The missing link between long-term stimulation of nicotinic receptors and the increases of acetylcholine release and vasodilation in the cerebral cortex of aged rats

Sae Uchida, Harumi Hotta, Hidemi Misawa, Koichiro Kawashima

Research output: Contribution to journalArticle

6 Citations (Scopus)

Abstract

In adult rats (4-9 months), chronic nicotine infusion increases the basal level of acetylcholine (ACh) release in the cerebral cortex and enhances responses of cortical ACh release and cortical vasodilation elicited by nucleus basalis of Meynert (NBM) stimulation. In the present study, we examined whether these effects of nicotine are detected in aged rats. Aged rats (27-30 months) received sustained subcutaneous nicotine (100 μg/kg/h) or saline for 14 days. Under urethane anesthesia, ACh release and regional blood flow in the parietal cortex were measured. The basal level of ACh release in the cerebral cortex was not changed by chronic nicotine. In addition, the magnitudes of ACh release and vasodilation by NBM stimulation were similar between the saline-treated and nicotine-treated groups. The lack of an effect of chronic nicotine in aged rats may be due to a decrease in nicotinic receptors in the cerebral cortex during aging (Nordberg et al., J Neurosci Res 31:103-111, 1992).

Original languageEnglish
Pages (from-to)95-101
Number of pages7
JournalJournal of Physiological Sciences
Volume63
Issue number2
DOIs
Publication statusPublished - 2013

Fingerprint

Nicotinic Receptors
Nicotine
Vasodilation
Cerebral Cortex
Acetylcholine
Basal Nucleus of Meynert
Parietal Lobe
Urethane
Regional Blood Flow
Anesthesia

Keywords

  • Acetylcholine release
  • Aging
  • Chronic nicotine
  • Cortical cerebral blood flow
  • Nucleus basalis of Meynert
  • Rat

ASJC Scopus subject areas

  • Physiology

Cite this

@article{59603d20253c4a0491b750b24972b5cd,
title = "The missing link between long-term stimulation of nicotinic receptors and the increases of acetylcholine release and vasodilation in the cerebral cortex of aged rats",
abstract = "In adult rats (4-9 months), chronic nicotine infusion increases the basal level of acetylcholine (ACh) release in the cerebral cortex and enhances responses of cortical ACh release and cortical vasodilation elicited by nucleus basalis of Meynert (NBM) stimulation. In the present study, we examined whether these effects of nicotine are detected in aged rats. Aged rats (27-30 months) received sustained subcutaneous nicotine (100 μg/kg/h) or saline for 14 days. Under urethane anesthesia, ACh release and regional blood flow in the parietal cortex were measured. The basal level of ACh release in the cerebral cortex was not changed by chronic nicotine. In addition, the magnitudes of ACh release and vasodilation by NBM stimulation were similar between the saline-treated and nicotine-treated groups. The lack of an effect of chronic nicotine in aged rats may be due to a decrease in nicotinic receptors in the cerebral cortex during aging (Nordberg et al., J Neurosci Res 31:103-111, 1992).",
keywords = "Acetylcholine release, Aging, Chronic nicotine, Cortical cerebral blood flow, Nucleus basalis of Meynert, Rat",
author = "Sae Uchida and Harumi Hotta and Hidemi Misawa and Koichiro Kawashima",
year = "2013",
doi = "10.1007/s12576-012-0239-2",
language = "English",
volume = "63",
pages = "95--101",
journal = "Journal of Physiological Sciences",
issn = "1880-6546",
publisher = "Springer Japan",
number = "2",

}

TY - JOUR

T1 - The missing link between long-term stimulation of nicotinic receptors and the increases of acetylcholine release and vasodilation in the cerebral cortex of aged rats

AU - Uchida, Sae

AU - Hotta, Harumi

AU - Misawa, Hidemi

AU - Kawashima, Koichiro

PY - 2013

Y1 - 2013

N2 - In adult rats (4-9 months), chronic nicotine infusion increases the basal level of acetylcholine (ACh) release in the cerebral cortex and enhances responses of cortical ACh release and cortical vasodilation elicited by nucleus basalis of Meynert (NBM) stimulation. In the present study, we examined whether these effects of nicotine are detected in aged rats. Aged rats (27-30 months) received sustained subcutaneous nicotine (100 μg/kg/h) or saline for 14 days. Under urethane anesthesia, ACh release and regional blood flow in the parietal cortex were measured. The basal level of ACh release in the cerebral cortex was not changed by chronic nicotine. In addition, the magnitudes of ACh release and vasodilation by NBM stimulation were similar between the saline-treated and nicotine-treated groups. The lack of an effect of chronic nicotine in aged rats may be due to a decrease in nicotinic receptors in the cerebral cortex during aging (Nordberg et al., J Neurosci Res 31:103-111, 1992).

AB - In adult rats (4-9 months), chronic nicotine infusion increases the basal level of acetylcholine (ACh) release in the cerebral cortex and enhances responses of cortical ACh release and cortical vasodilation elicited by nucleus basalis of Meynert (NBM) stimulation. In the present study, we examined whether these effects of nicotine are detected in aged rats. Aged rats (27-30 months) received sustained subcutaneous nicotine (100 μg/kg/h) or saline for 14 days. Under urethane anesthesia, ACh release and regional blood flow in the parietal cortex were measured. The basal level of ACh release in the cerebral cortex was not changed by chronic nicotine. In addition, the magnitudes of ACh release and vasodilation by NBM stimulation were similar between the saline-treated and nicotine-treated groups. The lack of an effect of chronic nicotine in aged rats may be due to a decrease in nicotinic receptors in the cerebral cortex during aging (Nordberg et al., J Neurosci Res 31:103-111, 1992).

KW - Acetylcholine release

KW - Aging

KW - Chronic nicotine

KW - Cortical cerebral blood flow

KW - Nucleus basalis of Meynert

KW - Rat

UR - http://www.scopus.com/inward/record.url?scp=84874413042&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=84874413042&partnerID=8YFLogxK

U2 - 10.1007/s12576-012-0239-2

DO - 10.1007/s12576-012-0239-2

M3 - Article

VL - 63

SP - 95

EP - 101

JO - Journal of Physiological Sciences

JF - Journal of Physiological Sciences

SN - 1880-6546

IS - 2

ER -