| pubmed-article:1668353 | rdf:type | pubmed:Citation | lld:pubmed |
| pubmed-article:1668353 | lifeskim:mentions | umls-concept:C0021289 | lld:lifeskim |
| pubmed-article:1668353 | lifeskim:mentions | umls-concept:C0034721 | lld:lifeskim |
| pubmed-article:1668353 | lifeskim:mentions | umls-concept:C0034693 | lld:lifeskim |
| pubmed-article:1668353 | lifeskim:mentions | umls-concept:C0019564 | lld:lifeskim |
| pubmed-article:1668353 | lifeskim:mentions | umls-concept:C0243192 | lld:lifeskim |
| pubmed-article:1668353 | lifeskim:mentions | umls-concept:C0206529 | lld:lifeskim |
| pubmed-article:1668353 | pubmed:dateCreated | 1992-8-31 | lld:pubmed |
| pubmed-article:1668353 | pubmed:abstractText | 1. The effects of metabotropic glutamate receptor agonists on excitatory synaptic transmission in the CA1 region of rat hippocampal slices (11-30 days) were studied using extracellular and whole-cell patch-clamp recording techniques. 2. Trans-1-amino-1,3-cyclopentanedicarboxylic acid (trans-ACPD; 25-100 microM) reversibly depressed excitatory postsynaptic currents (EPSCs) without affecting presynaptic fibre excitability or EPSC reversal potential. 3. Ibotenate (25 microM) or L-glutamate (250 microM), in the presence of the N-methyl-D-aspartate (NMDA) receptor antagonist, D-2-amino-5-phosphonovaleric acid (APV, 50-75 microM), depressed the EPSC amplitude while inducing no detectable inward current. L-2-Amino-4-phosphonobutyrate (L-AP4, 25-100 microM), the phosphonic derivative of glutamate, also depressed EPSC amplitude and caused no detectable inward current. 4. The NMDA receptor-mediated component of the EPSC recorded in the presence of the non-NMDA receptor antagonist, 6-cyano-7-nitroquinoxaline-2,3-dione (CNQX, 20-30 microM) was depressed by trans-ACPD, L-AP4, or quisqualate (1-2 microM). 5. The response to ionophoretic application of alpha-amino-3-hydroxy-5-methyl-4-isoxazole propionic acid (AMPA) was unaffected by trans-ACPD or L-AP4 although the simultaneously recorded EPSC was strongly depressed. In addition, paired-pulse facilitation (50-75 ms interstimulus interval) was reversibly enhanced by trans-ACPD or L-AP4. These results indicate that the depression of synaptic transmission likely was mediated by a presynaptic 'autoreceptor'. 6. The effects of trans-ACPD or L-AP4 on synaptic transmission decreased significantly over ages 12-30 days and were minimal in adult (greater than 80 days) slices. 7. The depression of synaptic transmission caused by trans-ACPD or L-AP4 was not altered following the induction of long-term potentiation (LTP). 8. The results indicate that metabotropic glutamate receptor agonists suppress excitatory synaptic transmission in CA1 pyramidal cells by an action at a presynaptic site. This effect is developmentally regulated and is maximally expressed during the first postnatal month. | lld:pubmed |
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| pubmed-article:1668353 | pubmed:language | eng | lld:pubmed |
| pubmed-article:1668353 | pubmed:journal | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:1668353 | pubmed:citationSubset | IM | lld:pubmed |
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| pubmed-article:1668353 | pubmed:status | MEDLINE | lld:pubmed |
| pubmed-article:1668353 | pubmed:month | Dec | lld:pubmed |
| pubmed-article:1668353 | pubmed:issn | 0022-3751 | lld:pubmed |
| pubmed-article:1668353 | pubmed:author | pubmed-author:BaskysAA | lld:pubmed |
| pubmed-article:1668353 | pubmed:author | pubmed-author:MalenkaR CRC | lld:pubmed |
| pubmed-article:1668353 | pubmed:issnType | Print | lld:pubmed |
| pubmed-article:1668353 | pubmed:volume | 444 | lld:pubmed |
| pubmed-article:1668353 | pubmed:owner | NLM | lld:pubmed |
| pubmed-article:1668353 | pubmed:authorsComplete | Y | lld:pubmed |
| pubmed-article:1668353 | pubmed:pagination | 687-701 | lld:pubmed |
| pubmed-article:1668353 | pubmed:dateRevised | 2009-11-18 | lld:pubmed |
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| pubmed-article:1668353 | pubmed:year | 1991 | lld:pubmed |
| pubmed-article:1668353 | pubmed:articleTitle | Agonists at metabotropic glutamate receptors presynaptically inhibit EPSCs in neonatal rat hippocampus. | lld:pubmed |
| pubmed-article:1668353 | pubmed:affiliation | Department of Psychiatry, University of California, San Francisco 94143. | lld:pubmed |
| pubmed-article:1668353 | pubmed:publicationType | Journal Article | lld:pubmed |
| pubmed-article:1668353 | pubmed:publicationType | In Vitro | lld:pubmed |
| pubmed-article:1668353 | pubmed:publicationType | Research Support, U.S. Gov't, P.H.S. | lld:pubmed |
| pubmed-article:1668353 | pubmed:publicationType | Research Support, Non-U.S. Gov't | lld:pubmed |
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