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Article Role of Delayed Nonsynaptic Neuronal Plasticity in Long-Term Associative Memory

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Article Role of Delayed Nonsynaptic Neuronal Plasticity in Long-Term Associative Memory Current Biology 16, 1269–1279, July 11, 2006 ª2006 Elsevier Ltd All rights reserved DOI 10.1016/j.cub.2006.05.049 Article Role of Delayed Nonsynaptic Neuronal Plasticity in Long-Term Associative Memory Ildiko´ Kemenes,1 Volko A. Straub,1,3 memory, and we describe how this information can be Eugeny S. Nikitin,1 Kevin Staras,1,4 Michael O’Shea,1 translated into modified network and behavioral output. Gyo¨ rgy Kemenes,1,2,* and Paul R. Benjamin1,2,* 1 Sussex Centre for Neuroscience Introduction Department of Biological and Environmental Sciences School of Life Sciences It is now widely accepted that nonsynaptic as well as University of Sussex synaptic plasticity are substrates for long-term memory Falmer, Brighton BN1 9QG [1–4]. Although information is available on how nonsy- United Kingdom naptic plasticity can emerge from cellular processes active during learning [3], far less is understood about how it is translated into persistently modified behavior. Summary There are, for instance, important unanswered ques- tions regarding the timing and persistence of nonsynap- Background: It is now well established that persistent tic plasticity and the relationship between nonsynaptic nonsynaptic neuronal plasticity occurs after learning plasticity and changes in synaptic output. In this paper and, like synaptic plasticity, it can be the substrate for we address these important issues by looking at an long-term memory. What still remains unclear, though, example of learning-induced nonsynaptic plasticity is how nonsynaptic plasticity contributes to the altered (somal depolarization), its onset and persistence, and neural network properties on which memory depends. its effects on synaptically mediated network activation Understanding how nonsynaptic plasticity is translated in an experimentally tractable molluscan model system. into modified network and behavioral output therefore Unlike previous studies investigating nonsynaptic represents an important objective of current learning plasticity (reviewed in [3]), we used a single-trial asso- and memory research. ciative learning paradigm to induce long-term memory. Results: By using behavioral single-trial classical condi- This allowed a precise temporal analysis of nonsynaptic tioning together with electrophysiological analysis and electrical changes after learning and made it possible to calcium imaging, we have explored the cellular mecha- relate these changes to various postacquisition stages nisms by which experience-induced nonsynaptic electri- of memory formation at the behavioral and neural levels. cal changes in a neuronal soma remote from the synaptic This was not possible with multitrial learning paradigms, region are translated into synapticand circuit level effects. used in previous work investigating learning-induced We show that after single-trial food-reward conditioning nonsynaptic plasticity in molluscan feeding systems in the snail Lymnaea stagnalis, identified modulatory [5–7]. Moreover, we have isolated the learning-induced neurons that are extrinsic to the feeding network become nonsynaptic change to a neuron that is extrinsic to the persistently depolarized between 16 and 24 hr after train- synaptic network directly responsible for the generation ing. This is delayed with respect to early memory forma- of the conditioned and unconditioned behavior. This al- tion but concomitant with the establishment and duration lowed us to examine the contribution of nonsynaptic of long-term memory. The persistent nonsynaptic change plasticity to the conditioned response independently is extrinsic to and maintained independently of synaptic of any synaptic changes that might occur in the circuit effects occurring within the network directly responsible generating the behavior. In other examples, nonsynaptic for the generation of feeding. Artificial membrane poten- plasticity was shown to occur in neurons that are tial manipulation and calcium-imaging experiments directly responsible for the generation of both the suggest a novel mechanism whereby the somal depolar- unconditioned and conditioned behavior, making it diffi- ization of an extrinsic neuron recruits command-like cult to determine the independent contributions of intrinsic neurons of the circuit underlying the learned nonsynaptic and synaptic plasticity to altered network behavior. output [6–11]. Conclusions: We show that nonsynaptic plasticity in an Here, we target identified extrinsic modulatory neu- extrinsic modulatory neuron encodes information that rons, known in Lymnaea as the cerebral giant cells enables the expression of long-term associative (CGCs, Figure 1A). These paired serotonergic giant neu- rons and their homologs in other molluscs (e.g., Aplysia [12]) play a permissive role in feeding behavior ([13, 14] and Figure 1B) but have no direct role in the generation *Correspondence: [email protected] (G.K.); p.r.benjamin@ of the rhythmic feeding motor pattern [13–16]. By per- sussex.ac.uk (P.R.B.) forming electrophysiological analyses in semi-intact 2 These authors contributed equally to this work. preparations (Figure 1C), we show that in animals sub- 3 Present address: Department of Cell Physiology and Pharmacol- jected to a single pairing of amyl-acetate (the CS) with ogy, Faculty of Medicine and Biological Sciences, University of sucrose (the US), the CGCs have a more positive Leicester, Leicester LE1 9HN, United Kingdom. 4 Present address: Medical Research Council Laboratory for Molec- membrane potential than in unpaired control animals. ular and Cell Biology, University College London, London WC1E The depolarization is sufficient to increase the network 6BT, United Kingdom. response to the CS, emerges between 16 and 24 hr Current Biology 1270 Figure 1. Location and Axonal Branching Pattern of the Extrinsic Modulatory Cerebral Giant Cells and Their Synaptic Connections to the Intrinsic Circuit that Generates Feeding Motor Behavior in Lymnaea (A) The paired (left and right) CGCs send their main axon branches into the buccal ganglia (bg) via the cerebro-buccal connectives (cbc) and have side branches within the cerebral ganglia. Their main sensory inputs from the lips are from the median lip nerves (mln). The axonal branching pattern shown here is based on preparations (n > 10) in which both CGCs were intrasomatically filled with the Alexa Fluor 488 dye (Molecular Probes, Leiden, The Netherlands). (B) The electrically and chemically coupled CGCs provide widespread monosynaptic inputs to the buccal feeding central pattern generator (CPG) and motoneurons. Phasic modulatory cerebral-buccal interneurons (CBIs), CPG interneurons (types N1, N2, and N3), and motoneurons (types B1–B10, some of which also have CPG properties [54]), intrinsic to the feeding network, are primarily responsible for the generation of the rhythmic motor pattern underlying feeding. The CGCs have an extrinsic, state-setting or permissive function in feeding [13, 14]. (C) The semi-intact preparation that allows chemosensory stimulation of the lips, intracellular recording from the CGCs and intrinsic neurons of the feeding network (see Figures 2–5), and extracellular recording of CBI activity from the cbc (see Figure 8). The CPG neurons are located in the gray areas in the buccal ganglia. The interneurons (CGC, CBIs) and motoneurons (B1, B3, B4) recorded in the present work are labeled on the left side of the diagram only. _/\/\/\/\_, electrotonic synapse; I___, excitatory connection; __, inhibitory connection, I___, biphasic, excitatory/ inhibitory connection. postconditioning, and persists as long as the long-term tested for their behavioral feeding response to the CS memory. The depolarization of the CGC soma spreads (amyl-acetate) at 1, 2, 3, 7, or 14 days after conditioning to local axonal regions and increases the strength of (Figure 2A). At each time point, the trained animals re- CGC postsynaptic responses. Depolarization of the sponded significantly (at least p < 0.05, Figure 2A) CGC also leads to an increase in presynaptic calcium more strongly to the CS than the controls, indicating levels, a mechanism by which presynaptic depolariza- associative learning. tion can regulate synaptic function [17]. At the network The membrane potentials of the CGCs in semi-intact level, we show that CGC depolarization increases the lip-CNS preparations (Figure 1C) made from randomly spike response to the CS in feeding command interneu- selected trained and control animals also were recorded rons, leading to the activation of feeding. These experi- at each time point. The CGC membrane potential was ments reveal a novel mechanism that links nonsynaptic significantly (at least p < 0.05, Figure 2B) different plasticity occurring outside a behavioral network to between the trained and control groups on each day of modified output arising within the network. the investigation (Figure 2B). We also measured CGC input resistance, spike fre- Results quency, threshold, amplitude, duration, and after-hyper- polarization that might have been affected by condition- Single-Trial Conditioning Leads to Long-Term ing. We found no significant differences between the Memory and Persistent Depolarization of an trained and control groups in these electrical parameters Extrinsic Modulatory Interneuron at any of the time points (data not shown, example traces First, we examined whether single-trial conditioning from the Day 14 experiment are shown in Figure 2B). leads to electrophysiological changes in the CGCs con- Next, we focused our attention to the pre-24 hr period comitant
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