Neonatal primary neuronal death induced by capsaicin and axotomy involves an apoptotic mechanism

Tomosada Sugimoto, Chun Xiao, Hiroyuki Ichikawa

Research output: Contribution to journalArticle

45 Citations (Scopus)

Abstract

To clarify the mechanism of capsaicin-induced primary neuronal cell death, newborn and adult rats were given a subcutaneous injection of capsaicin (50 mg/kg). Neonatal capsaicin injection induced neuronal apoptosis in the trigeminal ganglion. Apoptotic neurons had peripheral stacks of long parallel endoplasmic reticulum that are characteristic to primary neurons of the B-type, and exhibited nucleoplasmic condensation, nuclear shrinkage and cytoplasmic fragmentation. Light microscopically, apoptotic neurons exhibited a sign of DNA fragmentation as revealed by a nick end labelling method. The proportion of apoptotic cells was quite low during the first 12 h after capsaicin injection (<1%), rapidly increase to 10.44% by 24 h, and decreased to 0.29% by 48 h. Normal and vehicle control levels of apoptosis were <1%. Nerve growth factor (NGF, 0.5 mg/kg) simultaneously administered with capsaicin reduced the incidence of apoptosis by about 35% at 24 h post- injection. Neonatal transection of the infraorbital nerve induced neuronal apoptosis similar to that produced by the neonatal capsaicin in the maxillary division of the trigeminal ganglion. Unlike capsaicin, however, the neurotomy-induced apoptosis was seen in neurons of both the A- and B-types. Neither the capsaicin injection nor the neurotomy induced apoptosis in adult rats, though mitochondrial swelling similar to that seen at 0.5 h after neonatal capsaicin was observed after capsaicin injection in adults. The results indicate that the capsaicin-induced and nerve injury-induced primary neuronal damages in newborn rats share a common final pathway, apoptosis.

Original languageEnglish
Pages (from-to)147-154
Number of pages8
JournalBrain Research
Volume807
Issue number1-2
DOIs
Publication statusPublished - Oct 5 1998

Fingerprint

Axotomy
Capsaicin
Apoptosis
Injections
Neurons
Trigeminal Ganglion
Nerve Growth Factor
Mitochondrial Swelling
DNA Fragmentation
Subcutaneous Injections
Endoplasmic Reticulum
Cell Death

Keywords

  • Apoptosis
  • Capsaicin
  • Nerve growth factor
  • Nerve injury
  • Primary neuron
  • Trigeminal ganglion

ASJC Scopus subject areas

  • Neuroscience(all)

Cite this

Neonatal primary neuronal death induced by capsaicin and axotomy involves an apoptotic mechanism. / Sugimoto, Tomosada; Xiao, Chun; Ichikawa, Hiroyuki.

In: Brain Research, Vol. 807, No. 1-2, 05.10.1998, p. 147-154.

Research output: Contribution to journalArticle

Sugimoto, Tomosada ; Xiao, Chun ; Ichikawa, Hiroyuki. / Neonatal primary neuronal death induced by capsaicin and axotomy involves an apoptotic mechanism. In: Brain Research. 1998 ; Vol. 807, No. 1-2. pp. 147-154.
@article{b7ffe58add7d4c2b9c711714a657313e,
title = "Neonatal primary neuronal death induced by capsaicin and axotomy involves an apoptotic mechanism",
abstract = "To clarify the mechanism of capsaicin-induced primary neuronal cell death, newborn and adult rats were given a subcutaneous injection of capsaicin (50 mg/kg). Neonatal capsaicin injection induced neuronal apoptosis in the trigeminal ganglion. Apoptotic neurons had peripheral stacks of long parallel endoplasmic reticulum that are characteristic to primary neurons of the B-type, and exhibited nucleoplasmic condensation, nuclear shrinkage and cytoplasmic fragmentation. Light microscopically, apoptotic neurons exhibited a sign of DNA fragmentation as revealed by a nick end labelling method. The proportion of apoptotic cells was quite low during the first 12 h after capsaicin injection (<1{\%}), rapidly increase to 10.44{\%} by 24 h, and decreased to 0.29{\%} by 48 h. Normal and vehicle control levels of apoptosis were <1{\%}. Nerve growth factor (NGF, 0.5 mg/kg) simultaneously administered with capsaicin reduced the incidence of apoptosis by about 35{\%} at 24 h post- injection. Neonatal transection of the infraorbital nerve induced neuronal apoptosis similar to that produced by the neonatal capsaicin in the maxillary division of the trigeminal ganglion. Unlike capsaicin, however, the neurotomy-induced apoptosis was seen in neurons of both the A- and B-types. Neither the capsaicin injection nor the neurotomy induced apoptosis in adult rats, though mitochondrial swelling similar to that seen at 0.5 h after neonatal capsaicin was observed after capsaicin injection in adults. The results indicate that the capsaicin-induced and nerve injury-induced primary neuronal damages in newborn rats share a common final pathway, apoptosis.",
keywords = "Apoptosis, Capsaicin, Nerve growth factor, Nerve injury, Primary neuron, Trigeminal ganglion",
author = "Tomosada Sugimoto and Chun Xiao and Hiroyuki Ichikawa",
year = "1998",
month = "10",
day = "5",
doi = "10.1016/S0006-8993(98)00788-4",
language = "English",
volume = "807",
pages = "147--154",
journal = "Brain Research",
issn = "0006-8993",
publisher = "Elsevier",
number = "1-2",

}

TY - JOUR

T1 - Neonatal primary neuronal death induced by capsaicin and axotomy involves an apoptotic mechanism

AU - Sugimoto, Tomosada

AU - Xiao, Chun

AU - Ichikawa, Hiroyuki

PY - 1998/10/5

Y1 - 1998/10/5

N2 - To clarify the mechanism of capsaicin-induced primary neuronal cell death, newborn and adult rats were given a subcutaneous injection of capsaicin (50 mg/kg). Neonatal capsaicin injection induced neuronal apoptosis in the trigeminal ganglion. Apoptotic neurons had peripheral stacks of long parallel endoplasmic reticulum that are characteristic to primary neurons of the B-type, and exhibited nucleoplasmic condensation, nuclear shrinkage and cytoplasmic fragmentation. Light microscopically, apoptotic neurons exhibited a sign of DNA fragmentation as revealed by a nick end labelling method. The proportion of apoptotic cells was quite low during the first 12 h after capsaicin injection (<1%), rapidly increase to 10.44% by 24 h, and decreased to 0.29% by 48 h. Normal and vehicle control levels of apoptosis were <1%. Nerve growth factor (NGF, 0.5 mg/kg) simultaneously administered with capsaicin reduced the incidence of apoptosis by about 35% at 24 h post- injection. Neonatal transection of the infraorbital nerve induced neuronal apoptosis similar to that produced by the neonatal capsaicin in the maxillary division of the trigeminal ganglion. Unlike capsaicin, however, the neurotomy-induced apoptosis was seen in neurons of both the A- and B-types. Neither the capsaicin injection nor the neurotomy induced apoptosis in adult rats, though mitochondrial swelling similar to that seen at 0.5 h after neonatal capsaicin was observed after capsaicin injection in adults. The results indicate that the capsaicin-induced and nerve injury-induced primary neuronal damages in newborn rats share a common final pathway, apoptosis.

AB - To clarify the mechanism of capsaicin-induced primary neuronal cell death, newborn and adult rats were given a subcutaneous injection of capsaicin (50 mg/kg). Neonatal capsaicin injection induced neuronal apoptosis in the trigeminal ganglion. Apoptotic neurons had peripheral stacks of long parallel endoplasmic reticulum that are characteristic to primary neurons of the B-type, and exhibited nucleoplasmic condensation, nuclear shrinkage and cytoplasmic fragmentation. Light microscopically, apoptotic neurons exhibited a sign of DNA fragmentation as revealed by a nick end labelling method. The proportion of apoptotic cells was quite low during the first 12 h after capsaicin injection (<1%), rapidly increase to 10.44% by 24 h, and decreased to 0.29% by 48 h. Normal and vehicle control levels of apoptosis were <1%. Nerve growth factor (NGF, 0.5 mg/kg) simultaneously administered with capsaicin reduced the incidence of apoptosis by about 35% at 24 h post- injection. Neonatal transection of the infraorbital nerve induced neuronal apoptosis similar to that produced by the neonatal capsaicin in the maxillary division of the trigeminal ganglion. Unlike capsaicin, however, the neurotomy-induced apoptosis was seen in neurons of both the A- and B-types. Neither the capsaicin injection nor the neurotomy induced apoptosis in adult rats, though mitochondrial swelling similar to that seen at 0.5 h after neonatal capsaicin was observed after capsaicin injection in adults. The results indicate that the capsaicin-induced and nerve injury-induced primary neuronal damages in newborn rats share a common final pathway, apoptosis.

KW - Apoptosis

KW - Capsaicin

KW - Nerve growth factor

KW - Nerve injury

KW - Primary neuron

KW - Trigeminal ganglion

UR - http://www.scopus.com/inward/record.url?scp=0032487626&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=0032487626&partnerID=8YFLogxK

U2 - 10.1016/S0006-8993(98)00788-4

DO - 10.1016/S0006-8993(98)00788-4

M3 - Article

C2 - 9757021

AN - SCOPUS:0032487626

VL - 807

SP - 147

EP - 154

JO - Brain Research

JF - Brain Research

SN - 0006-8993

IS - 1-2

ER -