Aversive stimulus properties of scopolamine

Abstract

The drug state produced in rats by intraperitoneal injections of scopolamine hydrobromide (1.2 mg/kg) was treated as a putative aversive US. This US was paired with a distinctive spatial location in a shuttle box for 6 of 12 daily sessions by confining the subject to one side following scopolamine and to the other side following saline (6 sessions). Two groups of 8 subjects each received zero and 20 min post-injection delays respectively. Following zero delay, but not 20 min delay, subjects avoided the side associated with scopolamine in drug-free, free choice tests. This is evidence that the immediate post-injection drug state induced by scopolamine is aversive.

The Role of Identified Neurotransmitter Systems in the Response of Insular Cortex to Unfamiliar Taste: Activation of ERK1–2 and Formation of a Memory Trace

“…We were concerned with the possibility that the drugs microinjected into the IC might themselves induce visceral malaise, because a variety of drugs, including neurotransmitter antagonists, may induce malaise when administered systemically (MacMahon et al, 1981;Asin and Montana, 1989;Bures and Buresova, 1989). Although the drugs in our study were locally microinjected into the IC, and, moreover, this was done before the taste was presented, i.e., in a backward conditioning situation that is not expected to lead to efficient associations, we could not exclude the possibility that subtle malaise might develop that lingers throughout and after the time during which the tastant is consumed and become associated with the experienced taste.…”

Taste reactivity responses elicited by cocaine-, phencyclidine-, and methamphetamine-paired sucrose solutions.

“…Reinforcing US agents that do not produce aversive TR responses 2 g/kg ip (familiar) 1-5 mg/kg ip 0.5-7.5 mg/kg ip 2-80 mg/kg sc 0.4-0.8 mg/kg sc 1 mg/kg ip Davies & Parker, 1990Parker, 1982, 1984Parker & Carvell, 1986;Parker & McLeod, 1992;Zalaquett & Parker, 1989Parker & Brosseau, 1990Parker, 1988bParker, 1991Parker & Carvell, 1986 Nonreinforcing US agents that do not produce aversive TR responses Footshock 0.3-0.6 mA Pelchat et al, 1983 Lactose (40%) 10 min oral access Pelchat et al, 1983;Simbayi et al, 1986 Naltrexone 0.01-10 mg/kg ip Parker & Rennie, 1992 produce a conditioned place aversion (e.g., Asin, Wirtshafer, & Tabakoff, 1985;Best, Best, & Mickley, 1973;Cunningham, 1979;Davies & Parker, in press;Jorenby, Steinpreis, Sherman, & Baker, 1990;MacMahon, Blampied, & Hughes, 1981;Mucha, van der Kooy, O'Shaughnessey, & Bucenieks, 1982;Parker, 1992;Reid, Hunter, Beauman, Hubbel, 1985;Sherman, Hickis, Rice, Rusiniak, & Garcia, 1983;van der Kooy, O'Shaughnessey, Mucha, & Kalant, 1983;Wall, Hinson, Schmidt, Johnston, & Streather, 1990) or to be ineffective reinforcers in place conditioning or self-administration paradigms (e.g., Costello, Carlson, Glick, & Bryda, 1989;Davies & Parker, 1990;Fudala, Teoh, & Iwamoto, 1985;Parker, 1992;Winger, Young, & Woods, 1985). Physostigmine and neostigmine, which are acetylcholinesterase inhibitors, have not been assessed for their ability to produce place conditioning or self-administration, although physostigmine has been demonstrated to suppress responding for food reinforcement (e.g., Lui, 1991) a...…”

“…A feature shared by all US agents presented in the upper section of Table 1 is their inability to serve as a reinforcer in place conditioning and drug self-administration paradigms. At the dosage levels tested, novel alcohol (2–3 g/kg), apomorphine (15 mg/kg), fenfluramine (3 mg/kg), lithium (12−127.2 mg/kg), methylscopolamine (1 mg/kg), nicotine (1.2–2 mg/kg sc), and scopolamine (1 mg/kg) have been demonstrated to produce a conditioned place aversion (e.g., Asin, Wirtshafer, & Tabakoff, 1985; Best, Best, & Mickley, 1973; Cunningham, 1979; Davies & Parker, in press; Jorenby, Steinpreis, Sherman, & Baker, 1990; MacMahon, Blampied, & Hughes, 1981; Mucha, van der Kooy, O'Shaughnessey, & Bucenieks, 1982; Parker, 1992; Reid, Hunter, Beauman, Hubbel, 1985; Sherman, Hickis, Rice, Rusiniak, & Garcia, 1983; van der Kooy, O'Shaughnessey, Mucha, & Kalant, 1983; Wall, Hinson, Schmidt, Johnston, & Streather, 1990) or to be ineffective reinforcers in place conditioning or self-administration paradigms (e.g., Costello, Carlson, Glick, & Bryda, 1989; Davies & Parker, 1990; Fudala, Teoh, & Iwamoto, 1985; Parker, 1992; Winger, Young, & Woods, 1985). Physostigmine and neostigmine, which are acetylcholinesterase inhibitors, have not been assessed for their ability to produce place conditioning or self-administration, although physostigmine has been demonstrated to suppress responding for food reinforcement (e.g., Lui, 1991) and to produce dysphoria in humans (Risch et al, 1980).…”