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Long-Term Potentiation Differentially Affects Two Components of Synaptic Proc. Nati. Acad. Sci. USA Vol. 85, pp. 9346-9350, December 1988 Neurobiology Long-term potentiation differentially affects two components of synaptic responses in hippocampus (plasticity/N-methyl-D-aspartate/D-2-amino-5-phosphonovglerate/facilitation) DOMINIQUE MULLER*t AND GARY LYNCH Center for the Neurobiology of Learning and Memory, University of California, Irvine, CA 92717 Communicated by Leon N Cooper, September 6, 1988 (receivedfor review June 20, 1988) ABSTRACT We have used low magnesium concentrations ing electrode was positioned in field CAlb between two and the specific antagonist D-2-amino-5-phosphonopentanoate stimulating electrodes placed in fields CAla and CAlc; this (D-AP5) to estimate the effects of long-term potentiation (LTP) allowed us to activate separate inputs to a common pool of on the N-methyl-D-aspartate (NMDA) and non-NMDA recep- target cells. Stimulation voltages were adjusted to produce tor-mediated components of postsynaptic responses. LTP in- field EPSPs of -1.5 mV and did not elicit population spikes duction resulted in a considerably larger potentiation of non- in any of the responses included for data analysis. NMDA as opposed to NMDA receptor-related currents. In- Paired-pulse facilitation was produced by applying two creasing the size of postsynaptic potentials with greater stimulation pulses separated by 30 or 50 ms to the same stimulation currents or with paired-pulse facilitation produced stimulating electrode and LTP was induced by patterned opposite effects; i.e., those aspects ofthe response dependent on burst stimulation-i.e., 10 bursts delivered at 5 Hz, each NMDA receptor's increased to a greater degree than did those burst being composed of four pulses at 100 Hz (see ref. 5). components mediated by non-NMDA receptors. These results Suppression of Inhibitory Potentials with "Priming" Stim- pose new constraints on hypotheses about the locus and nature ulation. The NMDA receptor ionophore is blocked in a ofLTP and strongly suggest that postsynaptic modifications ate voltage-dependent fashion by magnesium ions (14, 15). As a part of the effect. consequence, antagonists of the receptor [e.g., D-2-amino-5- phosphonopentanoate (D-AP5)] have little effect on field Long-term potentiation (LTP), a long-lasting increase in EPSPs elicited by single-stimulation pulses in slices main- synaptic efficacy observed in hippocampus (1) and elsewhere tained in normal medium. Two procedures were used in the in forebrain (2), has attracted interest as a possible substrate present experiments to reduce the blockade of the receptor of behavioral memory (3). While considerable progress has channel and allow response components mediated by NMDA been made in identifying the cellular events that trigger LTP receptors to appear. First, the concentration ofmagnesium in (4-7), the final and stable modifications that underlie the the medium was reduced from 1 mM to 10-20 uM. As increased synaptic potency remain to be resolved. In an previously shown (10), however, this manipulation by itself effort to restrict the list of proposed mechanisms, we have does not reliably result in the development of a large tested the possibility that LTP has selective effects on postsynaptic response component sensitive to D-AP5. Pre- different components of the postsynaptic response. Recent sumably, because of the small amount of magnesium still work has identified conditions under which a sizable portion present in the medium, the degree and duration of the of the field excitatory postsynaptic potential (EPSP) elicited depolarization produced by a single field EPSP are not by afferent stimulation is blocked by antagonists of the N- sufficient to counteract the voltage-dependent blockade of methyl-D-aspartate (NMDA) receptor (8-10). Here we report the receptor channel. However, when the feedforward in- that the NMDA and non-NMDA components of synaptic hibitory postsynaptic potentials (IPSPs) that normally ac- responses in hippocampus are differently affected by LTP, company and truncate synaptic responses in hippocampus the pattern of results being opposite that observed with (16) are removed, then a sizable portion of the field EPSP is paired-pulse facilitation, an effect attributed to increased blocked by NMDA receptor antagonists (8, 10). Accordingly, transmitter release (11-13). we used a technique referred to as priming (see ref. 5 and Fig. la for an illustration) to suppress feedforward IPSPs. Feed- forward IPSPs exhibit a short (-0.5 s) refractory period once MATERIAL AND METHODS having been activated (5, 6, 16), an effect that is readily Hippocampal slices (450 ,m thick) were prepared and main- apparent in experiments using two separate inputs (Schaffer- tained as described elsewhere in a surface recording chamber commissural fibers) to a common pool of intermeurons and and continuously perfused with a medium containing in mM: pyramidal cells. If one collection of afferents (the "priming NaCl, 124; KCl, 3; KH2PO4, 1.25; CaC12, 3; MgCI2, 1; input") is used to trigger the excitatory as well as inhibitory NaHCO3, 26; glucose, 10; L-ascorbate, 2 (pH 7.4). The slices potentials in the target region, then the responses to the were kept at 350C and oxygenated with 95% 02/5% Co2. second (or "test") input activated 200 ms later are largely After an hour of recovery, the perfusion medium was free of IPSPs. The intracellularly recorded afterhyperpolari- switched to a solution containing only 10 or 20 tLM magne- zation produced by feedforward IPSPs is suppressed (Fig. sium, which was perfused for another hour before the lb), while the repolarization phase of the field EPSP mea- experiments were started. sured with extracellular electrodes is prolonged (Fig. lc). As Responses were evoked by stimulation of the Schaffer- commissural projections in the stratum radiatum offield CA1 Abbreviations: LTP, long-term potentiation; NMDA, N-methyl- and recorded with glass micropipettes (1-5 Mfl). The record- D-aspartate; EPSP, excitatory postsynaptic potential; IPSP, inhibi- tory postsynaptic potential; D-AP5, D-2-amino-5-phosphonopen- tanoate. The publication costs of this article were defrayed in part by page charge *Present address: Department of Pharmacology, Geneva School of payment. This article must therefore be hereby marked "advertisement" Medicine, CMU, 1206 Geneva, Switzerland. in accordance with 18 U.S.C. §1734 solely to indicate this fact. tTo whom reprint requests should be addressed. 9346 Downloaded by guest on September 28, 2021 Neurobiology: Muller and Lynch Proc. Natl. Acad. Sci. USA 85 (1988) 9347 shown in Fig. ic, priming has a comparable effect on control a Priming paradigm responses as it does on field potentials that had been increased either by induction of LTP or with paired-pulse facilitation. The results show that after suppression ofthe fast IPSPs, the primed responses evoked in all three conditions are characterized by a similar time course, since they can be superimposed after normalization of their amplitude. 2 mU Effect of D-AP5 on Responses Evoked with Paired-Pulse Stimulation, Increased Stimulation Intensity, or Following 40 ms LTP Induction. Paired-pulse facilitation was produced by applying two pulses separated by 30 or 50 ms to a group of afferents terminating in a dendritic field that had been primed b Intracellular EPSPs by stimulation of a second input 200 ms earlier (Fig. 1). The area of the postsynaptic responses evoked by the first and second pulses to the test input was measured before and after application of D-AP5 (50-125 ,uM) to the medium. In some cases, the drug was washed out of the slices and the same experiment was repeated. Comparisons were thus made of the degree of paired-pulse facilitation found in the presence 5 mU and absence of the NMDA receptor antagonists. To assess the effect of D-AP5 on responses of different sizes, primed EPSPs were evoked by applying alternatively 20 ms stimulation pulses of different intensities to the same stimu- lation electrode. The area of both responses was then c Extracellular EPSPs measured before and after application of the drug. Two types ofexperiments were conducted to determine the Control Potentiation Facilitation effect of D-AP5 on potentiated responses. In nine cases, we tested for the effect of the drug on control responses, and then, following a washout period (40-60 min), LTP was induced and D-AP5 was reintroduced at the same concen- tration. In some cases, the control responses were evoked by using a paired-pulse paradigm, thus allowing for a direct 1 mu comparison of the effect of D-AP5 on facilitated and poten- 10 ms tiated responses (see Fig. 3). In five other experiments, we used two independent, equal-sized test inputs to the same Superimposed dendritic field in addition to the priming input (i.e., three stimulation electrodes activating converging afferents were used). LTP was then induced on one ofthe test inputs and the effect ofa single application ofD-AP5 (50 ,4M) was measured on potentiated and control responses. In some cases, control responses were also evoked using a paired-pulse paradigm, FIG. 1. Priming paradigm. (a) Illustration ofthe paradigm used to allowing for a direct comparison of the effect of the receptor suppress feedforward inhibitory responses. The records show the antagonist on control, facilitated, and potentiated responses. field potentials collected by one recording electrode and elicited on The two types of LTP experiments (i.e., single vs. sequential priming and test inputs by two different stimulating electrodes. The application of D-AP5) generated similar results. responses to a pair of priming pulses are shown at the beginning of the trace, while those elicited by paired-pulse (50-ms interpulse interval) stimulation ofthe test input 200 ms later are illustrated at the RESULTS end ofthe record. Recordings with (arrowhead) and without priming are superimposed. (b) Effect ofthe priming paradigm on intracellular As anticipated, the combination of priming and low magne- EPSPs. The afterhyperpolarization that reflects synaptically medi- sium medium resulted in field EPSPs that contained a ated IPSPs and that normally shortens the dendritic EPSP to significant component that was blocked by D-AP5 (Fig.
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