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Uptake and release of serotonin in rat cerebrovascular nerves after subarachnoid hemorrhage

Szabo, Csaba; Emilsson, Kjell; Hardebo, Jan Erik LU ; Nystedt, Sverker LU and Owman, Christer (1992) In Stroke: a journal of cerebral circulation 23(1). p.54-61
Abstract
BACKGROUND AND PURPOSE: Serotonin released from platelets has been suggested as one substance causing the vasospasm following subarachnoid hemorrhage. We studied whether such serotonin is able to constrict pial vessels. METHODS: We studied the uptake of serotonin in pial perivascular nerves by immunohistochemistry. We measured the contractile response in rat basilar artery after in vitro incubation with serotonin and during electrical field stimulation of perivascular nerves following experimental subarachnoid hemorrhage. RESULTS: After incubation with serotonin, electrical field stimulation caused a tetrodotoxin- and ketanserin-blockable contractile response. We observed no such response in vessels from rats treated with 6-hydroxydopamine... (More)
BACKGROUND AND PURPOSE: Serotonin released from platelets has been suggested as one substance causing the vasospasm following subarachnoid hemorrhage. We studied whether such serotonin is able to constrict pial vessels. METHODS: We studied the uptake of serotonin in pial perivascular nerves by immunohistochemistry. We measured the contractile response in rat basilar artery after in vitro incubation with serotonin and during electrical field stimulation of perivascular nerves following experimental subarachnoid hemorrhage. RESULTS: After incubation with serotonin, electrical field stimulation caused a tetrodotoxin- and ketanserin-blockable contractile response. We observed no such response in vessels from rats treated with 6-hydroxydopamine or after blockade of serotonin uptake. After subarachnoid hemorrhage, a pronounced network of serotonin-immunoreactive nerve fibers was demonstrated in the vessel wall. In vessels from control rats, no serotonin fibers were seen, and in vessels from 6-hydroxydopamine-treated animals with subarachnoid hemorrhage only a few such fibers were seen. Electrical field stimulation of the basilar artery from rats tested 2 or 16 hours (but not 10 minutes or 24 hours) after subarachnoid hemorrhage showed contractile responses that were prevented by tetrodotoxin, ketanserin, and prior 6-hydroxydopamine treatment. CONCLUSIONS: Our study demonstrates a capacity of the perivascular sympathetic nerves to take up serotonin both in vitro and during the early phase of subarachnoid hemorrhage. Such uptake may help to remove excess serotonin from the subarachnoid space. Only if serotonin is subsequently released upon nerve activation may minor smooth muscle contraction develop. (Less)
Please use this url to cite or link to this publication:
author
organization
publishing date
type
Contribution to journal
publication status
published
subject
in
Stroke: a journal of cerebral circulation
volume
23
issue
1
pages
54 - 61
publisher
American Heart Association
external identifiers
  • pmid:1530992
  • scopus:0026542018
ISSN
1524-4628
language
English
LU publication?
yes
id
feb076d5-9487-47d8-8d53-37baf64b7336 (old id 1106669)
alternative location
http://stroke.ahajournals.org/cgi/reprint/23/1/54
date added to LUP
2008-08-12 08:58:41
date last changed
2017-01-01 07:26:54
@article{feb076d5-9487-47d8-8d53-37baf64b7336,
  abstract     = {BACKGROUND AND PURPOSE: Serotonin released from platelets has been suggested as one substance causing the vasospasm following subarachnoid hemorrhage. We studied whether such serotonin is able to constrict pial vessels. METHODS: We studied the uptake of serotonin in pial perivascular nerves by immunohistochemistry. We measured the contractile response in rat basilar artery after in vitro incubation with serotonin and during electrical field stimulation of perivascular nerves following experimental subarachnoid hemorrhage. RESULTS: After incubation with serotonin, electrical field stimulation caused a tetrodotoxin- and ketanserin-blockable contractile response. We observed no such response in vessels from rats treated with 6-hydroxydopamine or after blockade of serotonin uptake. After subarachnoid hemorrhage, a pronounced network of serotonin-immunoreactive nerve fibers was demonstrated in the vessel wall. In vessels from control rats, no serotonin fibers were seen, and in vessels from 6-hydroxydopamine-treated animals with subarachnoid hemorrhage only a few such fibers were seen. Electrical field stimulation of the basilar artery from rats tested 2 or 16 hours (but not 10 minutes or 24 hours) after subarachnoid hemorrhage showed contractile responses that were prevented by tetrodotoxin, ketanserin, and prior 6-hydroxydopamine treatment. CONCLUSIONS: Our study demonstrates a capacity of the perivascular sympathetic nerves to take up serotonin both in vitro and during the early phase of subarachnoid hemorrhage. Such uptake may help to remove excess serotonin from the subarachnoid space. Only if serotonin is subsequently released upon nerve activation may minor smooth muscle contraction develop.},
  author       = {Szabo, Csaba and Emilsson, Kjell and Hardebo, Jan Erik and Nystedt, Sverker and Owman, Christer},
  issn         = {1524-4628},
  language     = {eng},
  number       = {1},
  pages        = {54--61},
  publisher    = {American Heart Association},
  series       = { Stroke: a journal of cerebral circulation},
  title        = {Uptake and release of serotonin in rat cerebrovascular nerves after subarachnoid hemorrhage},
  volume       = {23},
  year         = {1992},
}