Long-term plasticity in cingulate cortex requires both NMDA and metabotropic glutamate receptor activation.
Eur J Pharmacol
; 310(1): 19-27, 1996 Aug 22.
Article
en En
| MEDLINE
| ID: mdl-8880063
We tested whether induction of homosynaptic long-term potentiation and long-term depression of synaptic strength in posterior cingulate cortex requires NMDA and/or metabotropic glutamate (mGlu) receptor activation. In in-vitro slices of rat posterior cingulate cortex, the NMDA receptor antagonist D-2-amino-5-phosphonopentanoic acid (D-AP5; 15-20 microM) blocked induction of both long-term potentiation and long-term depression of mono- and polysynaptic population potentials in deep laminae. In contrast, DL-2-amino-3-phosphonopropionic acid (DL-AP3; 15-25 microM), a selective mGlu receptor antagonist, blocked homosynaptic long-term potentiation and long-term depression of monosynaptic transmission, but was ineffective in blocking the induction of either type of plasticity at polysynaptically-driven sites. The selective mGlu receptor agonist, trans-1-aminocyclopentane-1,3-dicarboxylic acid (ACPD), induced a marked depression of subicular-evoked monosynaptic potentials which reversed upon drug washout, but produced little depression of polysynaptic responses. We conclude that metabotropic glutamate receptor activation is necessary for the induction of long-term synaptic plasticity only at monosynaptic subiculo-cingulate terminals, while NMDA receptor activation is necessary for the induction of long-term potentiation/long-term depression of both mono- and polysynaptic pathways.
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Colección:
01-internacional
Base de datos:
MEDLINE
Asunto principal:
Receptores de Glutamato
/
Receptores de N-Metil-D-Aspartato
/
Transmisión Sináptica
/
Giro del Cíngulo
Límite:
Animals
Idioma:
En
Revista:
Eur J Pharmacol
Año:
1996
Tipo del documento:
Article
País de afiliación:
Estados Unidos
Pais de publicación:
Países Bajos