Effects of nicotine on brain 1-phosphatidylinositol-4-phosphate and 1-phosphatidylinositol-3,4-bisphosphate synthesis and metabolism-possible relationship to nicotine-induced behaviors

Robert Hitzemann, Reiko Natsuki, Horace H. Loh

Research output: Contribution to journalArticle

3 Citations (Scopus)

Abstract

The effects of nicotine and other cholinergic drugs on the initial incorporation of 32Pi, and [3H]glycerol into 1-phosphatidylinositol-4-phosphate(DPI)and 1-phosphatidylinsitol-3,4-bisphosphate (TPI) in the rat brain microsomal fraction were studied. Nicotine and eserine significantly decreased and mecamylamine increased [32P]- and [3H]TPI levels. Atropine had no effect on labeled TPI levels. Dose-effect studies for nicotine revealed that as little as 0.1 mg/kg of nicotine, i.p., significantly decreased the accumulation of labeled TPI. It was concluded that pharmacologically relevant and nonconvulsive doses of nicotine can markedly affect brain polyphosphoinositide synthesis and/or metabolism; the nature of the effects is consistent with theories suggesting that the conversion of TPI to DPI will release membrane lipid bound Ca2+ and, thus, increase membrane excitability.

Original languageEnglish (US)
Pages (from-to)2519-2523
Number of pages5
JournalBiochemical Pharmacology
Volume27
Issue number21
DOIs
StatePublished - 1978
Externally publishedYes

Fingerprint

Nicotine
Metabolism
Brain
Mecamylamine
Phosphatidylinositol Phosphates
Physostigmine
Membrane Lipids
Atropine
Glycerol
Cholinergic Agents
Rats
phosphatidylinositol 4-phosphate
phosphatidylinositol 3,4-diphosphate
Membranes

ASJC Scopus subject areas

  • Pharmacology

Cite this

@article{3f84236ae38b415fabdf742bed9a798a,
title = "Effects of nicotine on brain 1-phosphatidylinositol-4-phosphate and 1-phosphatidylinositol-3,4-bisphosphate synthesis and metabolism-possible relationship to nicotine-induced behaviors",
abstract = "The effects of nicotine and other cholinergic drugs on the initial incorporation of 32Pi, and [3H]glycerol into 1-phosphatidylinositol-4-phosphate(DPI)and 1-phosphatidylinsitol-3,4-bisphosphate (TPI) in the rat brain microsomal fraction were studied. Nicotine and eserine significantly decreased and mecamylamine increased [32P]- and [3H]TPI levels. Atropine had no effect on labeled TPI levels. Dose-effect studies for nicotine revealed that as little as 0.1 mg/kg of nicotine, i.p., significantly decreased the accumulation of labeled TPI. It was concluded that pharmacologically relevant and nonconvulsive doses of nicotine can markedly affect brain polyphosphoinositide synthesis and/or metabolism; the nature of the effects is consistent with theories suggesting that the conversion of TPI to DPI will release membrane lipid bound Ca2+ and, thus, increase membrane excitability.",
author = "Robert Hitzemann and Reiko Natsuki and Loh, {Horace H.}",
year = "1978",
doi = "10.1016/0006-2952(78)90319-2",
language = "English (US)",
volume = "27",
pages = "2519--2523",
journal = "Biochemical Pharmacology",
issn = "0006-2952",
publisher = "Elsevier Inc.",
number = "21",

}

TY - JOUR

T1 - Effects of nicotine on brain 1-phosphatidylinositol-4-phosphate and 1-phosphatidylinositol-3,4-bisphosphate synthesis and metabolism-possible relationship to nicotine-induced behaviors

AU - Hitzemann, Robert

AU - Natsuki, Reiko

AU - Loh, Horace H.

PY - 1978

Y1 - 1978

N2 - The effects of nicotine and other cholinergic drugs on the initial incorporation of 32Pi, and [3H]glycerol into 1-phosphatidylinositol-4-phosphate(DPI)and 1-phosphatidylinsitol-3,4-bisphosphate (TPI) in the rat brain microsomal fraction were studied. Nicotine and eserine significantly decreased and mecamylamine increased [32P]- and [3H]TPI levels. Atropine had no effect on labeled TPI levels. Dose-effect studies for nicotine revealed that as little as 0.1 mg/kg of nicotine, i.p., significantly decreased the accumulation of labeled TPI. It was concluded that pharmacologically relevant and nonconvulsive doses of nicotine can markedly affect brain polyphosphoinositide synthesis and/or metabolism; the nature of the effects is consistent with theories suggesting that the conversion of TPI to DPI will release membrane lipid bound Ca2+ and, thus, increase membrane excitability.

AB - The effects of nicotine and other cholinergic drugs on the initial incorporation of 32Pi, and [3H]glycerol into 1-phosphatidylinositol-4-phosphate(DPI)and 1-phosphatidylinsitol-3,4-bisphosphate (TPI) in the rat brain microsomal fraction were studied. Nicotine and eserine significantly decreased and mecamylamine increased [32P]- and [3H]TPI levels. Atropine had no effect on labeled TPI levels. Dose-effect studies for nicotine revealed that as little as 0.1 mg/kg of nicotine, i.p., significantly decreased the accumulation of labeled TPI. It was concluded that pharmacologically relevant and nonconvulsive doses of nicotine can markedly affect brain polyphosphoinositide synthesis and/or metabolism; the nature of the effects is consistent with theories suggesting that the conversion of TPI to DPI will release membrane lipid bound Ca2+ and, thus, increase membrane excitability.

UR - http://www.scopus.com/inward/record.url?scp=0018186221&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=0018186221&partnerID=8YFLogxK

U2 - 10.1016/0006-2952(78)90319-2

DO - 10.1016/0006-2952(78)90319-2

M3 - Article

VL - 27

SP - 2519

EP - 2523

JO - Biochemical Pharmacology

JF - Biochemical Pharmacology

SN - 0006-2952

IS - 21

ER -