Decrease in core temperature as an indication of cholinergic overdrive during amitriptyline withdrawal.

S C Dilsaver; M J Majchrzak

doi:10.1016/0006-3223(87)90109-0

Home/Archive/PubMed

PubMed · 3676377

Decrease in core temperature as an indication of cholinergic overdrive during amitriptyline withdrawal.

S C Dilsaver·M J Majchrzak

View original source ↗Export metadata ↓

Abstract

The source did not provide an abstract. Follow the original record for more information.

Explore related subjects

Amitriptyline Animals Body Temperature Regulation Male Rats Rats, Inbred Strains Receptors, Cholinergic Substance Withdrawal Syndrome Journal Article Research Support, U.S. Gov't, P.H.S.

Keep this discovery

Explore connections, maps & timelines

BibTeX RIS

S C Dilsaver, M J Majchrzak. 1987. Decrease in core temperature as an indication of cholinergic overdrive during amitriptyline withdrawal.. https://doi.org/10.1016/0006-3223(87)90109-0

Cite the original work for its findings. Save a collection to share your selection of sources.

KEEP EXPLORING

Related citations

PubMed1992

High-performance liquid chromatographic determination of amitriptyline and its main metabolites using a silica column with reversed-phase eluent. Application in mice.

A method was developed for the assay of amitriptyline, amitriptyline N-oxide, nortriptyline, desmethylnortriptyline and E (trans) and Z (cis) isomers of 10-hydroxyamitriptyline and of 10-hydroxynortriptyline in plasma and brain of animals, using high-performance liquid chromatography with ultraviolet detection (254 nm). Single extraction was performed at pH 10.5 from 0.25 ml of plasma or 1 ml of brain mixture. Chromatographic separations were achieved with a silica column and an aqueous methanol mobile phase containing ammonia. This procedure offers high sensitivity (8-10 ng/ml), high linearity (r > 0.99) and acceptable precision (coefficient of variation < or = 13.3%). The method was used to determine levels of amitriptyline and its major metabolites in mice 30 min after a single intraperitoneal administration of amitriptyline (20 mg/kg).

Amitriptyline↗

PubMed1992

Antidepressants inhibit spontaneous oscillations of intracellular Ca2+ concentration in rat cortical cultured neurons.

In rat cortical cultured neurons, spontaneous oscillations in the intracellular Ca2+ concentration ([Ca2+]i) were observed by direct [Ca2+]i measurements using the fluorescent indicator fura-2. These [Ca2+]i responses were eliminated by the removal of extracellular Ca2-, L-type Ca2+ channel blockers or a glutamate receptor antagonist. Three antidepressants (amitriptyline, imipramine and mianserin) suppressed the [Ca2+]i oscillations in the range of 1-50 microM. In addition, amitriptyline inhibited high K(+)-and glutamate-induced [Ca2+]i increases with IC50 values of 19 and 27 microM, respectively. Imipramine and mianserin also inhibited the high K(+)-induced [Ca2+]i increases with IC50 values of 45 and 24 microM, respectively. These results suggest that blocking actions by the antidepressants on voltage-dependent Ca2+ influx and glutamate receptor-mediated Ca2+ influx may be involved in the suppression of the [Ca2+]i oscillations.

Amitriptyline↗

PubMed1992

Amitriptyline inhibits striatal efflux of neurotransmitters via blockade of voltage-dependent Na+ channels.

Amitriptyline, a tricyclic antidepressant, almost completely inhibited veratridine- or scorpion toxin-evoked efflux of endogenous dopamine (DA) and gamma-aminobutyric acid (GABA) from rat striatal slices without any effects of 30 mM K+ or 4-aminopyridine on basal and evoked efflux. The effects of amitriptyline on glutamate efflux were comparable to those on DA or GABA efflux. These effects of amitriptyline can be well explained by its blockade of voltage-dependent Na+ channels and may be independent of other activities of this drug such as re-uptake inhibition of monoamines and blockade of K+ channels.

Amitriptyline↗