Effect of disconnecting the orbital prefrontal cortex from the nucleus accumbens core on inter-temporal choice behaviour: A quantitative analysis
- 作者：G. Bezzina ; S. Body ; T.H.C. Cheung ; C.L. Hampson ; C.M. Bradshaw ; E. Szabadi ; I.M. Anderson ; J.F.W. Deakin
- 关键词：Orbital prefrontal cortex ; Nucleus accumbens core ; Disconnection lesion ; Inter-temporal choice ; Delay discounting ; Rat
- 刊名：Behavioural Brain Research
- 出版年：2008
- 期刊代码：3_01664328
- 类别：neu
- 出版时间：22 August 2008
- 卷：191
- 期：2
- 页码：272-279
- 文件大小：1195 K
摘要
Previous experiments showed that destruction of the orbital prefrontal cortex (OPFC) or the nucleus accumbens core (AcbC) in rats altered choice between two delayed food reinforcers. Application of a quantitative model of inter-temporal choice suggested that lesions of either structure increased the delay-dependent degradation of reinforcer value (delay discounting); destruction of the OPFC (but not the AcbC) also increased the relative value of the larger reinforcer. This experiment examined the effect of disconnecting the OPFC from the AcbC on inter-temporal choice. Rats received excitotoxin-induced contralateral lesions of the OPFC and AcbC (disconnection), severing of the anterior corpus callosum (callosotomy), a combined lesion (disconnection + callosotomy) or sham lesions. They were trained in a discrete-trials progressive delay schedule to press levers A and B for a sucrose solution. Responses on A delivered 50 μl of the solution after a delay dA; responses on B delivered 100 μl after a delay dB. dB increased across blocks of trials; dA was manipulated across phases of the experiment. Indifference delay, dB(50) (value of dB corresponding to 50%choice of B), was estimated for each rat in each phase, and linear indifference functions (dB(50) vs. dA) were derived. The disconnection + callosotomy group showed a lower intercept of the indifference function (implying a higher rate of delay discounting) than the sham-lesioned group; the disconnection group showed a similar but less robust effect, whereas the callosotomy group did not differ significantly from the sham-lesioned group. The results suggest that OPFC–AcbC connections are involved in delay discounting of food reinforcers, but provide no evidence for an involvement of OPFC–AcbC connections in regulating sensitivity to reinforcer size.