Effect of NGF treatment on outcome measures in a rat model of middle cerebral artery occlusion

T. A. Kent, M. Quast, Giulio Taglialatela, C. Rea, J. Wei, Z. Tao, J. Regino Perez-Polo

Research output: Contribution to journalArticle

15 Citations (Scopus)

Abstract

Ischemic insults to the brain result in a time-dependent increase in neuronal death that is responsible for some of the functional deficits associated with stroke. Our working hypothesis is that ischemia results in a prompt depletion of high energy phosphate species resulting in decreased pH and glutathione levels in brain in a temporal and spatial pattern that disrupts nerve growth factor homeostasis and increases neuronal apoptosis. Here we show hemispheric depletion of active phosphate species after ischemia. Also, we observed that the striatum is an early target for oxidative stress that is followed by energy metabolic impairment and altered neurotrophin levels that were detected by noninvasive magnetic resonance imaging (MRI) measurements of cytotoxicity and conventional biochemical determinations of apoptosis, glutathione, and nerve growth factor (NGF) protein levels in a pattern distinct from that observed in the hippocampus. Furthermore, early assessment of intracellular pH by 31P-magnetic resonance spectroscopy (31P-MRS) was a predictor of later infarct development as determined by MRI. We also show that pretreatment with pharmacological doses of NGF did not have overall significant beneficial consequences on irreversible ischemia in an intraluminal unilateral irreversible model of stroke in rat brain.

Original languageEnglish (US)
Pages (from-to)357-369
Number of pages13
JournalJournal of Neuroscience Research
Volume55
Issue number3
DOIs
StatePublished - Feb 1 1999

Fingerprint

Middle Cerebral Artery Infarction
Nerve Growth Factor
Ischemia
Outcome Assessment (Health Care)
Glutathione
Brain
Stroke
Phosphates
Magnetic Resonance Imaging
Apoptosis
Nerve Growth Factors
Hippocampus
Oxidative Stress
Homeostasis
Magnetic Resonance Spectroscopy
Pharmacology
Proteins

Keywords

  • Glutathione
  • Magnetic resonance imaging
  • Middle cerebral artery occlusion
  • Nerve growth factor
  • Nuclear magnetic resonance
  • Stroke

ASJC Scopus subject areas

  • Neuroscience(all)

Cite this

Effect of NGF treatment on outcome measures in a rat model of middle cerebral artery occlusion. / Kent, T. A.; Quast, M.; Taglialatela, Giulio; Rea, C.; Wei, J.; Tao, Z.; Perez-Polo, J. Regino.

In: Journal of Neuroscience Research, Vol. 55, No. 3, 01.02.1999, p. 357-369.

Research output: Contribution to journalArticle

Kent, T. A. ; Quast, M. ; Taglialatela, Giulio ; Rea, C. ; Wei, J. ; Tao, Z. ; Perez-Polo, J. Regino. / Effect of NGF treatment on outcome measures in a rat model of middle cerebral artery occlusion. In: Journal of Neuroscience Research. 1999 ; Vol. 55, No. 3. pp. 357-369.
@article{ddb8a033cc4f431abbdda29aaee1410d,
title = "Effect of NGF treatment on outcome measures in a rat model of middle cerebral artery occlusion",
abstract = "Ischemic insults to the brain result in a time-dependent increase in neuronal death that is responsible for some of the functional deficits associated with stroke. Our working hypothesis is that ischemia results in a prompt depletion of high energy phosphate species resulting in decreased pH and glutathione levels in brain in a temporal and spatial pattern that disrupts nerve growth factor homeostasis and increases neuronal apoptosis. Here we show hemispheric depletion of active phosphate species after ischemia. Also, we observed that the striatum is an early target for oxidative stress that is followed by energy metabolic impairment and altered neurotrophin levels that were detected by noninvasive magnetic resonance imaging (MRI) measurements of cytotoxicity and conventional biochemical determinations of apoptosis, glutathione, and nerve growth factor (NGF) protein levels in a pattern distinct from that observed in the hippocampus. Furthermore, early assessment of intracellular pH by 31P-magnetic resonance spectroscopy (31P-MRS) was a predictor of later infarct development as determined by MRI. We also show that pretreatment with pharmacological doses of NGF did not have overall significant beneficial consequences on irreversible ischemia in an intraluminal unilateral irreversible model of stroke in rat brain.",
keywords = "Glutathione, Magnetic resonance imaging, Middle cerebral artery occlusion, Nerve growth factor, Nuclear magnetic resonance, Stroke",
author = "Kent, {T. A.} and M. Quast and Giulio Taglialatela and C. Rea and J. Wei and Z. Tao and Perez-Polo, {J. Regino}",
year = "1999",
month = "2",
day = "1",
doi = "10.1002/(SICI)1097-4547(19990201)55:3<357::AID-JNR11>3.0.CO;2-W",
language = "English (US)",
volume = "55",
pages = "357--369",
journal = "Journal of Neuroscience Research",
issn = "0360-4012",
publisher = "Wiley-Liss Inc.",
number = "3",

}

TY - JOUR

T1 - Effect of NGF treatment on outcome measures in a rat model of middle cerebral artery occlusion

AU - Kent, T. A.

AU - Quast, M.

AU - Taglialatela, Giulio

AU - Rea, C.

AU - Wei, J.

AU - Tao, Z.

AU - Perez-Polo, J. Regino

PY - 1999/2/1

Y1 - 1999/2/1

N2 - Ischemic insults to the brain result in a time-dependent increase in neuronal death that is responsible for some of the functional deficits associated with stroke. Our working hypothesis is that ischemia results in a prompt depletion of high energy phosphate species resulting in decreased pH and glutathione levels in brain in a temporal and spatial pattern that disrupts nerve growth factor homeostasis and increases neuronal apoptosis. Here we show hemispheric depletion of active phosphate species after ischemia. Also, we observed that the striatum is an early target for oxidative stress that is followed by energy metabolic impairment and altered neurotrophin levels that were detected by noninvasive magnetic resonance imaging (MRI) measurements of cytotoxicity and conventional biochemical determinations of apoptosis, glutathione, and nerve growth factor (NGF) protein levels in a pattern distinct from that observed in the hippocampus. Furthermore, early assessment of intracellular pH by 31P-magnetic resonance spectroscopy (31P-MRS) was a predictor of later infarct development as determined by MRI. We also show that pretreatment with pharmacological doses of NGF did not have overall significant beneficial consequences on irreversible ischemia in an intraluminal unilateral irreversible model of stroke in rat brain.

AB - Ischemic insults to the brain result in a time-dependent increase in neuronal death that is responsible for some of the functional deficits associated with stroke. Our working hypothesis is that ischemia results in a prompt depletion of high energy phosphate species resulting in decreased pH and glutathione levels in brain in a temporal and spatial pattern that disrupts nerve growth factor homeostasis and increases neuronal apoptosis. Here we show hemispheric depletion of active phosphate species after ischemia. Also, we observed that the striatum is an early target for oxidative stress that is followed by energy metabolic impairment and altered neurotrophin levels that were detected by noninvasive magnetic resonance imaging (MRI) measurements of cytotoxicity and conventional biochemical determinations of apoptosis, glutathione, and nerve growth factor (NGF) protein levels in a pattern distinct from that observed in the hippocampus. Furthermore, early assessment of intracellular pH by 31P-magnetic resonance spectroscopy (31P-MRS) was a predictor of later infarct development as determined by MRI. We also show that pretreatment with pharmacological doses of NGF did not have overall significant beneficial consequences on irreversible ischemia in an intraluminal unilateral irreversible model of stroke in rat brain.

KW - Glutathione

KW - Magnetic resonance imaging

KW - Middle cerebral artery occlusion

KW - Nerve growth factor

KW - Nuclear magnetic resonance

KW - Stroke

UR - http://www.scopus.com/inward/record.url?scp=0033081976&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=0033081976&partnerID=8YFLogxK

U2 - 10.1002/(SICI)1097-4547(19990201)55:3<357::AID-JNR11>3.0.CO;2-W

DO - 10.1002/(SICI)1097-4547(19990201)55:3<357::AID-JNR11>3.0.CO;2-W

M3 - Article

VL - 55

SP - 357

EP - 369

JO - Journal of Neuroscience Research

JF - Journal of Neuroscience Research

SN - 0360-4012

IS - 3

ER -