Capsaicin exhibits neuroprotective effects in a model of transient global cerebral ischemia in Mongolian gerbils

Simona Pegorini, Daniela Braida, Chiara Verzoni, Chiara Guerini-Rocco, Gian Giacomo Consalez, Laura Croci, Mariaelvina Sala

Research output: Contribution to journalArticle

Abstract

Capsaicin, the irritant principle of hot peppers, is a vanilloid agonist known to activate the transient receptor potential channel vanilloid subfamily member 1 (VR1), recently reported to be involved in neurodegeneration. The present study investigated the role of VR1 in a model of global cerebral ischemia in gerbils. Over the dose range tested, capsaicin (0.01, 0.025, 0.05, 0.2 and 0.6 mg kg -1), given 5 min after recirculation, dose-dependently antagonized the ischemia-induced electroencephalographic total spectral power decrease and restored relative frequency band distribution evaluated 7 days after ischemia. Capsaicin, at all tested doses, fully prevented ischemia-induced hyperlocomotion evaluated 1 day after ischemia. Capsaicin dose-dependently antagonized ischemia-induced memory impairment evaluated in a passive avoidance task, 3 days after ischemia. Capsaicin showed a dose-dependent hypothermic effect evaluated for 2 h after recirculation. At 7 days after ischemia, a progressive survival of pyramidal cells in the CA1 subfield in capsaicin-treated gerbils, with a maximum of 80%, at a dose of 0.2 mg kg -1, was obtained. The selective VR1 antagonist, capsazepine (0.01 mg kg -1), reversed capsaicin-induced protective effects, in a competitive manner. These results suggest that the neuroprotective effect of capsaicin may be attributable, at least in part, to VR1 desensitizadon and provide a valuable target for development of interventional pharmacological strategies.

Original languageEnglish
Pages (from-to)727-735
Number of pages9
JournalBritish Journal of Pharmacology
Volume144
Issue number5
DOIs
Publication statusPublished - Mar 2005

Fingerprint

Gerbillinae
Capsaicin
Transient Ischemic Attack
Neuroprotective Agents
Ischemia
Transient Receptor Potential Channels
Capsicum
Pyramidal Cells
Irritants
Brain Ischemia
Pharmacology

Keywords

  • CA1
  • Capsaicin
  • EEG
  • Ischemia
  • Memory
  • Motor activity
  • Neuroprotection
  • Rectal temperature
  • Vanilloid agonist
  • Vanilloid antagonist

ASJC Scopus subject areas

  • Pharmacology

Cite this

Capsaicin exhibits neuroprotective effects in a model of transient global cerebral ischemia in Mongolian gerbils. / Pegorini, Simona; Braida, Daniela; Verzoni, Chiara; Guerini-Rocco, Chiara; Consalez, Gian Giacomo; Croci, Laura; Sala, Mariaelvina.

In: British Journal of Pharmacology, Vol. 144, No. 5, 03.2005, p. 727-735.

Research output: Contribution to journalArticle

Pegorini, Simona ; Braida, Daniela ; Verzoni, Chiara ; Guerini-Rocco, Chiara ; Consalez, Gian Giacomo ; Croci, Laura ; Sala, Mariaelvina. / Capsaicin exhibits neuroprotective effects in a model of transient global cerebral ischemia in Mongolian gerbils. In: British Journal of Pharmacology. 2005 ; Vol. 144, No. 5. pp. 727-735.
@article{65186a8c840d4860845daeab38d99a53,
title = "Capsaicin exhibits neuroprotective effects in a model of transient global cerebral ischemia in Mongolian gerbils",
abstract = "Capsaicin, the irritant principle of hot peppers, is a vanilloid agonist known to activate the transient receptor potential channel vanilloid subfamily member 1 (VR1), recently reported to be involved in neurodegeneration. The present study investigated the role of VR1 in a model of global cerebral ischemia in gerbils. Over the dose range tested, capsaicin (0.01, 0.025, 0.05, 0.2 and 0.6 mg kg -1), given 5 min after recirculation, dose-dependently antagonized the ischemia-induced electroencephalographic total spectral power decrease and restored relative frequency band distribution evaluated 7 days after ischemia. Capsaicin, at all tested doses, fully prevented ischemia-induced hyperlocomotion evaluated 1 day after ischemia. Capsaicin dose-dependently antagonized ischemia-induced memory impairment evaluated in a passive avoidance task, 3 days after ischemia. Capsaicin showed a dose-dependent hypothermic effect evaluated for 2 h after recirculation. At 7 days after ischemia, a progressive survival of pyramidal cells in the CA1 subfield in capsaicin-treated gerbils, with a maximum of 80{\%}, at a dose of 0.2 mg kg -1, was obtained. The selective VR1 antagonist, capsazepine (0.01 mg kg -1), reversed capsaicin-induced protective effects, in a competitive manner. These results suggest that the neuroprotective effect of capsaicin may be attributable, at least in part, to VR1 desensitizadon and provide a valuable target for development of interventional pharmacological strategies.",
keywords = "CA1, Capsaicin, EEG, Ischemia, Memory, Motor activity, Neuroprotection, Rectal temperature, Vanilloid agonist, Vanilloid antagonist",
author = "Simona Pegorini and Daniela Braida and Chiara Verzoni and Chiara Guerini-Rocco and Consalez, {Gian Giacomo} and Laura Croci and Mariaelvina Sala",
year = "2005",
month = "3",
doi = "10.1038/sj.bjp.0706115",
language = "English",
volume = "144",
pages = "727--735",
journal = "British Journal of Pharmacology",
issn = "0007-1188",
publisher = "Wiley-Blackwell",
number = "5",

}

TY - JOUR

T1 - Capsaicin exhibits neuroprotective effects in a model of transient global cerebral ischemia in Mongolian gerbils

AU - Pegorini, Simona

AU - Braida, Daniela

AU - Verzoni, Chiara

AU - Guerini-Rocco, Chiara

AU - Consalez, Gian Giacomo

AU - Croci, Laura

AU - Sala, Mariaelvina

PY - 2005/3

Y1 - 2005/3

N2 - Capsaicin, the irritant principle of hot peppers, is a vanilloid agonist known to activate the transient receptor potential channel vanilloid subfamily member 1 (VR1), recently reported to be involved in neurodegeneration. The present study investigated the role of VR1 in a model of global cerebral ischemia in gerbils. Over the dose range tested, capsaicin (0.01, 0.025, 0.05, 0.2 and 0.6 mg kg -1), given 5 min after recirculation, dose-dependently antagonized the ischemia-induced electroencephalographic total spectral power decrease and restored relative frequency band distribution evaluated 7 days after ischemia. Capsaicin, at all tested doses, fully prevented ischemia-induced hyperlocomotion evaluated 1 day after ischemia. Capsaicin dose-dependently antagonized ischemia-induced memory impairment evaluated in a passive avoidance task, 3 days after ischemia. Capsaicin showed a dose-dependent hypothermic effect evaluated for 2 h after recirculation. At 7 days after ischemia, a progressive survival of pyramidal cells in the CA1 subfield in capsaicin-treated gerbils, with a maximum of 80%, at a dose of 0.2 mg kg -1, was obtained. The selective VR1 antagonist, capsazepine (0.01 mg kg -1), reversed capsaicin-induced protective effects, in a competitive manner. These results suggest that the neuroprotective effect of capsaicin may be attributable, at least in part, to VR1 desensitizadon and provide a valuable target for development of interventional pharmacological strategies.

AB - Capsaicin, the irritant principle of hot peppers, is a vanilloid agonist known to activate the transient receptor potential channel vanilloid subfamily member 1 (VR1), recently reported to be involved in neurodegeneration. The present study investigated the role of VR1 in a model of global cerebral ischemia in gerbils. Over the dose range tested, capsaicin (0.01, 0.025, 0.05, 0.2 and 0.6 mg kg -1), given 5 min after recirculation, dose-dependently antagonized the ischemia-induced electroencephalographic total spectral power decrease and restored relative frequency band distribution evaluated 7 days after ischemia. Capsaicin, at all tested doses, fully prevented ischemia-induced hyperlocomotion evaluated 1 day after ischemia. Capsaicin dose-dependently antagonized ischemia-induced memory impairment evaluated in a passive avoidance task, 3 days after ischemia. Capsaicin showed a dose-dependent hypothermic effect evaluated for 2 h after recirculation. At 7 days after ischemia, a progressive survival of pyramidal cells in the CA1 subfield in capsaicin-treated gerbils, with a maximum of 80%, at a dose of 0.2 mg kg -1, was obtained. The selective VR1 antagonist, capsazepine (0.01 mg kg -1), reversed capsaicin-induced protective effects, in a competitive manner. These results suggest that the neuroprotective effect of capsaicin may be attributable, at least in part, to VR1 desensitizadon and provide a valuable target for development of interventional pharmacological strategies.

KW - CA1

KW - Capsaicin

KW - EEG

KW - Ischemia

KW - Memory

KW - Motor activity

KW - Neuroprotection

KW - Rectal temperature

KW - Vanilloid agonist

KW - Vanilloid antagonist

UR - http://www.scopus.com/inward/record.url?scp=15944389904&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=15944389904&partnerID=8YFLogxK

U2 - 10.1038/sj.bjp.0706115

DO - 10.1038/sj.bjp.0706115

M3 - Article

C2 - 15678080

AN - SCOPUS:15944389904

VL - 144

SP - 727

EP - 735

JO - British Journal of Pharmacology

JF - British Journal of Pharmacology

SN - 0007-1188

IS - 5

ER -