scholarly journals Alterations in Serotonin and Neuropeptide Y Content of Cerebrovascular Sympathetic Nerves following Experimental Subarachnoid Hemorrhage

1989 ◽  
Vol 9 (3) ◽  
pp. 271-279 ◽  
Author(s):  
A. Jackowski ◽  
A. Crockard ◽  
G. Burnstock ◽  
J. Lincoln
Keyword(s):  
Subarachnoid Hemorrhage ◽  
Neuropeptide Y ◽  
Sympathetic Nerve ◽  
Blood Clot ◽  
Cerebral Arteries ◽  
Immunohistochemical Analysis ◽  
Sympathetic Nerves ◽  
Nerve Fibers ◽  
Arterial Blood ◽  
Experimental Subarachnoid Hemorrhage

The effect of an experimental subarachnoid hemorrhage (SAH) upon neurotransmitter content in sympathetic nerves supplying the major cerebral arteries of the rat has been examined by immunohistochemical analysis and high performance liquid chromatography with electrochemical detection (HPLC–ECD). In particular, changes that occur in sympathetic nerve content of the vasoconstrictor agents serotonin (5-HT) and neuropeptide Y (NPY), which are colocalized with noradrenaline, were assessed. Subarachnoid hemorrhage was induced by a single injection of autologous arterial blood into the cerebrospinal fluid (CSF) space of the cisterna magna. The density of 5-HT-containing and NPY-containing perivascular nerve fibers per unit area of vessels was measured at defined intervals from 15 min to 5 days post-SAH. In addition, an HPLC study was performed to quantify the actual amounts of 5-HT and noradrenaline present in circle of Willis vessels at 3 h post-SAH. Comparison was made with sham-operated animals and animals that received a cisternal injection of buffered saline in place of blood. Our results reveal a major increase in cerebrovascular sympathetic nerve content of serotonin, arising by uptake, presumably from subarachnoid blood clot, within the first 3 h post-SAH. Neuropeptide Y content, however, decreased from 3 up to 48 h posthemorrhage. By 3 days post-SAH, when the majority of subarachnoid clot had resorbed, the sympathetic nerve content of both NPY and 5-HT was restored to normal. This pattern of change was not observed in either sham-operated or saline-injected controls.

Cerebral perivascular nerves in subarachnoid hemorrhage

1986 ◽  
Vol 65 (4) ◽  
pp. 531-539 ◽  
Author(s):  
Hideaki Hara ◽  
Michael Nosko ◽  
Bryce Weir
Keyword(s):  
Subarachnoid Hemorrhage ◽  
Blood Clot ◽  
Autologous Blood ◽  
Nerve Fibers ◽  
Content Type ◽  
Arterial Blood ◽  
Mild Reduction ◽  
Perivascular Nerves ◽  
Basilar Arteries ◽  
Repeat Angiography

✓ The authors have studied the changes induced by subarachnoid hemorrhage (SAH) in the density and distribution of cerebral perivascular nerves in monkeys and rats. The SAH was induced in monkeys by placement of an autologous blood clot after opening the basal cisterns over the arteries of the circle of Willis on one side. In the rat study, SAH was induced by injection of autologous arterial blood into the cisterna magna. The nerves examined were adrenergic nerves, acetylcholinesterase (AChE)-containing nerves, vasoactive intestinal polypeptide (VIP)-like immunoreactive nerves, and substance P-like immunoreactive nerves. In the monkey study, all animals underwent baseline cerebral angiography, then had repeat angiography just before sacrifice on Day 2, 7, 28, or 70 after SAH. Two sham-operated monkeys underwent the surgical procedure without clot placement and were sacrificed on postoperative Day 7, after repeat angiography. Clot placement in monkeys reduced staining of all middle cerebral artery (MCA) perivascular nerves for between 2 and 28 days post-SAH. The number of stained nerve fibers of MCA's on the non-operated side was slightly reduced on Days 2 and 7 after SAH. Sham-operated monkeys showed a mild reduction of staining in all nerves, but only on the operated side. Cerebral vasospasm was observed on all angiograms taken on Days 2 and 7 following SAH. No vasospasm was found in normal or sham-operated monkeys. The disappearance of nerve staining without associated vasospasm was found on the operated side of the sham-operated monkeys and on the clot side of the animal sacrificed on Day 28 after SAH. Rats sacrificed on Days 2 and 7 post-SAH showed reduction in adrenergic and VIP-like immunoreactive staining around basilar arteries, while nerves containing AChE were not affected. Saline-injected rats exhibited no change in the appearance of perivascular innervation. These results suggest that SAH as well as surgical manipulation of the vessel wall caused a reduction of the studied substances in cerebral perivascular nerves. This reduction in immunoreactive staining of perivascular nerves did not correlate with the development of angiographic vasospasm after SAH.

Ultrastructural evidence of arterial denervation following experimental subarachnoid hemorrhage

1986 ◽  
Vol 64 (2) ◽  
pp. 292-297 ◽  
Author(s):  
Thomas A. Duff ◽  
Grayson Scott ◽  
John A. Feilbach
Keyword(s):  
Subarachnoid Hemorrhage ◽  
Prolonged Exposure ◽  
Cerebral Arteries ◽  
Content Type ◽  
Ultrastructural Evidence ◽  
Experimental Subarachnoid Hemorrhage ◽  
Catecholamine Histofluorescence ◽  
Increased Sensitivity ◽  
The Media ◽  
Adult Cats

✓ Loss of catecholamine histofluorescence, increased sensitivity to norepinephrine, and changes in alpha1 receptor binding have led to the proposal that denervation hypersensitivity may play a role in cerebrovascular spasm. Because the significance of these alterations has remained unclear, the present study was undertaken to determine whether there was direct ultrastructural evidence of arterial denervation following experimental subarachnoid hemorrhage. Under general anesthesia, adult cats were subjected to pre-pontine injection of blood or serum (5 to 7 ml) via a transclival approach. The animals were sacrificed 4, 7, or 10 days later and basilar artery segments were prepared for electron microscopy. Control vessels appeared normal, whereas those bathed in blood revealed unequivocal changes in neural and supporting elements, including: 1) disintegration of both clear- and dense-core vesicles; 2) fragmentation of varicosities; 3) loss of Schwann cell cytoplasm; and 4) axonal degeneration. These changes were most pronounced 7 days after instillation of blood, and correlated in time with maximal injury of the media and endothelium. Although the development of smooth-muscle hypersensitivity remains unsettled, this study indicates that prolonged exposure to blood can cause extensive denervation of cerebral arteries.

scholarly journals Nerve Fibers Containing Neuropeptide Y in the Cerebrovascular Bed: Immunocytochemistry, Radioimmunoassay, and Vasomotor Effects

1987 ◽  
Vol 7 (1) ◽  
pp. 45-57 ◽  
Author(s):  
L. Edvinsson ◽  
J. R. Copeland ◽  
P. C. Emson ◽  
J. McCulloch ◽  
R. Uddman
Keyword(s):  
Neuropeptide Y ◽  
Blood Vessels ◽  
Superior Cervical Ganglion ◽  
Cerebral Arteries ◽  
Nerve Fibers ◽  
Calcium Entry Blocker ◽  
Cervical Ganglion ◽  
Prostaglandin F ◽  
6 Hydroxydopamine

Perivascular nerve fibers containing neuropeptide Y (NPY)-like immunoreactivity were identified around cerebral blood vessels of human, cat, guinea pig, rat, and mouse. The major cerebral arteries were invested by dense plexuses; veins, small arteries, and arterioles were accompanied by few fibers. Removal of the superior cervical ganglion resulted in a reduction of NPY-like material in pial vessels and dura mater. Pretreatment with 6-hydroxydopamine or reserpine reduced the number of visible NPY fibers and the concentration of NPY in rat cerebral vessels. Sequential immuno-staining with antibodies toward dopamine-β-hydroxylase (DBH) (an enzyme involved in the synthesis of noradrenaline) and NPY revealed an identical localization of DBH and NPY in nerve cell bodies in the superior cervical ganglion and in perivascular fibers of pial blood vessels, suggesting their coexistence. Administration of NPY in vitro resulted in concentration-dependent contractions that were not modified by a sympathectomy. The contractions induced by noradrenaline, 5-hydroxytryptamine, and prostaglandin F2α and the dilator responses to calcitonin gene-related peptide were not modified by NPY in rat cerebral arteries. However, the constrictor response to NPY was reduced by 70% in the presence of the calcium entry blocker nifedipine, and abolished following incubation in a calcium-free buffer. These data suggest an interaction of NPY at a postsynaptic site, which for induction of contraction may open calcium channels in the sarcolemma of cerebral arteries.

Changes of neuropeptide immunoreactivity in cerebrovascular nerve fibers after experimentally produced SAH

1987 ◽  
Vol 66 (5) ◽  
pp. 741-747 ◽  
Author(s):  
Yoshihiko Uemura ◽  
Tetsuo Sugimoto ◽  
Shinichiro Okamoto ◽  
Hajime Handa ◽  
Noboru Mizuno
Keyword(s):  
Body Weight ◽  
Subarachnoid Hemorrhage ◽  
Substance P ◽  
Unit Area ◽  
Single Injection ◽  
Nerve Fibers ◽  
The Other ◽  
Content Type ◽  
Arterial Blood ◽  
Fine Print

✓ The immunoreactivity of vasoactive intestinal polypeptide (VIP)-, substance P (SP)-, and neuropeptide Y (NPY)-containing nerve fibers in the basilar artery (BA) and proximal portion of the middle cerebral artery (M1) was immunohistochemically examined in the dog after experimentally produced subarachnoid hemorrhage (SAH). The SAH was produced by a single injection of fresh autologous arterial blood (1 ml/kg body weight) into the cisterna magna. The density (the averaged number of nerve fibers in a unit area) of VIP-, SP-, and NPY-immunoreactive perivascular nerve fibers in the M1 segment and the BA was markedly decreased (5% to 40% of the normal value) immediately after the injection. The density of VIP- and SP-immunoreactive perivascular fibers increased 2 or 3 weeks after SAH and became normal by the 63rd day after injection. On the other hand, no substantial recovery was observed in the density of NPY-immunoreactive perivascular fibers by 63 days after injection.

Subarachnoid hemorrhage—induced upregulation of the 5-HT1B receptor in cerebral arteries in rats

2003 ◽  
Vol 99 (1) ◽  
pp. 115-120 ◽  
Author(s):  
Jacob Hansen-Schwartz ◽  
Natalie Løvland Hoel ◽  
Cang-Bao Xu ◽  
Niels-Aage Svendgaard ◽  
Lars Edvinsson
Keyword(s):  
Subarachnoid Hemorrhage ◽  
Real Time ◽  
Cerebral Vasospasm ◽  
Cerebral Arteries ◽  
Specific Treatment ◽  
Content Type ◽  
Sequence Of Events ◽  
Arterial Blood ◽  
Receptor Phenotype ◽  
Fine Print

Object. Cerebral vasospasm following subarachnoid hemorrhage (SAH) leads to reduced blood flow in the brain. Inspired by organ culture—induced changes in the receptor phenotype of cerebral arteries, the authors investigated possible changes in the 5-hydroxytryptamine (HT) receptor phenotype after experimental SAH. Methods. Experimental SAH was induced in rats by using an autologous prechiasmatic injection of arterial blood. Two days later, the middle cerebral artery (MCA), posterior communicating artery (PCoA), and basilar artery (BA) were harvested and examined functionally with the aid of a sensitive in vitro pharmacological method and molecularly by performing quantitative real-time reverse transcription—polymerase chain reaction (PCR). In the MCA and BA the 5-HT1B receptor was upregulated, as determined through both functional and molecular analysis. In response to selective 5-HT1 receptor agonists both the negative logarithm of the 50% effective concentration was increased (one log unit in the MCA and one half unit in the BA), as was the agonist's potency (increased by 50% in the MCA and doubled in the BA). In addition, the authors found an approximately fourfold increase in the number of copies of messenger RNA coding for the 5-HT1B receptor as determined by quantitative real-time PCR. In the PCoA no upregulation of the 5-HT1B receptor was observed. Conclusions. Changes in the receptor phenotype in favor of contractile receptors may well represent the end stage in a sequence of events leading from SAH to the actual development of cerebral vasospasm. Insight into the mechanism of upregulation may provide new targets for developing specific treatment against cerebral vasospasm.

Neuropeptide Y as a presynaptic modulator of norepinephrine release from the sympathetic nerve fibers in the pig pineal gland

2015 ◽  
Vol 18 (1) ◽  
pp. 53-61 ◽  
Author(s):  
N. Ziółkowska ◽  
B. Lewczuk ◽  
B. Przybylska-Gornowicz
Keyword(s):  
Pineal Gland ◽  
Neuropeptide Y ◽  
Sympathetic Nerve ◽  
Nerve Fibers ◽  
Adrenergic Nerve ◽  
Sympathetic Nerve Fibers ◽  
Uk 14,304 ◽  
Mammalian Pineal Gland ◽  
Pharmacologically Active

Abstract Norepinephrine (NE) released from the sympathetic nerve endings is the main neurotransmitter controlling melatonin synthesis in the mammalian pineal gland. Although neuropeptide Y (NPY) co-exists with NE in the pineal sympathetic nerve fibers it also occurs in a population of non-adrenergic nerve fibers located in this gland. The role of NPY in pineal physiology is still enigmatic. The present study characterizes the effect of NPY on the depolarization-evoked 3H-NE release from the pig pineal explants. The explants of the pig pineal gland were loaded with 3H-NE in the presence of pargyline and superfused with Tyrode medium. They were exposed twice to the modified Tyrode medium containing 60 mM of K+ to evoke the 3H-NE release via depolarization. NPY, specific agonists of Y1- and Y2-receptors and pharmacologically active ligands of α2-adrenoceptors were added to the medium before and during the second depolarization. The radioactivity was measured in medium fractions collected every 2 minutes during the superfusion. NPY (0.1 – 10 μM) significantly decreased the depolarization-induced 3H-NE release. Similar effect was observed after the treatment with Y2-agonist: NPY13-36, but not with Y1-agonist: [Leu31, Pro34]-NPY. The tritium overflow was lower in the explants exposed to the 5 μM NPY and 1 μM rauwolscine than to rauwolscine only. The effects of 5 μM NPY and 0.05 μM UK 14,304 on the depolarization-evoked 3H-NE release were additive. The results show that NPY is involved in the regulation of NE release from the sympathetic terminals in the pig pineal gland, inhibiting this process via Y2-receptors.

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