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Query: UMLS:C0002622 (amnesia)
 5,520 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Training chicks on a one-trial passive avoidance task results in a cellular cascade over the subsequent hours. Phosphorylation of the presynaptic phosphokinase C substrate B-50 is followed by immediate-early gene expression and increased synthesis of pre- and postsynaptic glycoproteins, increases in dendritic spine densities, synapse and synaptic vesicle numbers, and a prolonged increase in neuronal bursting. Many of these effects have been localized to two forebrain regions: the left intermediate medial hyperstriatum ventrale and the lobus parolfactorius. Pretraining lesions in the left intermediate medial hyperstriatum ventrale, or post-training lesions in the lobus parolfactorius result in amnesia. These and related results lead to models of memory storage based on multiple representation by way of synaptic stabilization through glycoprotein synaptic recognition molecules.
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PMID:How chicks make memories: the cellular cascade from c-fos to dendritic remodelling. 172 May 78

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.
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PMID:Memory formation in the chick depends on membrane-bound protein kinase C. 229 19

Several evidences demonstrate that protein kinase C (PKC) is involved in hippocampal long-term potentiation (LTP) and in different forms of learning, including inhibitory avoidance training in rats. Here, we evaluated the levels of conventional PKC isozymes (alpha, betaI, betaII, gamma) in synaptic plasma membrane (SPM) fractions isolated from hippocampus of rats subjected to a one-trial inhibitory avoidance paradigm. At 0, 30 and 120 min after training, there was a significant increase in the total amount of PKCbetaI. Densitometric analysis of the immunoblots showed an increase of 142+/-11% at 0 min, 193+/-16% at 30 min and 156+/-6% at 120 min after training relative to shocked control values. No changes were found in PKCbetaI levels in SPM fractions of the shocked animals relative to naive control values. No training-specific increments in the levels of PKCalpha, betaII and gamma were observed at any time point tested. However, an increase in PKCgamma levels was found in trained and shocked animals sacrificed 120 min after each experimental procedure. In addition, bilateral microinjections of a fairly selective inhibitor of PKCbetaI isozyme into the CA1 of the dorsal hippocampus produced amnesia when given 10 min before training, or 50, 110, but not 170 min, after training. Thus, the present findings demonstrate the participation of PKCbetaI in the early synaptic events responsible for the acquisition and consolidation of an inhibitory avoidance learning, and suggest a putative role of this presynaptic isozyme on the enhanced PKC-dependent B-50/GAP-43 phosphorylation previously detected by us during this associative learning.
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PMID:Involvement of hippocampal PKCbetaI isoform in the early phase of memory formation of an inhibitory avoidance learning. 1067 91