Reference

Discriminative stimulus effects of a low dose of apomorphine in the rat

Discriminative stimulus effects of a low dose of apomorphine in the rat. Tang, A. H.; Franklin, S. R. (Upjohn Co., Kalamazoo, MI 49001, USA). Psychopharmacology (Berlin), 91(1), 61-6 (English) 1987. CODEN: PSCHDL.There are some reagents with their cas registry numbers 18426-20-5 and 4205-90-7 are used in this study. ISSN: 0033-3158. DOCUMENT TYPE: Journal CA Section: 1 (Pharmacology) The discriminative stimulus (DS) effect of apomorphine [58-00-4] was investigated in rats trained in a 2-lever, food-reinforcement procedure. Rats were given s.c. injections of saline or 0.1 mg/kg apomorphine 15 min before training sessions. The training dose of apomorphine was chosen to activate dopamine autoreceptors selectively. Stimulus generalization studies demonstrated that the DS effects generalized completely to other direct-acting dopaminergic agonists such as N-n-propylnorapomorphine [18426-20-5], pergolide mesylate [66104-23-2], lergotrile mesylate [51473-23-5], and bromocriptine [25614-03-3]. The indirect-acting dopamine agonists (+)amphetamine [51-64-9], cocaine [50-36-2], and methylphenidate [113-45-1] produced predominantly saline-appropriate lever responses. The DS effect of apomorphine at the training dose was incompletely antagonized by haloperidol [52-86-8] or metoclopramide [364-62-5]. The dopaminergic antagonists tested, however, also partially generalized to apomorphine. Both enantiomers of 3-(3-hydroxyphenyl)-N-n-propylpiperidine (3-PPP) produced apomorphine-appropriate lever choice with the (-)-enantiomer [85966-89-8] being slightly more potent. The discriminative property of this (0.1 mg/kg) dose of apomorphine has characteristics consistent with selective dopamine autoreceptor activation. .

Stimulation of adenylate cyclase in relation to dopamine-induced long-term enhancement (LTE) of muscarinic depolarization in the rabbit superior cervical ganglion

Stimulation of adenylate cyclase in relation to dopamine-induced long-term enhancement (LTE) of muscarinic depolarization in the rabbit superior cervical ganglion. Mochida, Sumiko; Kobayashi, Haruo; Libet, Benjamin (Dep. Physiol., Tokyo Med. Coll., Tokyo 160, Japan). J. 7683-59-2 and 60-92-4 are cas registry numbers. These chemicals are also mentioned in this article. Neurosci., 7(2), 311-18 (English) 1987. CODEN: JNRSDS. ISSN: 0270-6474. DOCUMENT TYPE: Journal CA Section: 2 (Mammalian Hormones) Dopamine (DA) [51-61-6] (15 mM), its analog, 2-amino-6,7-dihyroxy-1,2,3,4-tetrahydronaphthalene [53463-78-8], and a D2 receptor antagonist, metoclopramide [364-62-5] each can induce both the long-term enhancement (LTE) of the slow muscarinic depolarizing response to methacholine (MCh) [55-92-5] and an increase in ganglionic cAMP [60-92-4]. Conversely, antagonists of DA-induced LTE also depress DA-induced rises in cAMP; these antagonists include haloperidol (1 mM), both (+) and (-) enantiomers of butaclamol (0.7-7 mM), flupenthixol (1 mM), and (+)-R-8-chloro-2,3,4,5-tetrahydro-3-methyl-5-phenyl-1H-3-benzazepine- 7-ol (SCH-23390) (7mM). The selective D2 antagonists sulpiride (10 mM) and domperidone (10 mM) affect neither DA action. a2-Adrenergic agonists (a-methyl-norepinephrine and clonidine) produce no LTE; a-antagonists dihydroergotamine (35 mM) does not affect either DA action, although it can completely block the hyperpolarizing response to DA or other catecholamines. b-Antagonist propranolol (5 mM) partially depresses DA-induced LTE. Butaclamol and propranolol in combination can completely block the cAMP rise induced by DA. b-Agonist isoproterenol [7683-59-2] can induce appreciable LTE of MCh depolariziation, but this LTE is not depressed by propranolol (10 mM). Isoproterenol can elicit a substantial rise in cAMP. Evidently, LTE of slow muscarinic depolarizing responses is induced via activation of a DA receptor that is coupled to adenylate cylase [9012-42-4] and resembles, but is not identical to, D1 receptors described in the brain. The induction of LTE by isoproterenol may reflect an ability to activate this DA receptor to some extent, rather than its addnl. activation of a b-receptor. In contrast to the cAMP produced at the DA receptor, cAMP formed via activation of b-receptors in this ganglion appears to be ineffective for inducing LTE of muscarinic responses. .