title: Long-term plasticity in cingulate cortex requires both NMDA and metabotropic glutamate receptor activation.
abstract: 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.
authors.affiliation: Department of Neuroscience, Albert Einstein College of Medicine, Bronx, NY 10461, USA. hedberg@aecom.yu.edu
authors.forename: T G
authors.initials: TG
authors.lastname: Hedberg
authors.forename: P K
authors.initials: PK
authors.lastname: Stanton
mesh_terms: D000818:Animals; D004558:Electric Stimulation; D005071:Evoked Potentials / Q000502:physiology; D005260:Female; D006179:Gyrus Cinguli / Q000502:physiology*; D066298:In Vitro Techniques; D017774:Long-Term Potentiation; D051381:Rats; D017470:Receptors, Glutamate / Q000502:physiology*; D016194:Receptors, N-Methyl-D-Aspartate / Q000502:physiology*; D009435:Synaptic Transmission / Q000502:physiology*
chemical_list: D017470:Receptors, Glutamate; D016194:Receptors, N-Methyl-D-Aspartate