Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0598853 (forgetting)
 3,232 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Long-term depression (LTD) of synaptic transmission is a candidate for a neuronal model of forgetting and is considered to be important in learning and memory. The present study employed extracellular recording in the CA1 pyramidal cell layer of rat hippocampal slices following orthodromic stimulation of Schaffer collateral fibres in stratum radiatum. Muscimol induced a time and concentration-dependent LTD at a frequency of stimulation of 0.01 Hz or in the absence of stimulation. The LTD was reversed by stimulation at 1 Hz. The ability of muscimol to act via GABAA receptors was confirmed by the ability of bicuculline (5 microM) to reverse the LTD. The NMDA non-selective glutamate antagonists kynurenate, failed to modify the LTD. receptor antagonist 2-AP5, the selective metabotropic antagonist L(+)AP3 and the non-selective glutamate antagonists kynurenate, failed to modify the LTD. (1S,3R)-ACPD, a selective agonist at metabotropic receptors, did not induce LTD. The lack of involvement of glutamate receptors in muscimol induced LTD in our protocol may indicate a novel type of long-lasting synaptic depression
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PMID:Glutamate-independent long term depression in rat hippocampus by activation GABAA receptors. 862 54

Convergent data indicate that certain substances that interact with N-methyl-D-aspartate (NMDA) receptors or metabotropic glutamate receptors (mGluRs) do not affect acquisition processes per se, or retrieval, but interfere specifically with the formation of memory traces. This action differs widely in its amplitude and time-course according to the learning task used. We showed that systemic injection of the competitive NMDA receptor antagonists, gamma-L-glutamyl-L-aspartate (gamma-LGLA) and 3-(2-carboxypiperazin-4-yl)propyl-1-phosphonate (CPP), or intracerebroventricular infusion of D-2-amino-5-phosphonovalerate (D-AP5), immediately following acquisition of a Y-maze avoidance learning task in mice, deeply impaired retention of the temporal component of the task (leaving the start alley within the first 5 s of a trial), which significantly improved in controls during the hours following acquisition. In contrast the same substances had no or only slight effects on retention of the discrimination component (choice of the correct alley), which did not improve over time in control animals. This retention deficit did not appear to be due to an action on acquisition, retrieval and/or forgetting processes, or to state-dependent effects. Moreover, gamma-LGLA, CPP or AP5, when administered immediately after partial acquisition of a food-reinforced bar-press task, suppressed the spontaneous improvement in post-training performance observed in control mice 24 h after the training session. (R,S)-alpha-methyl-4-carboxyphenylglycine (MCPG), an antagonist of mGluRs, also suppressed the post-training performance increment and its effects were antagonized by the co-administration of trans-ACPD, an agonist of mGluRs. Post-training improvement of performance over time is thought to reflect an active and dynamic process, leading to the organization of memory traces. According to this hypothesis, our results suggest that synaptic plasticity mediated by NMDA receptors and/or mGluRs activation is involved in mechanisms underlying long-term consolidation of memory traces.
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PMID:Are glutamate receptors specifically implicated in some forms of memory processes? 983 91