Abstract

BackgroundMemory is the ability to store, retain, and later retrieve information that has been learned. Intermediate term memory (ITM) that persists for up to 3 h requires new protein synthesis. Long term memory (LTM) that persists for at least 24 h requires: DNA transcription, RNA translation, and the trafficking of newly synthesized proteins. It has been shown in a number of different model systems that NMDA receptors, protein kinase C (PKC) and mitogen activated protein kinase (MAPK) are all involved in the memory formation process.ResultsHere we show that snails trained in control conditions are capable of forming, depending on the training procedure used, either ITM or LTM. However, blockage of NMDA receptors (MK 801), inhibition of PKC (GF109203X hydrochloride) and MAPK activity (UO126) prevent the formation of both ITM and LTM.ConclusionsThe injection of either U0126 or GF109203X, which inhibit MAPK and PKC activity respectively, 1 hour prior to training results in the inhibition of both ITM and LTM formation. We further found that NMDA receptor activity was necessary in order for both ITM and LTM formation.

Highlights

  • Memory is the ability to store, retain, and later retrieve information that has been learned

  • We have found that while both Intermediate term memory (ITM) and Long term memory (LTM) depend upon new protein synthesis there is an additional requirement of altered gene activity for LTM formation [19,20,21,22,23]

  • Even more recently we have shown that an operant conditioning paradigm of the aerial respiratory behaviour that leads to LTM formation causes a significant increase in the expression of mitogen activated protein kinase kinase 1 (MEKK1), a member of the MAPK family of proteins, and the novel expression of the epsilon isoform of protein kinase C (PKC) [37]

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Summary

Introduction

Memory is the ability to store, retain, and later retrieve information that has been learned. Long term memory (LTM) that persists for at least 24 h requires: DNA transcription, RNA translation, and the trafficking of newly synthesized proteins It has been shown in a number of different model systems that NMDA receptors, protein kinase C (PKC) and mitogen activated protein kinase (MAPK) are all involved in the memory formation process. For memories lasting longer that a few minutes, the changes in synaptic strength and neuron excitability require a physical alteration of both the synaptic and membrane complement of proteins Strong evidence for this exists in the form of numerous studies showing the requirement of new protein synthesis and altered gene activity in order for long-term memories (LTM) to form [1,2,3,4]. Considerably less is known about the molecular mechanisms underlying memory formation in this animal

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