Ibotenic acid lesions of the medial septum retard delay eyeblink conditioning in rabbits (Oryctolagus cuniculus).

S. Berry and R. Thompson (1979) reported that electrolytic lesions of the medial septum significantly retard eyeblink conditioning. However, these electrolytic lesions were nonselective and may have also damaged the subcortical inputs to the hippocampus via the fimbria-fornix. In the present study, the medial septum was selectively lesioned with ibotenic acid in rabbits (Oryctolagus cuniculus), whose performance in a delay eyeblink conditioning paradigm was compared with that of intact controls. sham-operated controls, and intact controls given a systemic injection of scopolamine. Rabbits with selective medial septal lesions and rabbits receiving systemic scopolamine were significantly slower to condition than were intact and sham-lesioned rabbits. This finding demonstrates that the selective removal of the medial septum retards delay eyeblink conditioning in a manner similar to the disruption seen after systemic administration of scopolamine.

Selective hippocampal lesions disrupt a novel cue effect but fail to eliminate blocking in rabbit eyeblink conditioning.

The classical conditioning task of blocking involves the adding of a novel but redundant stimulus to a previously trained stimulus. Both blocking and novelty detection are thought to involve the hippocampus. Previously, Solomon (1977) found that nonselective aspiration lesions of the hippocampal region eliminated blocking in rabbit eyeblink conditioning. We tested the effects of selective ibotenic acid lesions of the hippocampus on blocking, as well as on novelty detection, when training is switched from a tone conditioned stimulus (CS) to a compound tone-light CS in eyeblink conditioning. Selective hippocampal lesions did not eliminate blocking but did lead to a facilitation of conditioned response (CR) acquisition to the tone and to the light, but not to the tone-light compound. Selective hippocampal lesions disrupted a CR decrement observed in sham surgical controls when transferred from tone training to tone-light training. It appears that although selective hippocampal lesions do not eliminate blocking in eyeblink conditioning, they do disrupt novelty detection and may facilitate learning to a previously blocked cue.

Blocking in rabbit eyeblink conditioning is not due to learned inattention: indirect support for an error correction mechanism of blocking.

Blocking is a classical conditioning task in which prior training to one cue such as a tone reduces learning about a second cue such as a light, when subsequently trained as a tone-light compound. Blocking has been theorized to come about through a US-modulated error correction mechanism by Rescorla & Wagner (1972) as well as through a mechanism of learned inattention as theorized by Mackintosh (1973). In the case of eyeblink conditioning, an error correction mechanism has been hypothesized to take place in the cerebellum while some form of inattention has been hypothesized to take place in the hippocampal region. The hypothesis we are testing is whether the mechanism of learned inattention is involved in blocking in rabbit eyeblink conditioning. If blocking in eyeblink conditioning is produced by a mechanism of learned inattention, then training to a previously blocked cue should be slower than training to that cue in a naïve animal. Rabbits that had received tone training followed by tone-light training exhibited blocking. Rabbits that had been previously blocked to the light acquired conditioned responses to the light at the same rate as naive rabbits. This finding failed to support the hypothesis that blocking in rabbit eyeblink conditioning is due to learned inattention, but does support the Rescorla-Wagner mechanism of error correction. The present finding along with previous work on error correction mechanism in the cerebellar-brainstem circuit (Kim et al., 1998) lend support to the theory that blocking, at least in rabbit eyeblink conditioning, seems to be due to an error correction mechanism rather than a learned inattention mechanism.