Extracellular release of serotonin following fluid-percussion brain injury in rats

Raul Busto, W. Dalton Dietrich, Mordecai Y T Globus, Ofelia Alonso, Myron Ginsberg

Research output: Contribution to journalArticle

43 Citations (Scopus)

Abstract

Serotonin has been implicated in the pathobiology of central nervous system trauma. Using microdialysis techniques, we performed measurements of extracellular serotonin release within the traumatized cerebral cortex of rats subjected to moderate fluid-percussion (F-P) brain injury. Twenty-four hours prior to TBI, a F-P interface was positioned parasagitally over the right cerebral cortex. On the second day, fasted rats were anesthetized with 70% nitrous oxide, 1% halothane, and 30% oxygen. Under controlled physiological conditions and normothermic brain temperature (37-37.5°C), rats were injured (n = 6) with a F-P pulse ranging from 1.8 to 2.0 atm. Following trauma, brain temperature was maintained for 4 h at 37°C. Sham trauma animals (n = 7) were treated in an identical manner. Brain trauma induced acute elevations in the extracellular levels of serotonin (p < 0.01, ANOVA) compared to sham-operated controls. For example, serotonin levels increased from 18.85 ± 7.12 pm/mL (mean ± SD) in baseline samples to 65.78 ± 11.36 in the first 10 min after trauma. The levels of serotonin remained significantly higher than control for the first 90-min sampling period. In parallel to the increase in serotonin levels after TBI, a significant 71.1% decrease (i.e., 182.29 ± 30.08 vs 52.75 ± 16.92) in extracellular 5- hydroxyindoleacetic acid (5-HIAA) levels was observed during the first 10 min after TBI. These data indicate that TBI is followed by a prompt increase in the extracellular levels of serotonin in cortical regions adjacent to the impact site. These neurochemical findings indicate that serotonin may play a significant role in the pathophysiology of TBI.

Original languageEnglish
Pages (from-to)35-42
Number of pages8
JournalJournal of Neurotrauma
Volume14
Issue number1
StatePublished - Jan 1 1997

Fingerprint

Percussion
Brain Injuries
Serotonin
Cerebral Cortex
Wounds and Injuries
Nervous System Trauma
Hydroxyindoleacetic Acid
Temperature
Microdialysis
Brain
Nitrous Oxide
Halothane
Analysis of Variance
Central Nervous System
Oxygen

Keywords

  • microdialysis
  • serotonin
  • traumatic brain injury

ASJC Scopus subject areas

  • Clinical Neurology
  • Neuroscience(all)

Cite this

Extracellular release of serotonin following fluid-percussion brain injury in rats. / Busto, Raul; Dalton Dietrich, W.; Globus, Mordecai Y T; Alonso, Ofelia; Ginsberg, Myron.

In: Journal of Neurotrauma, Vol. 14, No. 1, 01.01.1997, p. 35-42.

Research output: Contribution to journalArticle

Busto, Raul ; Dalton Dietrich, W. ; Globus, Mordecai Y T ; Alonso, Ofelia ; Ginsberg, Myron. / Extracellular release of serotonin following fluid-percussion brain injury in rats. In: Journal of Neurotrauma. 1997 ; Vol. 14, No. 1. pp. 35-42.
@article{6ab547bdf0e24094823686283dc316f5,
title = "Extracellular release of serotonin following fluid-percussion brain injury in rats",
abstract = "Serotonin has been implicated in the pathobiology of central nervous system trauma. Using microdialysis techniques, we performed measurements of extracellular serotonin release within the traumatized cerebral cortex of rats subjected to moderate fluid-percussion (F-P) brain injury. Twenty-four hours prior to TBI, a F-P interface was positioned parasagitally over the right cerebral cortex. On the second day, fasted rats were anesthetized with 70{\%} nitrous oxide, 1{\%} halothane, and 30{\%} oxygen. Under controlled physiological conditions and normothermic brain temperature (37-37.5°C), rats were injured (n = 6) with a F-P pulse ranging from 1.8 to 2.0 atm. Following trauma, brain temperature was maintained for 4 h at 37°C. Sham trauma animals (n = 7) were treated in an identical manner. Brain trauma induced acute elevations in the extracellular levels of serotonin (p < 0.01, ANOVA) compared to sham-operated controls. For example, serotonin levels increased from 18.85 ± 7.12 pm/mL (mean ± SD) in baseline samples to 65.78 ± 11.36 in the first 10 min after trauma. The levels of serotonin remained significantly higher than control for the first 90-min sampling period. In parallel to the increase in serotonin levels after TBI, a significant 71.1{\%} decrease (i.e., 182.29 ± 30.08 vs 52.75 ± 16.92) in extracellular 5- hydroxyindoleacetic acid (5-HIAA) levels was observed during the first 10 min after TBI. These data indicate that TBI is followed by a prompt increase in the extracellular levels of serotonin in cortical regions adjacent to the impact site. These neurochemical findings indicate that serotonin may play a significant role in the pathophysiology of TBI.",
keywords = "microdialysis, serotonin, traumatic brain injury",
author = "Raul Busto and {Dalton Dietrich}, W. and Globus, {Mordecai Y T} and Ofelia Alonso and Myron Ginsberg",
year = "1997",
month = "1",
day = "1",
language = "English",
volume = "14",
pages = "35--42",
journal = "Journal of Neurotrauma",
issn = "0897-7151",
publisher = "Mary Ann Liebert Inc.",
number = "1",

}

TY - JOUR

T1 - Extracellular release of serotonin following fluid-percussion brain injury in rats

AU - Busto, Raul

AU - Dalton Dietrich, W.

AU - Globus, Mordecai Y T

AU - Alonso, Ofelia

AU - Ginsberg, Myron

PY - 1997/1/1

Y1 - 1997/1/1

N2 - Serotonin has been implicated in the pathobiology of central nervous system trauma. Using microdialysis techniques, we performed measurements of extracellular serotonin release within the traumatized cerebral cortex of rats subjected to moderate fluid-percussion (F-P) brain injury. Twenty-four hours prior to TBI, a F-P interface was positioned parasagitally over the right cerebral cortex. On the second day, fasted rats were anesthetized with 70% nitrous oxide, 1% halothane, and 30% oxygen. Under controlled physiological conditions and normothermic brain temperature (37-37.5°C), rats were injured (n = 6) with a F-P pulse ranging from 1.8 to 2.0 atm. Following trauma, brain temperature was maintained for 4 h at 37°C. Sham trauma animals (n = 7) were treated in an identical manner. Brain trauma induced acute elevations in the extracellular levels of serotonin (p < 0.01, ANOVA) compared to sham-operated controls. For example, serotonin levels increased from 18.85 ± 7.12 pm/mL (mean ± SD) in baseline samples to 65.78 ± 11.36 in the first 10 min after trauma. The levels of serotonin remained significantly higher than control for the first 90-min sampling period. In parallel to the increase in serotonin levels after TBI, a significant 71.1% decrease (i.e., 182.29 ± 30.08 vs 52.75 ± 16.92) in extracellular 5- hydroxyindoleacetic acid (5-HIAA) levels was observed during the first 10 min after TBI. These data indicate that TBI is followed by a prompt increase in the extracellular levels of serotonin in cortical regions adjacent to the impact site. These neurochemical findings indicate that serotonin may play a significant role in the pathophysiology of TBI.

AB - Serotonin has been implicated in the pathobiology of central nervous system trauma. Using microdialysis techniques, we performed measurements of extracellular serotonin release within the traumatized cerebral cortex of rats subjected to moderate fluid-percussion (F-P) brain injury. Twenty-four hours prior to TBI, a F-P interface was positioned parasagitally over the right cerebral cortex. On the second day, fasted rats were anesthetized with 70% nitrous oxide, 1% halothane, and 30% oxygen. Under controlled physiological conditions and normothermic brain temperature (37-37.5°C), rats were injured (n = 6) with a F-P pulse ranging from 1.8 to 2.0 atm. Following trauma, brain temperature was maintained for 4 h at 37°C. Sham trauma animals (n = 7) were treated in an identical manner. Brain trauma induced acute elevations in the extracellular levels of serotonin (p < 0.01, ANOVA) compared to sham-operated controls. For example, serotonin levels increased from 18.85 ± 7.12 pm/mL (mean ± SD) in baseline samples to 65.78 ± 11.36 in the first 10 min after trauma. The levels of serotonin remained significantly higher than control for the first 90-min sampling period. In parallel to the increase in serotonin levels after TBI, a significant 71.1% decrease (i.e., 182.29 ± 30.08 vs 52.75 ± 16.92) in extracellular 5- hydroxyindoleacetic acid (5-HIAA) levels was observed during the first 10 min after TBI. These data indicate that TBI is followed by a prompt increase in the extracellular levels of serotonin in cortical regions adjacent to the impact site. These neurochemical findings indicate that serotonin may play a significant role in the pathophysiology of TBI.

KW - microdialysis

KW - serotonin

KW - traumatic brain injury

UR - http://www.scopus.com/inward/record.url?scp=0031039481&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=0031039481&partnerID=8YFLogxK

M3 - Article

C2 - 9048309

AN - SCOPUS:0031039481

VL - 14

SP - 35

EP - 42

JO - Journal of Neurotrauma

JF - Journal of Neurotrauma

SN - 0897-7151

IS - 1

ER -