evidence that the modulation of gastrointestinal motility by PYY, PP, and NPY in the thoracic spinal cord is through different mechanisms.Key words: PP-fold peptides, duodenum, colon, atropine.

Peripheral modulation of duodenal and colonic motility and arterial pressure by neuropeptide Y, neuropeptide Y fragment 13–36, peptide YY, and pancreatic polypeptide in rats: cholinergic mechanisms

1993 ◽  
Vol 71 (10-11) ◽  
pp. 768-775 ◽  
Author(s):  
S. A. Wager-Pagé ◽  
E. Raizada ◽  
W. Veale ◽  
J. S. Davison
Keyword(s):  
Arterial Pressure ◽  
Neuropeptide Y ◽  
Gastrointestinal Motility ◽  
Pancreatic Polypeptide ◽  
Peptide Yy ◽  
Colonic Motility ◽  
Intraluminal Pressure ◽  
Rat Colon ◽  
Excitatory Effect ◽  
Anesthetized Rats

The pancreatic polypeptide-fold (PP-fold) peptides neuropeptide Y (NPY), peptide YY (PYY), and pancreatic polypeptide (PP) (500 pmol/kg) increased duodenal and colonic intraluminal pressure of urethane-anesthetized rats following intravenous (iv) bolus injections. Increases in mean arterial pressure (MAP) accompanied the excitatory effects of NPY and PYY on gastrointestinal motility in these rats during the same time period. Atropine attenuated PYY's excitatory effect on duodenal pressure of rats. Excitatory effects of NPY, PYY, and PP (iv) on rat colon were not mediated via the muscarinic receptors. In the presence of hexamethonium, a nicotinic antagonist, PP (iv) increased colonic pressure to a greater extent than when administered alone. This observation suggested that PP had an inhibitory effect on colonic motility, which was not apparent as a result of the larger excitatory component. The nicotinic antagonist did not modulate the effects of peripherally administered NPY or PYY on duodenal or colonic motility in anesthetized rats. The Y2 receptor ligand, NPY (13–36) (iv) (500 pmol/kg), increased duodenal and colonic pressure in rats to the same extent as the full NPY molecule. Therefore, the peripheral effect of PYY and NPY on duodenal and colonic motility in rats may be mediated via Y2 receptors. NPY and PYY (iv) initially increased MAP, which then return to baseline values. Unlike NPY and PYY (iv) which produced short-term hypertensive effects, PP (iv) decreased MAP. Atropine did not attenuate the hypertensive effects of PYY and NPY (iv); however, the hypotensive effect of PP (iv) was blocked by atropine. The effects of the PP-fold peptides on MAP were not altered in the presence of hexamethonium. MAP in anesthetized rats was not modulated by NPY (13–36) (iv). Peripheral modulation of MAP by the PP-fold peptides does not correspond with alterations in gastrointestinal motility observed in these studies.Key words: pancreatic polypeptide-fold peptides, duodenum, colon, atropine.

The peripheral modulation of duodenal and colonic motility in rats by the pancreatic polypeptide-fold family: Neuropeptide Y, peptide YY, and pancreatic polypeptide

Peptides ◽  
1993 ◽  
Vol 14 (2) ◽  
pp. 153-160 ◽  
Author(s):  
S.A. Wager-Pagé ◽  
B. Ghazali ◽  
W. Anderson ◽  
W.L. Veale ◽  
J.S. Davison
Keyword(s):  
Neuropeptide Y ◽  
Pancreatic Polypeptide ◽  
Peptide Yy ◽  
Colonic Motility ◽  
Fold Family

Neuropeptide Y, peptide YY, and pancreatic polypeptide modulate duodenal and colonic motility at a thoracic spinal site in rats

Peptides ◽  
1992 ◽  
Vol 13 (4) ◽  
pp. 807-813 ◽  
Author(s):  
S.A. Wager-Pagé ◽  
B. Ghazali ◽  
W. Anderson ◽  
W.L. Veale ◽  
J.S. Davison
Keyword(s):  
Neuropeptide Y ◽  
Pancreatic Polypeptide ◽  
Peptide Yy ◽  
Colonic Motility ◽  
Thoracic Spinal

A5 noradrenergic unit activity and sympathetic nerve discharge in rats

1991 ◽  
Vol 261 (2) ◽  
pp. R393-R402 ◽  
Author(s):  
D. H. Huangfu ◽  
N. Koshiya ◽  
P. G. Guyenet
Keyword(s):  
Spinal Cord ◽  
Arterial Pressure ◽  
Sympathetic Nerve ◽  
Unit Recording ◽  
Thoracic Spinal Cord ◽  
Aortic Depressor Nerve ◽  
Thoracic Spinal ◽  
A5 Area ◽  
6 Hydroxydopamine ◽  
Nerve Discharge

Unit recording experiments were designed to determine whether A5 noradrenergic neurons contribute to the generation of the splanchnic sympathetic nerve discharge (SSND) of halothane-anesthetized rats. Neurons (presumed A5 cells) were selected on the following bases: location in the ventrolateral tegmentum rostrolateral to facial nucleus (FN), antidromic (AD) activation from thoracic spinal cord, and complete inhibition by clonidine (10-15 micrograms/kg iv). These cells (n = 59) had low rates of spontaneous firing (1.4 +/- 0.2 spikes/s) and slow conduction velocities (2.6 +/- 0.2 m/s). The AD activation of seven of eight neurons was abolished within 1 h after intraspinal microinjection of 6-hydroxydopamine (4 micrograms), but the drug failed to affect the AD responses of eight sympathoexcitatory cells located caudal to the FN (control cells). The terminal fields of 16 A5 area neurons were found in the intermediolateral cell column of the spinal cord. Most neurons (63%, 37/59) were inhibited by raising arterial pressure and by train stimulation of the aortic depressor nerve (ADN, 47%, 9/20). A few cells responded to ADN stimulation but not to arterial pressure elevation or vice versa. The discharge of the cells was correlated to the SSND and preceded a peak of SSND by 69 +/- 6 ms (12/29 in intact and 3/9 in debuffered rats). We conclude that 40% of A5 cells may have a visceral vasomotor sympathoexcitatory function.

Spinal and peripheral modulation of gastric acid secretion and arterial pressure by neuropeptide Y, peptide YY, and pancreatic polypeptide in rats

Peptides ◽  
1993 ◽  
Vol 14 (6) ◽  
pp. 1299-1308 ◽  
Author(s):  
S.A. Wager-Pagé ◽  
G. Rosenbaum ◽  
W.L. Veale ◽  
J.S. Davison
Keyword(s):  
Arterial Pressure ◽  
Acid Secretion ◽  
Neuropeptide Y ◽  
Gastric Acid Secretion ◽  
Gastric Acid ◽  
Pancreatic Polypeptide ◽  
Peptide Yy

Neuropeptide Y-immunoreactive synapses in the intermediolateral cell column of rat and rabbit thoracic spinal cord

1990 ◽  
Vol 108 (3) ◽  
pp. 243-248 ◽  
Author(s):  
I.J. Llewellyn-Smith ◽  
J.B. Minson ◽  
D.A. Morilak ◽  
J.R. Oliver ◽  
J.P. Chalmers
Keyword(s):  
Spinal Cord ◽  
Neuropeptide Y ◽  
Cell Column ◽  
Thoracic Spinal Cord ◽  
Thoracic Spinal

THERE ARE FEW CATECHOLAMINE- OR NEUROPEPTIDE Y-CONTAINING SYNAPSES IN THE INTERMEDIOLATERAL CELL COLUMN OF RAT THORACIC SPINAL CORD

1991 ◽  
Vol 18 (2) ◽  
pp. 111-115 ◽  
Author(s):  
Ida J. Llewellyn-Smith ◽  
Jane B. Minson ◽  
Paul M. Pilowsky ◽  
John P. Chalmers
Keyword(s):  
Spinal Cord ◽  
Neuropeptide Y ◽  
Cell Column ◽  
Thoracic Spinal Cord ◽  
Thoracic Spinal

Cardiovascular neurons of brain stem with projections to spinal cord

1984 ◽  
Vol 247 (6) ◽  
pp. R1009-R1016 ◽  
Author(s):  
D. L. Brown ◽  
P. G. Guyenet
Keyword(s):  
Spinal Cord ◽  
Arterial Pressure ◽  
Ventrolateral Medulla ◽  
Cervical Cord ◽  
Thoracic Spinal Cord ◽  
Antidromic Activation ◽  
Axonal Projections ◽  
Thoracic Spinal ◽  
Cardiovascular Neurons ◽  
Pressure Changes

In urethan-anesthetized rats a portion of the rostral ventrolateral medulla, the intermediate portion of the nucleus paragigantocellularis lateralis, was explored electrophysiologically for spinally projecting cardiovascular neurons. Spinal projections were demonstrated for 48 of 300 units tested for antidromic activation following spinal cord stimulation. The cardiovascular nature of units was tested by monitoring unit activity during transient changes in arterial pressure. A total of 47 cardiovascular neurons were identified; of these, 43 showed activities inversely correlated with arterial pressure and changes in activity closely coupled in time to arterial pressure changes. At high arterial pressures these neurons also displayed activities phasically linked to the cardiac cycle. Of these 43 neurons, 13 projected to or through the thoracic cord and 5 to or through the cervical cord. Axonal conduction velocities averaged 4.7 m/s. A second type of cardiovascular neuron (4 units of 47) was found that increased activity as arterial pressure increased. Three of these neurons projected to the cord. These results provide evidence for tonically active, baroreceptor-inhibited neurons with axonal projections to the thoracic spinal cord.

Spontaneous Herniation of the Thoracic Spinal Cord: A Case Report

2001 ◽  
Vol 45 (4) ◽  
pp. 353 ◽  
Author(s):  
Sung Chan Jin ◽  
Seoung Ro Lee ◽  
Dong Woo Park ◽  
Kyung Bin Joo
Keyword(s):  
Spinal Cord ◽  
Case Report ◽  
Thoracic Spinal Cord ◽  
Thoracic Spinal ◽  
Spontaneous Herniation
Sign in / Sign up

Export Citation Format

Share Document