ABSTRACT
Piribedil produces a pronounced hypothermia both in mice and rats. This hypothermia was prevented by previous administration of dopamine receptor blocking agents (spiperone in mice and rats, pimozide in mice), tricyclic antidepressant drugs (imipramine, clomipramine, desipramine) in mice and LSD in rats. Administration of agents acting on serotonin receptors (cyproheptadine, p-chlorophenylalanine) or of a classical anticholinergic drug, atropine, did not change the hypothermizing effect of piribedil in rats. Thus, the hypothermia produced by piribedil is apparently similar to that produced by apomorphine. The possibility of a secondary stimulation of serotonergic receptors through direct stimulatory action of piribedil on dopamine neurons is discussed.
Subject(s)
Body Temperature/drug effects , Piperazines/pharmacology , Piribedil/pharmacology , Animals , Antidepressive Agents, Tricyclic/pharmacology , Depression, Chemical , Drug Interactions , Female , Male , Mice , Neurons/physiology , Rats , Receptors, Dopamine/drug effects , Receptors, Muscarinic/drug effects , Serotonin/physiology , Time FactorsABSTRACT
Nomifensine, a new antidepressant drug, affects the central noradrenergic neurons in the rat. Nomifensine does not affect the noradrenaline level in the brain, but retards the depletion of noradrenaline after inhibition of its synthesis. Apomorphine and dimethylaminoadamantane accelerate the depletion of noradrenaline and amphetamine does not affect it. Nomifensine potentiates the flexor reflex of the hind paw of a spinal rat and depresses the body temperature.
Subject(s)
Antidepressive Agents/pharmacology , Brain Chemistry/drug effects , Isoquinolines/pharmacology , Animals , Apomorphine/pharmacology , Bis(4-Methyl-1-Homopiperazinylthiocarbonyl)disulfide/pharmacology , Body Temperature/drug effects , Dextroamphetamine/pharmacology , Ditiocarb/pharmacology , Drug Interactions , Male , Norepinephrine/analysis , Rats , Reflex/drug effects , Time FactorsABSTRACT
The central action of nomifensine (NF), a new antidepressive drug, was studied in rats and mice. NF stimulates locomotor activity in normal animals as well as in animals whose motor activity has been depressed by reserpine, alpha-methyltyrosine (alpha-MT), bis-(4-methyl-1-homopiperazinyl-thiocarbonyl)-disulfide (Fla-63) or phenoxybenzamine. The sedation produced by alpha-MT plus reserpine or by spiroperidol is not affected by NF. NF induces stereotypy in the rat and antagonizes the catalepsy induced in the rat by neuroleptics, pilocarpine and arecoline. The catalepsy induced by alpha-MT plus reserpine is not influenced. NF elevates the brain levels of serotonin (5-HT) and 5-hydroxyindole acetic acid (5-HIAA) in the rat. These and previous results indicate that the profile of action of NF differs both from that of known tricyclic antidepressive drugs and that of dopaminergic stimulants.
