Effects of alcohol and saccharin deprivations on concurrent ethanol and saccharin operant self-administration by alcohol-preferring (P) rats
- 作者：Jamie E. Toalston ; Scott M. Oster ; Kelly A. Kuc ; Tylene J. Pommer ; James M. Murphy ; Lawrence Lumeng ; Richard L. Bell ; William J. McBride ; Zachary A. Rodd
- 关键词：Alcohol deprivation effect ; Operant self-administration ; Alcohol-preferring P rats ; Repeated deprivations ; Saccharin self-administration
- 刊名：Alcohol
- 出版年：2008
- 期刊代码：1_07418329
- 类别：neu
- 出版时间：June 2008
- 卷：42
- 期：4
- 页码：277-284
- 文件大小：213 K
摘要
Consumption of sweet solutions has been associated with a reduction in withdrawal symptoms and alcohol craving in humans. The objective of the present study was to determine the effects of ethanol and saccharin (SACC) deprivations on operant oral self-administration. Alcohol-preferring (P) rats were allowed to lever press concurrently self-administer ethanol (15%vol/vol) and SACC (0.0125%g/vol) for 8 weeks. Rats were then maintained on daily operant access (nondeprived), deprived of both fluids (2 weeks), deprived of SACC and given 2 ml of ethanol daily, or deprived of ethanol and given 2 ml of SACC daily. All groups were then given 2 weeks of daily operant access to ethanol and SACC, followed by an identical second deprivation period. P rats responded more for ethanol than SACC. All deprived groups increased responding on the ethanol lever, but not on the SACC lever. Daily consumption of 2 ml ethanol decreased the duration of the alcohol deprivation effect (ADE). Home cage access to 2 ml of SACC also decreased the ADE but to a lesser extent than access to ethanol. A second deprivation period further increased and prolonged the expression of an ADE. These results show ethanol is a more salient reinforcer than SACC. With concurrent access to ethanol and SACC, P rats do not display a saccharin deprivation effect. Depriving P rats of both ethanol and SACC had the most pronounced effect on the magnitude and duration of the ADE, suggesting that there may be some interactions between ethanol and SACC in their CNS reinforcing effects.