A behavioural investigation of the function of glycoprotein fucosylation in learning and memory in the day-old domestic chicken.

Barber, Alistair John (1990). A behavioural investigation of the function of glycoprotein fucosylation in learning and memory in the day-old domestic chicken. PhD thesis The Open University.

DOI: https://doi.org/10.21954/ou.ro.0000fc5b

Abstract

Two new paradigms of learning in the day-old domestic chick were developed and tested. The first was a serial colour-discrimination passive avoidance task, similar to that used by Gibbs and Ng (1977), in which chicks were trained to discriminate between red and green stimuli by pairing one with the bitter taste of methylanthranilate. The second was a sickness-conditioned aversion task, similar to that developed by Garcia and Ervin (1968), in which chicks were trained to associate pecking at a stimulus with subsequent sickness, induced by lithium chloride injection.
2-Deoxy galactose (2-Dgal), a fucose analogue that inhibits the completion of brain fucosylglycoproteins, induced amnesia for both tasks when injected into both hemispheres of the forebrain before training. Amnesia was similarly induced for the passive avoidance task when 2-Dgal was injected into the right forebrain alone, but not the left forebrain. This indicates that fucosylglycoprotein incorporation has a more important function in the right forebrain after passive avoidance training.
No amnesia for the sickness-conditioned aversion task was detected after injection of 2- Dgal into either the left or the right forebrain alone. Thus either hemisphere was capable of learning this task but only one hemisphere was required.
2-Dgal was tested for a state-dependent action in both learning paradigms, by readministration of the drug before the retention test, in a 2x2 experimental design. The amnesia was not state-dependent, since readministration of 2-Dgal did not lead to recall of the learned response in either task. Thus the amnesia was not due to learned information becoming cue-dependent. Instead, amnesia was caused by the direct interruption of molecular processes necessary for memory formation.
The results are discussed in the context of previous biochemical and morphological findings concerning fucosylglycoprotein incorporation and synaptic remodeling.

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