Effects of TRH and DN-1417 on high potassium-evoked acetylcholine release from rat basal forebrain slices determined directly by radioimmunoassay

Takeshi Suzuki, Kazuko Fujimoto, Hisayo Oohata, Kawashima Koichiro

Research output: Contribution to journalArticle

8 Citations (Scopus)

Abstract

1. 1. High potassium (50 mM)-evoked acetylcholine (ACh) release from rat basal forebrain slices under conditions without an exogenous choline supply was determined using a radioimmunoassay for ACh. 2. 2. A consistent amount of ACh release was observed at each repetitive stimulation and ACh content in brain slices was not altered by potassium stimulations. These results indicate the existence of a large intracellular releasable ACh store, which is independent of new synthesis from exogenous choline. 3. 3. Atropine, even at a concentration of 10-6 M, did not affect the potassium-evoked ACh release. Thus, modulation of ACh release by the muscarinic autoreceptor was not revealed under the conditions employed. 4. 4. Thyrotropin-releasing hormone (TRH, 10-4 M) caused a slight and statistically insignificant increase in potassium-evoked ACh release. DN-1417, a TRH analogue, at a concentration of 10-4 M significantly increased potassium-evoked ACh release. These findings indicate that DN-1417 is able to enhance ACh output independently of ACh synthesis from exogenous choline.

Original languageEnglish
Pages (from-to)239-242
Number of pages4
JournalGeneral Pharmacology
Volume20
Issue number2
DOIs
Publication statusPublished - 1989

Fingerprint

Acetylcholine
Radioimmunoassay
Potassium
Choline
DN 1417
Basal Forebrain
Autoreceptors
Thyrotropin-Releasing Hormone
Atropine
Cholinergic Agents
Brain

ASJC Scopus subject areas

  • Pharmacology

Cite this

Effects of TRH and DN-1417 on high potassium-evoked acetylcholine release from rat basal forebrain slices determined directly by radioimmunoassay. / Suzuki, Takeshi; Fujimoto, Kazuko; Oohata, Hisayo; Koichiro, Kawashima.

In: General Pharmacology, Vol. 20, No. 2, 1989, p. 239-242.

Research output: Contribution to journalArticle

@article{2c19a92b63b442899b2f61d2bb69cf6f,
title = "Effects of TRH and DN-1417 on high potassium-evoked acetylcholine release from rat basal forebrain slices determined directly by radioimmunoassay",
abstract = "1. 1. High potassium (50 mM)-evoked acetylcholine (ACh) release from rat basal forebrain slices under conditions without an exogenous choline supply was determined using a radioimmunoassay for ACh. 2. 2. A consistent amount of ACh release was observed at each repetitive stimulation and ACh content in brain slices was not altered by potassium stimulations. These results indicate the existence of a large intracellular releasable ACh store, which is independent of new synthesis from exogenous choline. 3. 3. Atropine, even at a concentration of 10-6 M, did not affect the potassium-evoked ACh release. Thus, modulation of ACh release by the muscarinic autoreceptor was not revealed under the conditions employed. 4. 4. Thyrotropin-releasing hormone (TRH, 10-4 M) caused a slight and statistically insignificant increase in potassium-evoked ACh release. DN-1417, a TRH analogue, at a concentration of 10-4 M significantly increased potassium-evoked ACh release. These findings indicate that DN-1417 is able to enhance ACh output independently of ACh synthesis from exogenous choline.",
author = "Takeshi Suzuki and Kazuko Fujimoto and Hisayo Oohata and Kawashima Koichiro",
year = "1989",
doi = "10.1016/0306-3623(89)90023-2",
language = "English",
volume = "20",
pages = "239--242",
journal = "Vascular Pharmacology",
issn = "1537-1891",
publisher = "Elsevier Inc.",
number = "2",

}

TY - JOUR

T1 - Effects of TRH and DN-1417 on high potassium-evoked acetylcholine release from rat basal forebrain slices determined directly by radioimmunoassay

AU - Suzuki, Takeshi

AU - Fujimoto, Kazuko

AU - Oohata, Hisayo

AU - Koichiro, Kawashima

PY - 1989

Y1 - 1989

N2 - 1. 1. High potassium (50 mM)-evoked acetylcholine (ACh) release from rat basal forebrain slices under conditions without an exogenous choline supply was determined using a radioimmunoassay for ACh. 2. 2. A consistent amount of ACh release was observed at each repetitive stimulation and ACh content in brain slices was not altered by potassium stimulations. These results indicate the existence of a large intracellular releasable ACh store, which is independent of new synthesis from exogenous choline. 3. 3. Atropine, even at a concentration of 10-6 M, did not affect the potassium-evoked ACh release. Thus, modulation of ACh release by the muscarinic autoreceptor was not revealed under the conditions employed. 4. 4. Thyrotropin-releasing hormone (TRH, 10-4 M) caused a slight and statistically insignificant increase in potassium-evoked ACh release. DN-1417, a TRH analogue, at a concentration of 10-4 M significantly increased potassium-evoked ACh release. These findings indicate that DN-1417 is able to enhance ACh output independently of ACh synthesis from exogenous choline.

AB - 1. 1. High potassium (50 mM)-evoked acetylcholine (ACh) release from rat basal forebrain slices under conditions without an exogenous choline supply was determined using a radioimmunoassay for ACh. 2. 2. A consistent amount of ACh release was observed at each repetitive stimulation and ACh content in brain slices was not altered by potassium stimulations. These results indicate the existence of a large intracellular releasable ACh store, which is independent of new synthesis from exogenous choline. 3. 3. Atropine, even at a concentration of 10-6 M, did not affect the potassium-evoked ACh release. Thus, modulation of ACh release by the muscarinic autoreceptor was not revealed under the conditions employed. 4. 4. Thyrotropin-releasing hormone (TRH, 10-4 M) caused a slight and statistically insignificant increase in potassium-evoked ACh release. DN-1417, a TRH analogue, at a concentration of 10-4 M significantly increased potassium-evoked ACh release. These findings indicate that DN-1417 is able to enhance ACh output independently of ACh synthesis from exogenous choline.

UR - http://www.scopus.com/inward/record.url?scp=0024571418&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=0024571418&partnerID=8YFLogxK

U2 - 10.1016/0306-3623(89)90023-2

DO - 10.1016/0306-3623(89)90023-2

M3 - Article

C2 - 2565849

AN - SCOPUS:0024571418

VL - 20

SP - 239

EP - 242

JO - Vascular Pharmacology

JF - Vascular Pharmacology

SN - 1537-1891

IS - 2

ER -