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Memory formation in the chick depends on membrane-bound protein kinase C
R Burchuladze1, J Potter, S P Rose
1Brain and Behaviour Research Group, Open University, Milton Keynes, U.K.
Insights
Protein kinase C (PKC) activity is crucial for memory formation in chicks. Inhibiting PKC post-training impairs memory consolidation, suggesting its role in neural plasticity and learning.
Area of Science:
- Neuroscience
- Molecular Biology
- Behavioral Science
Background:
- Protein kinase C (PKC) is implicated in memory formation.
- PKC activity is regulated by translocation to synaptic membranes.
- PKC substrates, like B-50 protein, show altered phosphorylation after learning.
Purpose of the Study:
- To investigate the role of PKC in memory formation using a one-trial passive avoidance task in young chicks.
- To examine the effect of PKC inhibition on memory consolidation and neural plasticity.
Main Methods:
- Assayed PKC alpha/beta forms in synaptic membranes via immunological methods post-training.
- Administered PKC inhibitors (melittin, H7) intracerebrally before or after training.
- Assessed behavioral effects and memory retention (amnesia) in chicks.
Main Results:
- Training increased synaptic-membrane-bound PKC in the left IMHV.
- PKC inhibitors did not affect general behavior or initial training.
- Intracerebral inhibitor injections caused amnesia, specifically with left hemisphere administration.
- State-dependency was ruled out as an explanation for amnesia.
Conclusions:
- PKC plays a critical, lateralized role in the consolidation of passive avoidance memory.
- PKC translocation to synaptic membranes is associated with memory formation.
- PKC inhibition disrupts memory consolidation, highlighting its regulatory role in neural plasticity.
Abstract:
The role of protein kinase C (PKC) in the formation of memory for a one-trial passive avoidance task in 1-day-old chicks has been studied, following earlier observations that training on this task results in transient and lateralised changes in the phosphorylation state of presynaptic B-50 protein, a PKC substrate. In accord with hypotheses that the activity of PKC is regulated by translocation from cytosol to membrane, a significant increase was found in the fraction of the alpha/beta forms of the enzyme, assayed immunologically, present in a synaptic-membrane-bound, Triton-extractable form in the left intermediate medial hyperstriatum ventrale (IMHV) of chicks 30 min after training on the passive avoidance task. Two inhibitors of PKC, melittin (10 microliters, 120 microM) and H7 (10 microliters, 10 mM), if injected intracerebrally 10 min prior to or 10 min after training, were without effect on the general behaviour of the chicks or their training. However, these injections of the inhibitors produced amnesia in birds tested 3 h later. This effect was lateralised; only left hemisphere injections of the inhibitors produced amnesia. A possible state-dependency interpretation of these results was ruled out. The results are discussed in the context of hypotheses as to the regulatory role of PKC in neural plasticity and memory formation.