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The intermediate and medial hyperstriatum ventrale (IMHV) of the chick forebrain is a site of recognition memory for the learning process of imprinting. The results reported here demonstrate that neural cell adhesion molecules (NCAMs) play a time-dependent role in this recognition memory. Dark-reared chicks were trained, tested, and assigned a preference score as a measure of learning. Chicks with high preference scores were designated good learners and those with lower preference scores, poor learners. Controls were untrained. Tissue was removed, 9.5 hr or 24 hr after training, from the left and right IMHV, hyperstriatum accessorium, and posterior neostriatum. Three major NCAM isoforms (180, 140, and 120 kDa) were assayed. At 24 hr only, there was in left IMHV significantly more NCAM (for each isoform) in good learners than in the other 2 groups, and also a significant correlation between the amounts of NCAM and preference scores for all isoforms; the amount predicted by each regression line at preference score 50 (no learning) did not differ significantly from the mean value for untrained controls. There were no learning-related effects in either the hyperstriatum accessorium or the posterior neostriatum.

Although memory formation occurs in a sequence of pharmacologically dissociable stages, many models assume that this sequence is located within a single neuronal ensemble. Three forebrain areas in the young chick--the intermediate medial hyperstriatum ventrale (IMHV), the lobus parolfactorius (LPO), and the paleostriatum augmentatum--have been identified as important structures in mediating learning and memory processes. It has been shown that pretraining lesions placed to the left IMHV produce amnesia for a 1-trial passive avoidance task. posttraining lesions in the IMHV are not amnestic. The present study demonstrated that bilateral lesions to the LPO are amnestic but only if made subsequent to rather than before training. These results suggest that long-term storage of the memory is dependent on the LPO. Further experiments determined that in the absence of the LPO at training, the right IMHV can act a long-term memory storage site. In the absence of the right IMHV at training, other, as yet undetermined, areas can take up this role.

Apomorphine was found to disrupt memory consolidation in a dose-dependent manner on chicks trained on a 1-trial passive avoidance task with a strong aversant experience. Chicks injected with 4.0 mg/kg apomorphine displayed memory deficits at 180 min after learning and showed marked behavioral disturbances, including increased locomotion and increased pecking at the feet of conspecifics. Pretreatment with the dopamine antagonist haloperidol eliminated the memory disturbance induced by apomorphine and facilitated consolidation of memory in chicks given a weak (20% vol/vol methyl anthralinate) training experience. Time-of-retention data suggested that the memory disruption occurred from 120 min after learning, leading to the suggestion that dopamine-related modulation of the training experience may be involved in late-memory formation processes.

From Day 2 to Day 4 of life, chicks were fed daily in a large enclosure with 2 identical food caches, each filled with a different type of seed. On Day 5, binocular and monocular chicks were fed in their home cages 1 type of seed exclusively for 30 min. At test, soon after this devaluation phase, both binocular and right-eyed chicks chose the food caches containing the seeds that had not been devalued; in contrast, left-eyed chicks did not show a clear choice. Experiments revealed that the asymmetry was not due to lack of motivation, worse spatial memory, or inability to remember the consequences of devaluation by left-eyed chicks. Results suggest that young chicks can form declarative-like memories of the content of food caches. However, chicks using their left eye (which provides a supply mainly to the right hemisphere) failed to integrate memory of the content of food caches with memory of the consequences of devaluation.

Several experiments were conducted to examine the effects of intracranial injection of opioid peptides and antagonists on learning and memory in the chick. Pretraining injection of [[leu.sup.5]]enkephalin and the selective delta receptor agonist [D-[Pen.sup.2], L-[Pen.sup.5]]enkephalin (DPLPE) into the intermediate medial hyperstriatum ventrale (IMHV) produced impairment. ICL 174,864, a delta-selective antagonist, reversed the impairment produced by either [[leu.sup.5]]enkephalin or DPLPE, results indicating that delta receptors may play a role in learning in the chick and suggesting that the impairment produced by [[leu.sup.5]]enkephalin is mediated through delta opioid receptors. [beta]-endorphin produced a naloxone-reversible impairment in performance, which suggests that this impairment is mediated by opioid receptors. Bilateral injection of [beta]-endorphin into the IMHV produced impairment, as did unilateral injection into the right, but not left, IMHV. Only bilateral injections into IMHV of [[leu.sup.5]]enkephalin were effective. These results suggest that the effects of [beta]-endorphin are centrally mediated whereas the effects of [[leu.sup.5]]enkephalin may be localized to other brain regions or are peripherally mediated. These initial results suggest that opioids are associated with learning and memory in the chick.