Contribution of NMDA receptors to postsynaptic potentials and paired-pulse facilitation in identified neurons of the rat nucleus accumbens in vitro

Abstract

Summary. The principal aim of this study was to characterize the transmitter mechanisms mediating fast postsynaptic potentials in identified neurons of the rat nucleus accumbens. Using the biocytin-avidin labeling technique, impaled neurons were identified as medium spiny neurons. The basic membrane characteristics of these neurons were determined. Local electrical stimulation or stimulation of the corpus callosum elicited a depolarizing postsynaptic potential consisting of an EPSP often followed by an IPSP. The quisqualate/kainate receptor antagonist 6-cyano-7-nitroquinoxaline-2,3-dione (4 gM) abolished most of the depolarizing postsynaptic potential. The N-methyl-D-aspartate receptor antagonist D(-)-2-amino-5-phosphonopentanoic acid depressed a small part of the decay phase of the depolarizing postsynaptic potential. Paired-pulse facilitation of postsynaptic potentials was found using interstimulus-intervals between 10 and 150 ms. N-methyl-D-aspartate receptors were found to contribute only slightly to the facilitation of the decay phase of the depolarizing postsynaptic potential, but not to its rising phase. This contribution was particularly clear under conditions of reduced GABAA receptor mediated inhibition. The present study indicates that postsynaptic responses of medium spiny neurons in the nucleus accumbens to local stimulation or stimulation of neocortical afferents are primarily mediated by quisqualate/kainate receptors. The contribution of NMDA receptors is normally limited to a portion of the decay phase of these responses, but is enlarged in the absence of GABAergic inhibition and following paired-pulse stimulation.

A dynamical system-Markov model for active postsynaptic responses of muscle spindle afferent nerve

“…If comparing the total current with the NMDA current, it is easy to find that at the rising stage of the current, NMDA current imposes little effect, while at the falling phase, it contributes to the tail current of EPSC. Moreover, after repetitive stimulations, NMDA current gradually becomes remarkable and stable, consistent with experimental phenomena [27].…”

“…Non-NMDA current is dominant in EPSC [27], especially at the initial increasing stage of the current. However, non-NMDA receptors desensitize rapidly, and thus their currents decay very fast under the repetitive stimulations of the AP train.…”

“…Compared with non-NMDA receptors, the conductivity of NMDA receptors is larger, because they allow Ca 2+ to pass besides Na + and K + . However, experiments show that the contribution of NMDA current to EPSC is very small [27], and it only takes effect during the late components of EPSC for rapid signaling. Therefore, the number of NMDA receptors on the postsynaptic membrane is much smaller than that of non-NMDA ones.…”

AMPA/kainate, NMDA, and dopamine D1 receptor function in the nucleus accumbens core: A context-limited role in the encoding and consolidation of instrumental memory

“…It may be that AMPA/KA receptor blockade resulted in a larger learning impairment because of a concurrent decrease in the population of functionally active NMDA receptors, which are both glutamateand voltage-dependent (Nowak et al 1984). However, given the strong involvement of AMPA/KA receptors in driving NAc projection neurons, the larger learning impairment probably resulted from the complete inactivation of the affected portion of the nucleus, whereas NMDA (or D1) receptor blockade would have affected neuronal firing and plasticity to a lesser, yet significant, degree (Pennartz et al 1991;Hu and White 1996;Wolf et al 2004). Alternatively, it is possible that LY293558 administration has longer-lasting effects on neural function relative to AP-5 or SCH23990, but such effects may be negligible since rats that received the drug post-trial were able to learn normally on the following training sessions.…”

Inhibition of the Activity of a Neuronal κB‐Binding Factor by Glutamate

“…NMDA receptor-mediated signaling have kinetic differences that could explain the early elevation of NKBF by glutamate (Pennartz et al, 1991;Armstrong-James et al, 1993). Although these differences are on the order of milliseconds, they could be translated into larger distinctions by the involvement of additional signal transduction steps; for instance, phosphorylation-dependent events can convert NMDA receptor stimulation into a persistent, ligand-independent activation (Ben-Ari et al, 1992;Durand et al, 1993).…”