Reference

Effect of cholinergic drugs on methadone-induced catalepsy and stereotypies in rats treated chronically with methadone

Effect of cholinergic drugs on methadone-induced catalepsy and stereotypies in rats treated chronically with methadone. Ahtee, Liisa (Dep. Pharmacol., Univ. Helsinki, Helsinki, Finland). Eur.There are some reagents with their cas registry numbers 114-49-8 and 51-33-2 are used in this study. J. Pharmacol., 39(2), 203-13 (English) 1976. CODEN: EJPHAZ. DOCUMENT TYPE: Journal CA Section: 1 (Pharmacodynamics) In rats treated chronically with (.+-.)-methadone-HCl [125-56-4] antimuscarinic drugs potentiated and muscarinic drugs antagonized the cataleptic effect of acute methadone, whereas the antimuscarinic drugs tended to antagonize and the muscarinic drugs potentiated the methadone-induced sterotypies. Nicotine hydrogen (+)-tartrate [65-31-6] initially slightly potentiated and mecamylamine-HCl [826-39-1] antagonized the cataleptic effect of methadone. The actions of the cholinergic drugs on the extrapyramidal motor effects of methadone were most probably central, because methylscopolamine nitrate [51-33-2] and hexamethonium-HCl [60-25-3] had only very weak actions. Thus, the effects of antimuscarinic and muscarinic drugs on the catalepsy and sterotypies induced by methadone are opposite to their effects on the catalepsy and sterotypies produced by drugs which are thought to act on the postsynaptic dopaminergic receptors. .

The effect of nicotine on central catecholamine neurons and gonadotropin secretion

The effect of nicotine on central catecholamine neurons and gonadotropin secretion. I. Studies in the male rat. Fuxe, K.; Agnati, L.; Eneroth, P.; Gustafsson, J. A.; Hokfelt, T.; Lofstrom, A.; Skett, B.; Skett, P. (Dep. Histol., Karolinska Inst., Stockholm, Swed.). Med. Biol., 55(3), 148-57 (English) 1977. CODEN: MDBYAS. DOCUMENT TYPE: Journal CA Section: 1 (Pharmacodynamics) Nicotine tartrate (I tartrate) [65-31-6], I salicylate [29790-52-1], cotinine [486-56-6], and mecamylamine chloride [826-39-1] (10-5M) had only weak, if any, effects on 3H-labeled dopamine (DA) [51-61-6] and noradrenaline (NA) [51-41-2] uptake, retention, and release in various in vitro models. I in 4 doses of 2 mg/kg, i.p., (30 min intervals) caused a redn. of the catecholamine (CA) stores in the medial palisade zone (MPZ) of the median eminence but in no other brain region. I in 4 doses of 3 mg/kg (30 min intervals) caused a trend for NA depletion in whole brain. The redn. of spinal cord NA levels by I was nerve impulse dependent. During tyrosine hydroxylase inhibition, 4 doses of I (2-3 mg/kg; 30 min intervals) increased NA turnover in whole brain and reduced DA turnover in the nucleus caudatus. I in 4 doses of 2 mg/kg blocked the increase in serum prolactin [9002-62-4] levels caused by the tyrosine hydroxylase inhibitor .alpha.-methyltyrosine Me ester (H44/68), whereas the basal serum levels of prolactin and FSH were not affected. I may affect central DA and NA neurons via activation of central nicotinic acetylcholine receptors which are probably not located on the DA and NA nerve terminals. I may partly lower prolactin secretion via its effects on CA nerve terminals in the MPZ, since a pos. intraindividual correlation was found between prolactin levels and CA levels in the MPZ in the normal male rat. I may increase the activity in the DA nerve terminals of the MPZ, the DA being released into the portal system to act as a prolactin inhibitory factor at the anterior pituitary level.