Hippocampal lesions in rats differentially affect long- and short-trace eyeblink conditioning

Extensive previous research has implicated the hippocampus as an important structure for the acquisition of trace eyeblink conditioning. Evidence from multiple species and various lesioning methods shows that the disruption of conditioned responding (CR) may be partially dependent on the relative lengths of the conditioned stimulus (CS) period and the trace interval. The present study systematically manipulated the length of the CS and the trace interval while matching the interstimulus intervals (ISI) in rats with or without ibotenic acid hippocampal lesions. The long-trace interval condition had a CS duration of 50 ms and a trace interval of 500 ms. The short-trace interval condition had a 500 ms CS and a 50 ms trace interval. We found that control animals in the long-trace interval condition learned at a slower rate than the control animals in the short-trace interval condition. Lesioned animals in both the trace conditions showed deficits in acquisition. Lesioned animals in the short-trace interval condition acquired conditioned responses at a rate almost identical to that of the control animals in the long-trace interval condition. CR onset latencies were impaired for lesioned animals. Peak latencies were not different, indicating no difference in the adaptiveness of the CRs. These results suggest that while the hippocampus is important for acquisition of trace eyeblink conditioning, performance also depends on the parameters used for the task. In particular, the relative lengths of the CS period and the trace interval appear to be important.

[1]  D. Woodruff-Pak,et al.  Eyeblink classical conditioning in H.M.: delay and trace paradigms. , 1993, Behavioral neuroscience.

[2]  Louis D. Matzel,et al.  The Role of the Hippocampus in Trace Conditioning: Temporal Discontinuity or Task Difficulty? , 2001, Neurobiology of Learning and Memory.

[3]  L. Jarrard.  On the use of ibotenic acid to lesion selectively different components of the hippocampal formation , 1989, Journal of Neuroscience Methods.

[4]  J F Disterhoft,et al.  Impaired trace eyeblink conditioning in bilateral, medial-temporal lobe amnesia. , 1997, Behavioral neuroscience.

[5]  J. Steinmetz.  Brain substrates of classical eyeblink conditioning: a highly localized but also distributed system , 2000, Behavioural Brain Research.

[6]  Craig Weiss,et al.  Hippocampal lesions prevent trace eyeblink conditioning in the freely moving rat , 1999, Behavioural Brain Research.

[7]  C. Yeo,et al.  Hippocampal lesions and trace conditioning in the rabbit , 1987, Behavioural Brain Research.

[8]  R. F. Thompson,et al.  Hippocampus and trace conditioning of the rabbit's classically conditioned nictitating membrane response. , 1986, Behavioral neuroscience.

[9]  David G. Lavond,et al.  Trace conditioning: Abolished by cerebellar nuclear lesions but not lateral cerebellar cortex aspirations , 1985, Brain Research.

[10]  Richard F. Thompson,et al.  Hippocampectomy impairs the memory of recently, but not remotely, acquired trace eyeblink conditioned responses. , 1995, Behavioral neuroscience.

[11]  M. M. Patterson,et al.  Retention and acquisition of classical trace conditioned responses by rabbits with hippocampal lesions. , 1986, Behavioral neuroscience.