Post-training excitotoxic lesions of the dorsal hippocampus attenuate forward trace, backward trace, and delay fear conditioning in a temporally specific manner.
The present study sought to determine whether post-training excitotoxic lesions of the dorsal hippocampus would disrupt retention of fear conditioned using a trace procedure. Rats were trained using one of six procedures. Forward trace conditioning consisted of 10 trials in which a 16-s tone conditional stimulus (CS) was followed by a 28-s stimulus-free trace interval and then a mild footshock unconditional stimulus (US). We used two forms of delay conditioning where the tone and footshock co-terminated. Short delay used a 16-s tone and long delay used a 46-s tone. Backward trace conditioning was the same as forward trace, except that the order of the CS and US was reversed. CS-only and US-only were similar to forward trace except that the footshock or tone, respectively, was eliminated. One day later, animals received either an N-methyl-D-aspartate (NMDA)-induced lesion of the dorsal hippocampus or sham surgery. One week later, the rats were tested for freezing to the tone in a novel context. The next day, they were tested for freezing to the original training context. Hippocampal lesioned trace conditioned rats showed significantly less freezing during the tone compared with their sham lesioned controls. The lesion did not affect freezing during the tone in delay conditioning, nor in the other training conditions. During the 1-min period after tone offset, there was a trend in all hippocampal lesioned animals toward a deficit in freezing, compared with their corresponding sham lesioned controls, although only short delay, forward and backward trace groups showed a significant deficit. Hippocampal lesions also attenuated contextual conditioning. Thus, the hippocampus is critical for the consolidation and/or expression of a trace fear conditioned stimulus.
Quinn
Jennifer J
JJ
Department of Psychology, University of California, Los Angeles 90095, USA. jquinn@ucla.edu
Oommen
Santosh S
SS
Morrison
Glenn E
GE
Fanselow
Michael S
MS
D000818:Animals; D001927:Brain Diseases / Q000139:chemically induced* / Q000523:psychology*; D003213:Conditioning, Psychological / Q000502:physiology*; D018690:Excitatory Amino Acid Agonists; D005239:Fear / Q000502:physiology*; D006624:Hippocampus; D008297:Male; D016202:N-Methylaspartate; D051381:Rats; D020318:Rats, Long-Evans; D011930:Reaction Time / Q000502:physiology
D018690:Excitatory Amino Acid Agonists; D016202:N-Methylaspartate