FRINK Linked Data Fragments server

Matches in SemOpenAlex for { <https://semopenalex.org/work/W2003281978> ?p ?o ?g. }

• W2003281978 endingPage "54" @default.
• W2003281978 startingPage "45" @default.
• W2003281978 abstract "NG, K. T., B. S. O'DOWD, N. S. RICKARD, S. R. ROBINSON, M. E. GIBBS, C. RAINEY, W.-Q. ZHAO, G. L. SEDMAN AND L. HERTZ. Complex roles of glutamate in the Gibbs-Ng Model of one-trial aversive learning in the newborn chick. NEUROSCI BIOBEHAV REV 21 [1]45–54, 1997.—Glutamate is the most widespread excitatory transmitter in the CNS and is probably involved in LTP, a neural phenomenon which may be associated with learning and memory formation. Intracerebral injection of large amounts of glutamate between 5 min before and 2.5 min after passive avoidance learning in young chicks inhibits short-term memory, which occurs between 0 and 10 min post-learning in a three-stage model of memory formation first established by Gibbs and Ng [25][Physiol. Behav. 23:369–375; 1979]. This effect may be attributed to non-specific excitation. Blockade of glutamate uptake by l-aspartic acid β-hydroxamate also abolishes this stage of memory, provided the drug is administered within 2.5 min of learning. Interference with either the production of precursors for transmitter glutamate in astrocytes or with glutamate receptors is also detrimental to memory formation, but the effects appear much later. After its release from glutamatergic neurons, glutamate is, to a large extent, accumulated into astrocytes where it is converted to glutamine, which can be returned to glutamatergic neurons and reutilized for synthesis of transmitter glutamate, and partly oxidized as a metabolic substrate. The latter process leads to a net loss of transmitter glutamate which can be compensated for by de novo synthesis of a glutamate precursor α-ketoglutarate (αKG) in astrocytes, a process which is inhibited by the astrocyte-specific toxin fluoroacetate (R. A. Swanson, personal communication). Intracerebral injection of this toxin abolishes memory during an intermediate stage of memory processing occurring between 20 and 30 min post-training [50][Cog. Brain Res. 2:93–102; 1994]. Injection of methionine sulfoximine (MSO), a specific inhibitor of glutamine synthetase, which interferes with the re-supply of transmitter glutamate to neurons by inhibition of glutamine synthesis in astrocytes, has a similar effect. This effect of MSO is prevented by intracerebral injection of glutamate, glutamine, or a combination and αKG and alanine. MSO must be administered before learning, but does not interfere with acquisition since short-term memory remains intact. Administration of either the NMDA antagonist AP5, the AMPA antagonist DNQX, or the metabotropic receptor antagonist MCPF, also induces amnesia. Memory loss in each case does not occur until after 70 min post-training, during a protein synthesis-dependent long-term memory stage which begins at 60 min following learning. However, to be effective, AP5 must be administered within 60 s following learning, MCPG before 15 min post-learning, and DNQX between 15 and 25 min after learning. Together, these findings suggest that learning results in an immediate release of glutamate, followed by a secondary release of this transmitter at later stages of processing of the memory trace, and that one or both of these increases in extracellular glutamate concentration are essential for the consolidation of long-term memory. Since both fluoroacetate and MSO act exclusively on glial cells, the findings also show that neuronal-glial interactions are necessary during the establishment of memory. Copyright © 1996 Elsevier Science Ltd." @default.
• W2003281978 created "2016-06-24" @default.
• W2003281978 creator A5021821317 @default.
• W2003281978 creator A5028718070 @default.
• W2003281978 creator A5047240384 @default.
• W2003281978 creator A5047418672 @default.
• W2003281978 creator A5053150236 @default.
• W2003281978 creator A5061796601 @default.
• W2003281978 creator A5074071398 @default.
• W2003281978 creator A5084649968 @default.
• W2003281978 creator A5091770078 @default.
• W2003281978 date "1997-01-01" @default.
• W2003281978 modified "2023-09-29" @default.
• W2003281978 title "Complex Roles of Glutamate in the Gibbs—Ng Model of One-trial Aversive Learning in the New-born Chick" @default.
• W2003281978 cites W1119966406 @default.
• W2003281978 cites W1577989916 @default.
• W2003281978 cites W1963963391 @default.
• W2003281978 cites W1965900519 @default.
• W2003281978 cites W1968241424 @default.
• W2003281978 cites W1969501028 @default.
• W2003281978 cites W1976554671 @default.
• W2003281978 cites W1978507389 @default.
• W2003281978 cites W1979862266 @default.
• W2003281978 cites W1981030989 @default.
• W2003281978 cites W1984089779 @default.
• W2003281978 cites W1985639768 @default.
• W2003281978 cites W1990634611 @default.
• W2003281978 cites W1998678296 @default.
• W2003281978 cites W2002447155 @default.
• W2003281978 cites W2002517197 @default.
• W2003281978 cites W2003033533 @default.
• W2003281978 cites W2003058141 @default.
• W2003281978 cites W2005599435 @default.
• W2003281978 cites W2015593587 @default.
• W2003281978 cites W2018488830 @default.
• W2003281978 cites W2020065598 @default.
• W2003281978 cites W2022268886 @default.
• W2003281978 cites W2023567448 @default.
• W2003281978 cites W2024717575 @default.
• W2003281978 cites W2025801062 @default.
• W2003281978 cites W2029252387 @default.
• W2003281978 cites W2029529917 @default.
• W2003281978 cites W2030850051 @default.
• W2003281978 cites W2031347547 @default.
• W2003281978 cites W2037636017 @default.
• W2003281978 cites W2038162484 @default.
• W2003281978 cites W2039407495 @default.
• W2003281978 cites W2041316078 @default.
• W2003281978 cites W2044385789 @default.
• W2003281978 cites W2045176281 @default.
• W2003281978 cites W2046253429 @default.
• W2003281978 cites W2047887960 @default.
• W2003281978 cites W2049639693 @default.
• W2003281978 cites W2051069074 @default.
• W2003281978 cites W2052026392 @default.
• W2003281978 cites W2052617372 @default.
• W2003281978 cites W2054683291 @default.
• W2003281978 cites W2055475333 @default.
• W2003281978 cites W2056016753 @default.
• W2003281978 cites W2059361327 @default.
• W2003281978 cites W2059965794 @default.
• W2003281978 cites W2063957486 @default.
• W2003281978 cites W2067080574 @default.
• W2003281978 cites W2074391633 @default.
• W2003281978 cites W2075687876 @default.
• W2003281978 cites W2076075953 @default.
• W2003281978 cites W2079941612 @default.
• W2003281978 cites W2083840616 @default.
• W2003281978 cites W2084722225 @default.
• W2003281978 cites W2086818736 @default.
• W2003281978 cites W2091306165 @default.
• W2003281978 cites W2095097624 @default.
• W2003281978 cites W2127444824 @default.
• W2003281978 cites W2135711081 @default.
• W2003281978 cites W2156638143 @default.
• W2003281978 cites W2274170152 @default.
• W2003281978 cites W2337265064 @default.
• W2003281978 cites W313836430 @default.
• W2003281978 cites W3195435795 @default.
• W2003281978 cites W4244864219 @default.
• W2003281978 cites W4249919007 @default.
• W2003281978 doi "https://doi.org/10.1016/0149-7634(95)00079-8" @default.
• W2003281978 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/8994208" @default.
• W2003281978 hasPublicationYear "1997" @default.
• W2003281978 type Work @default.
• W2003281978 sameAs 2003281978 @default.
• W2003281978 citedByCount "63" @default.
• W2003281978 countsByYear W20032819782012 @default.
• W2003281978 countsByYear W20032819782017 @default.
• W2003281978 countsByYear W20032819782018 @default.
• W2003281978 countsByYear W20032819782020 @default.
• W2003281978 countsByYear W20032819782023 @default.
• W2003281978 crossrefType "journal-article" @default.
• W2003281978 hasAuthorship W2003281978A5021821317 @default.
• W2003281978 hasAuthorship W2003281978A5028718070 @default.
• W2003281978 hasAuthorship W2003281978A5047240384 @default.
• W2003281978 hasAuthorship W2003281978A5047418672 @default.
• W2003281978 hasAuthorship W2003281978A5053150236 @default.

• next