Behavioural Brain Research 173 (2006) 299–309 Research report Intrathecal infusions of anisomycin impact the learning deficit but not the learning effect observed in spinal rats that have received instrumental training Kyle M. Baumbauer a,∗ , Erin E. Young a , Kevin C. Hoy Jr. a , Jill L. France b , Robin L. Joynes b a Psychology Department, Texas A&M University, Mailstop 4235, College Station, TX 77843-4235, USA b Psychology Department, Kent State University, Kent, OH 44242, USA Received 12 December 2005; received in revised form 29 June 2006; accepted 30 June 2006 Abstract Previous research has shown that spinally transected rats will learn to maintain a flexion response when administered shock contingent upon leg position. In short, a contingency is arranged between shock delivery and leg extension so that Master rats exhibit an increase in flexion duration that lasts throughout the training session. Furthermore, when Master rats are later tested they reacquire the flexion response in fewer trials, indicative of some savings. As a control, a second group of spinal rats (Yoked rats) are given shock irrespective of leg position (noncontingent shock). These animals fail to show the same increase in leg flexion duration. Interestingly, when Yoked rats are later tested with a shock contingency in place, they still fail to learn (learning deficit). The present experiments were designed to determine whether both forms of instrumental learning in spinal animals require de novo protein synthesis. As such, we administered various doses of anisomycin intrathecally prior to training. Additionally, spinal rats were trained and tested either immediately or 24 h after test. We found that only the highest dose of anisomycin (125 g/l) had an effect in Yoked animals that were tested 24h after training. Specifically, the highest dose of anisomycin reversed the learning deficit in those animals. Moreover, anisomycin had a similar effect when administered prior to training and immediately following training, but not 6h after training. Finally, the results demonstrated that the observed effect of anisomycin was not due to state-dependency. © 2006 Elsevier B.V. All rights reserved. Keywords: Spinal cord; Spinal learning; Instrumental learning; Protein synthesis; Anisomycin 1. Introduction Recent research indicates that animals with spinal transec- tions will modify reflexive responses when exposed to various conditioning procedures [2,5,6,10,13,20,29,30,31]. Our labora- tory utilizes a simple instrumental training procedure (modified Master–Yoke paradigm) in which a contingency is established between leg position and the onset of shock. Spinal rats in the Master group receive shock to one hindleg whenever that leg is in an extended position. To control for the effects of shock per se, rats in a second group (Yoked group) receive the same amount and pattern of shock, only shock is delivered irrespective of their own leg position. During a 30 min training period, we find that ∗ Corresponding author. Tel.: +1 979 845 0378; fax: +1 979 845 4727. E-mail address: baumbauer@tamu.edu (K.M. Baumbauer). rats in the Master condition experience a response (leg down)- outcome (shock) contingency, while Yoked subjects do not. Consequently, Master rats learn to hold their legs in a flexed posi- tion while Yoked rats do not. A third group remains Unshocked for this training period. After training, when animals are later tested with contingent shock, Master and previously Unshocked animals will learn to hold their legs in a flexed position. Fur- thermore, Master rats reacquire the flexion response faster than the Unshocked rats, indicating a savings effect. Yoked animals, on the other hand, will fail to acquire the flexion response, even though they are tested with response-contingent shock, and are given the opportunity to learn about the response–outcome rela- tionship (learning deficit). Given our behavioral effects, we have become interested in investigating the underlying biological mechanisms respon- sible for this plasticity. Research has shown that the NMDA receptor is important for neuronal plasticity, and hence, the 0166-4328/$ – see front matter © 2006 Elsevier B.V. All rights reserved. doi:10.1016/j.bbr.2006.06.041