Effect of acute and chronic stress restraint on amphetamine-associated place preference: involvement of dopamine D and D receptors

NANCY CAPRILES 1, LILIANA M. CANCELA

EUROPEAN JOURNAL OF PHARMACOLOGY

ELSEVIER SCIENCE BV

Año: 1999 vol. 386 p. 127 - 134

0014-2999

The purpose of this study was to determine the D-amphetamine 1.0, 1.5 and 2 mgrkg i.p..-induced place preference in rats pre-exposed to acute or chronic restraint stress, using the conditioned place preference model. We also studied the involvement of opioid and dopamine mechanisms in the acute restraint stress-induced increase of D-amphetamine-induced place preference. A single restraint session 2 h. but not chronic restraint 2 hrday for 7 days. leading to adaptation to the stressor, enhanced the D-amphetamine-induced place preference. This enhancing effect was prevented by haloperidol administration 0.4 mgrkg i.p.., ".-sulpiride 60 mgrkg i.p.. orD-amphetamine 1.0, 1.5 and 2 mgrkg i.p..-induced place preference in rats pre-exposed to acute or chronic restraint stress, using the conditioned place preference model. We also studied the involvement of opioid and dopamine mechanisms in the acute restraint stress-induced increase of D-amphetamine-induced place preference. A single restraint session 2 h. but not chronic restraint 2 hrday for 7 days. leading to adaptation to the stressor, enhanced the D-amphetamine-induced place preference. This enhancing effect was prevented by haloperidol administration 0.4 mgrkg i.p.., ".-sulpiride 60 mgrkg i.p.. orD-amphetamine-induced place preference. A single restraint session 2 h. but not chronic restraint 2 hrday for 7 days. leading to adaptation to the stressor, enhanced the D-amphetamine-induced place preference. This enhancing effect was prevented by haloperidol administration 0.4 mgrkg i.p.., ".-sulpiride 60 mgrkg i.p.. or2 h. but not chronic restraint 2 hrday for 7 days. leading to adaptation to the stressor, enhanced the D-amphetamine-induced place preference. This enhancing effect was prevented by haloperidol administration 0.4 mgrkg i.p.., ".-sulpiride 60 mgrkg i.p.. or0.4 mgrkg i.p.., ".-sulpiride 60 mgrkg i.p.. or Rq.-SCH-23390 hydrochloride Rq.-7-chloro-8-hydroxy-3-methyl-1-phenyl-2,3,4,5-tetrahydro-1H-3-benzazepine hydrochloride, 30q.-SCH-23390 hydrochloride Rq.-7-chloro-8-hydroxy-3-methyl-1-phenyl-2,3,4,5-tetrahydro-1H-3-benzazepine hydrochloride, 30 mgrkg i.p.. 10–20 min prior to the acute restraint session. However, naltrexone pretreatment 1 or 2 mgrkg i.p.. failed to prevent the acute restraint-induced enhancement of D-amphetamine-induced place preference. These results suggest that: 1. the enhancement ofgrkg i.p.. 10–20 min prior to the acute restraint session. However, naltrexone pretreatment 1 or 2 mgrkg i.p.. failed to prevent the acute restraint-induced enhancement of D-amphetamine-induced place preference. These results suggest that: 1. the enhancement ofD-amphetamine-induced place preference. These results suggest that: 1. the enhancement of D-amphetamine-induced place preference occurred after a single restraint stress but not following chronic restraint stress, 2. the stimulation of both dopamine D1 and D2 receptors is necessary for the development of single restraint stress-induced enhancement of-amphetamine-induced place preference occurred after a single restraint stress but not following chronic restraint stress, 2. the stimulation of both dopamine D1 and D2 receptors is necessary for the development of single restraint stress-induced enhancement of1 and D2 receptors is necessary for the development of single restraint stress-induced enhancement of D-amphetamine-induced place preference and 3. apparently, an opioid system is not involved in this acute restraint-induced effect.-amphetamine-induced place preference and 3. apparently, an opioid system is not involved in this acute restraint-induced effect. q1999 Elsevier Science B.V. All rights reserved.1999 Elsevier Science B.V. All rights reserved.