Acquisition Of Long-term Memory Research Articles

Effect of ACEA 1021 on Neurotoxicity Induced by Dexamethasone — Initial Behavioral Study

Considerable evidence suggests that glucocorticoids (GCs) play an important role in neurodegeneration. Chronic elevated levels of GCs can result in neuronal degeneration of the hippocampal piramidal neurons, which are paralleled by cognitive deficits. Moreover, GCs potentiate stress or ischemia-induced accumulation of excitatory amino acids (EAA) in the extracellular space of hippocampus. ACEA 1021 (licostinel), a selective antagonist of the N-methyl-D-aspartate (NMDA) receptor, has been reported to prevent the excitotoxic action of high extracellular glutamate levels. The aim of this study was to investigate the effect of ACEA 1021 on neurotoxic effect of dexamethasone (DEX - a synthetic GCs receptor agonist). The experiments were carried out on Albino Swiss mice (25-30 g). ACEA 1021, at the doses: 1.25 and 2.5 mg/kg/day, ip, was administered 15 min before DEX (16 mg/kg/day, ip). The long-term memory acquisition (passive avoidance test) and the motor performance (“chimney” test) were evaluated 14 days after the drugs administration. The prolongation of climbing time in the “chimney” test and decrease of the retention time in the memory task of mice treated with DEX for 14 days. In mice treated with DEX for 14 days, ACEA 1021 at the both doses reduced the climbing time in the “chimney” test, at the dose of 1.25 mg/kg improved memory acquisition. The above findings suggest that ACEA 1021 could prevent the neurotoxic effects induced by DEX, but further study needs to be carried out to explain this effect.

Combinatory Actions of Co-transmitters in Dopaminergic Systems Modulate Drosophila Olfactory Memories.

Dopamine neurons (DANs) are extensively studied in the context of associative learning, in both vertebrates and invertebrates. In the acquisition of male and female Drosophila olfactory memory, the PAM cluster of DANs provides the reward signal, and the PPL1 cluster of DANs sends the punishment signal to the Kenyon cells (KCs) of mushroom bodies, the center for memory formation. However, thermo-genetical activation of the PPL1 DANs after memory acquisition impaired aversive memory, and that of the PAM DANs impaired appetitive memory. We demonstrate that the knockdown of glutamate decarboxylase, which catalyzes glutamate conversion to GABA in PAM DANs, potentiated the appetitive memory. In addition, the knockdown of glutamate transporter in PPL1 DANs potentiated aversive memory, suggesting that GABA and glutamate co-transmitters act in an inhibitory manner in olfactory memory formation. We also found that, in γKCs, the Rdl receptor for GABA and the mGluR DmGluRA mediate the inhibition. Although multiple-spaced training is required to form long-term aversive memory, a single cycle of training was sufficient to develop long-term memory when the glutamate transporter was knocked down, in even a single subset of PPL1 DANs. Our results suggest that the mGluR signaling pathway may set a threshold for memory acquisition to allow the organisms' behaviors to adapt to changing physiological conditions and environments.SIGNIFICANCE STATEMENT In the acquisition of olfactory memory in Drosophila, the PAM cluster of dopamine neurons (DANs) mediates the reward signal, while the PPL1 cluster of DANs conveys the punishment signal to the Kenyon cells of the mushroom bodies, which serve as the center for memory formation. We found that GABA co-transmitters in the PAM DANs and glutamate co-transmitters in the PPL1 DANs inhibit olfactory memory formation. Our findings demonstrate that long-term memory acquisition, which typically necessitates multiple-spaced training sessions to establish aversive memory, can be triggered with a single training cycle in cases where the glutamate co-transmission is inhibited, even within a single subset of PPL1 DANs, suggesting that the glutamate co-transmission may modulate the threshold for memory acquisition.

Urocanic acid facilitates acquisition of object recognition memory in mice

Trans-urocanic acid (UCA), an isomer of cis-UCA that is mainly located in the skin, has recently been reported to have a role in short-term working memory and in the consolidation, reconsolidation and retrieval of long-term memory. However, its effect on memory acquisition remains unclear. In the present study, the effect of UCA on short-term and long-term memory acquisition in mice was investigated using novel object recognition (NOR) and object location recognition (OLR) protocols that each involved three stages: habituation, sampling and testing. UCA was intraperitoneally injected 0.5 h pre-sampling, and the discrimination index during subsequent testing was determined in NOR and OLR tasks. The results showed that 10 mg/kg UCA significantly facilitated short-term and long-term memory acquisition in both types of tasks. Furthermore, 30 mg/kg UCA significantly facilitated long-term memory acquisition in the NOR task and tended to facilitate long-term memory acquisition in the OLR tasks but did not facilitate short-term memory acquisition in either task. Additionally, the enhancing role of UCA on memory acquisition was not dependent on changes of nonspecific responses, e.g. exploratory behavior and locomotor activity. The current study suggests that UCA facilitates short-term and long-term recognition memory acquisition, which further extends the functional role of UCA in the brain function.

Dr Cerebrolysin Improves Motor Abilities and Reverses the Long-Term Memory Acquisition Deficit in Rats with Hypoxic-Ischemic Encephalopathy

Background: Hypoxic-ischemic encephalopathy (HIE) is a neurological condition that leads to motor disabilities and even death in neonates. Unfortunately, few therapeutic alternatives can contribute to brain recovery after HIE damage. Cerebrolysin is a neuropeptide mixture that performs neuroprotective and neurotrophic effects on injured brain tissue after systemic administration. Aims: This study evaluates the effects of the Cerebrolysin intraperitoneal administration, Methods:10 mL/kg; once a day for 7 days, since postnatal day 8 (PD8) to PD14 on the neonatal neurobehavior in an HIE rat model was administrated. Results: Cerebrolysin administration after a hypoxic-ischemic insult minimized brain damage and increased cellular viability. Furthermore, this neuroprotective effect lasted until adulthood, improving some motor abnormalities and reversing the long-term memory acquisition deficit caused by HIE. Conclusion: Repeated Cerebrolysin administration can reduce HIE Motor Disabilities and Reverses the Long-Term Memory Acquisition Deficit in neonatal rats safely and effectively.

Anti-SARS-CoV-2 T-stem cell memory persists in ocrelizumab-treated MS patients

Background: Development of long-lasting anti-severe acute respiratory syndrome coronavirus 2 (SARS-CoV2) T-cell responses in persons with multiple sclerosis (pwMS) treated with ocrelizumab is questioned. Objective: Investigate antiviral T-cell responses after infection with SARS-CoV-2 in ocrelizumab-treated pwMS. Control groups included ocrelizumab-treated pwMS without SARS-CoV-2 infection, and non-MS individuals with and without SARS-CoV-2 infection. Methods: Peripheral blood mononuclear cells were stimulated with SARS-CoV-2 peptide pools and T-cell reactivity was assessed by ELISPOT for interferon (IFN)-γ detection, and by multiparametric fluorescence-activated cell sorting (FACS) analyses for assessment and characterization of T-cell activation. Results: ELISPOT assay against the spike and the N protein of SARS-CoV-2 displayed specific T-cell reactivity in 28/29 (96%) pwMS treated with ocrelizumab and infected by SARS-CoV-2, similar to infected persons without MS. This reactivity was present 1 year after infection and independent from the time of ocrelizumab infusion. FACS analysis following stimulation with SARS-CoV-2 peptide pools showed the presence of activation-induced markers (AIMs) in both CD4+ and CD8+ T-cell subsets in 96% and 92% of these individuals, respectively. Within naïve AIM+ CD4+ and CD8+ T-cells, we detected T memory stem cells, suggesting the acquisition of long-term memory. Conclusions: B-cell depletion using ocrelizumab does not impair the development of long-lasting anti-SARS-CoV-2 T-cell responses.

Involvement of medial prefrontal cortex canonical Wnt/β-catenin and non-canonical Wnt/Ca2+ signaling pathways in contextual fear memory in male rats

Wnt proteins activate different signaling pathways, such as the canonical Wnt/β-catenin signaling pathway and non-canonical β-catenin-independent signaling pathway and have been related to several functions in central nervous system, including learning and memory. However, whether these signaling pathways are required in the medial prefrontal cortex (mPFC) for fear memory acquisition, consolidation and retrieval remains unclear. To address this question, we submitted male rats to a contextual fear conditioning (CFC) paradigm, and administered canonical Wnt/β-catenin and non-canonical Wnt/Ca2+ signaling pathways inhibitors, DKK1 and SFRP1, respectively, into the prelimbic (PrL) subdivision of the mPFC at different moments and evaluated short-term and long-term memory acquisition, consolidation and retrieval. We found that blocking canonical Wnt/β-catenin and non-canonical Wnt/Ca2+ signaling pathways 15 min before or immediately after CFC training had no effect on STM and LTM of CFC, while their blockade 15 min before the retention test prevented the retrieval of STM and LTM of CFC. These results highlight the importance of the mPFC in fear memory retrieval demonstrating that both canonical Wnt/β-catenin and non-canonical Wnt/Ca2+ signaling pathways participate in this process. To understand how brain systems act on fear memories could provide a new target for the treatment of fear related disorders such as post-traumatic stress disorder and other anxiety disorders.

Effect of Berberine Isolated from Barberry Species by Centrifugal Partition Chromatography on Memory and the Expression of Parvalbumin in the Mouse Hippocampus Proper.

Neurodegenerative diseases associated with memory disturbances are important health issues occurring due to a prolonged life span. This article presents the results of a study targeting the emergence of a drug candidate with antiamnesic properties. The effect of berberine (BBR), an isoquinoline alkaloid isolated from the overground parts of Berberis sibirica Pall., on memory and expression of parvalbumin in the mouse hippocampus proper were determined. High-purity BBR was isolated by centrifugal partition chromatography from a methanolic extract from B. sibirica by using a methyl-tert-butyl ether and water (1:1 v/v) solvent system with 10 mmol/L of triethylamine and hydrochloric acid. In an in vivo study, we assessed the influence of the chronic administration of BBR on different stages of memory-related responses in mice. Our results indicated that the chronic administration of BBR in a higher dose (5 mg/kg) improves long-term memory acquisition in mice, as determined in the passive avoidance test. The hippocampal CA1–CA3 fields showed an increased number of parvalbumin-immunoreactive neurons (PV-IR) and nerve fibers as compared to the control. No significant changes in the dentate gyrus were observed between the groups. The HPLC-ESI-QTOF-MS/MS analysis of the biological material revealed the content of BBR as 363.4 ± 15.0 ng (4.11% of RSD) per brain, 15.06 ± 0.89 ng (5.91% of RSD) per hippocampus, and 54.45 ± 1.40 (4.05% of RSD) ng in 100 µL plasma. The study showed that BBR could be a factor influencing the expression of PV in hippocampal neurons. We speculate that BBR may modulate the level of Ca2+ in neurons and thus potentially act as a neuroprotective factor against neuronal damages.

Methamphetamine Inhibits Long-Term Memory Acquisition and Synaptic Plasticity by Evoking Endoplasmic Reticulum Stress.

Methamphetamine (MA), an illicit drug abused worldwide, leads to cognitive impairment and memory loss. However, the detailed mechanisms of MA-induced neurologic impairment are still unclear. The present study aimed to investigate the mechanisms of MA-induced inhibition of memory acquisition from the perspective of endoplasmic reticulum (ER) stress. ER stress, caused by the accumulation of wrongly folded proteins in the ER, is important for new protein synthesis, which further influence the formation of long-term memory. A subacute MA poisoning model of mice was established and several behavioral experiments were performed, including elevated plus maze, Morris water maze, electro-stimulus Y-maze, and novel object recognition tasks. The present results suggested that 4 days exposure to MA induced significant memory loss. Whereas, this damage to memory formation could be protected when mice were pre-treated with ER stress inhibitor, tauroursodeoxycholic acid (TUDCA). The results of Western blotting showed that subacute exposure to MA increased the expression levels of ER stress marker proteins, such as binding immunoglobulin protein, phosphorylated eukaryotic translation initiation factor 2α, cyclic AMP-dependent transcription factor (ATF)-4, ATF-6, and CCAAT-enhancer binding protein homologous protein. Meanwhile, the enhanced expression levels of these proteins were reversed by TUDCA, indicating that MA administration induced memory loss by evoking ER stress in the hippocampus. We also found that MA inhibited the induction of long-term potentiation (LTP) in the hippocampus. Nevertheless, LTP could be induced when mice were pre-treated with TUDCA. In conclusion, MA inhibited long-term memory acquisition and synaptic plasticity via ER stress.

Anabolic-androgenic steroids cycle administration decreases anxious-like behavior but does not affect long-term memory acquisition in rats

The steroid hormones are lipids in nature, which play crucial roles in several metabolic and behavioral pathways in mammals. Drug therapy uses sterol hormones for treating some disturbances linked with its deficiency; however, the illicit use of these hormones by amateur and elite athletes to enhance performance or body appearance may lead to several health issues. In this study we evaluated the anxious-like behavior and the long-term memory acquisition of male rats undergoing sedentary life-style or physical effort, with or without anabolic-androgenic steroids (ASC) treatment. The results showed a decrease in anxious-like behavioral levels in rats that received ASC treatment associated or not with physical effort, but this treatment did not affect the acquisition of long-term memory at the dose and experimental model assessed.

Mushroom Body Specific Transcriptome Analysis Reveals Dynamic Regulation of Learning and Memory Genes After Acquisition of Long-Term Courtship Memory in Drosophila.

The formation and recall of long-term memory (LTM) requires neuron activity-induced gene expression. Transcriptome analysis has been used to identify genes that have altered expression after memory acquisition, however, we still have an incomplete picture of the transcriptional changes that are required for LTM formation. The complex spatial and temporal dynamics of memory formation creates significant challenges in defining memory-relevant gene expression changes. The Drosophila mushroom body (MB) is a signaling hub in the insect brain that integrates sensory information to form memories across several different experimental memory paradigms. Here, we performed transcriptome analysis in the MB at two time points after the acquisition of LTM: 1 hr and 24 hr. The MB transcriptome was compared to biologically paired whole head (WH) transcriptomes. In both, we identified more transcript level changes at 1 hr after memory acquisition (WH = 322, MB = 302) than at 24 hr (WH = 23, MB = 20). WH samples showed downregulation of developmental genes and upregulation of sensory response genes. In contrast, MB samples showed vastly different changes in transcripts involved in biological processes that are specifically related to LTM. MB-downregulated genes were highly enriched for metabolic function. MB-upregulated genes were highly enriched for known learning and memory processes, including calcium-mediated neurotransmitter release and cAMP signaling. The neuron activity inducible genes Hr38 and sr were also specifically induced in the MB. These results highlight the importance of sampling time and cell type in capturing biologically relevant transcript level changes involved in learning and memory. Our data suggests that MB cells transiently upregulate known memory-related pathways after memory acquisition and provides a critical frame of reference for further investigation into the role of MB-specific gene regulation in memory.

PARP1-Erk synergism in proliferating cells.

A synergism between PARP1 and phosphorylated Erk mediating IEG (immediate early gene) expression has been recently reported in cerebral neurons and cardiomyocytes. Stimulation induced PARP-Erk synergism was required for IEG expression underlying synaptic plasticity and long-term memory acquisition during learning. It was similarly required for cardiomyocytes development. Here, we identified this mechanism in Erk-induced gene expression promoting proliferation. This mechanism can be targeted in malignant cells.

Modulation of learning and memory by the genetic disruption of circadian oscillator populations.

While a rich literature has documented that the efficiency of learning and memory varies across circadian time, a close survey of that literature reveals extensive heterogeneity in the time of day (TOD) when peak cognitive performance occurs. Moreover, most previous experiments in rodents have not focused on the question of discriminating which memory processes (e.g., working memory, memory acquisition, or retrieval) are modulated by the TOD. Here, we use assays of contextual fear conditioning and spontaneous alternation in WT (C57Bl/6 J) mice to survey circadian modulation of hippocampal-dependent memory at multiple timescales - including working memory (seconds to a few minutes), intermediate-term memory (a delay of thirty minutes), and acquisition and retrieval of long-term memory (a delay of two days). Further, in order to test the relative contributions of circadian timing mechanisms to the modulation of memory, a parallel set of studies were performed in mice lacking clock timing mechanisms. These transgenic mice lacked the essential circadian gene Bmal1, either globally (Bmal1 null) or locally (floxed Bmal1 mice, which lack Bmal1 in excitatory forebrain neurons, e.g. cortical and hippocampal neurons). Here, we show that in WT mice, retrieval (but not working memory, intermediate-term memory, or acquisition of long-term memory) is modulated by TOD. However, transgenic mouse models lacking Bmal1 - both globally, and only in forebrain excitatory neurons - show deficits regardless of the memory process tested (and lack circadian modulation of retrieval). These results provide new clarity regarding the impact of the TOD on hippocampal-dependent memory and support the key role of hippocampal and cortical circadian oscillations in circadian gating of cognition.

Adrenergic receptor β3 is involved in the memory consolidation process in mice.

Attention and emotion have a positive impact on memory formation, which is related to the activation of the noradrenergic system in the brain. The hippocampus and amygdala are fundamental structures in memory acquisition, which is modulated by noradrenaline through the noradrenergic receptors. Pharmacological studies suggest that memory acquisition depends on the action of both the β3 (β3-AR) and β2 (β2-AR) receptor subtypes. However, the use of animal models with specific knockout for the β3-AR receptor only (β3-ARKO) allows researchers to more accurately assess its role in memory formation processes. In the present study, we evaluated short- and long-term memory acquisition capacity in β3-ARKO mice and wild-type mice at approximately 60 days of age. The animals were submitted to the open field test, the elevated plus maze, object recognition, and social preference. The results showed that the absence of the β3-AR receptor caused no impairment in locomotion and did not cause anxious behavior, but it caused significant impairment of short- and long-term memory compared to wild-type animals. We also evaluated the expression of genes involved in memory consolidation. The mRNA levels for GLUT3, a glucose transporter expressed in the central nervous system, were significantly reduced in the amygdala, but not in the hippocampus of the β3-ARKO animals. Our results showed that β3-AR was involved in the process of acquisition of declarative memory, and its action may be due to the facilitation of glucose absorption in the amygdala.

A PARP1-ERK2 synergism is required for the induction of LTP.

Unexpectedly, a post-translational modification of DNA-binding proteins, initiating the cell response to single-strand DNA damage, was also required for long-term memory acquisition in a variety of learning paradigms. Our findings disclose a molecular mechanism based on PARP1-Erk synergism, which may underlie this phenomenon. A stimulation induced PARP1 binding to phosphorylated Erk2 in the chromatin of cerebral neurons caused Erk-induced PARP1 activation, rendering transcription factors and promoters of immediate early genes (IEG) accessible to PARP1-bound phosphorylated Erk2. Thus, Erk-induced PARP1 activation mediated IEG expression implicated in long-term memory. PARP1 inhibition, silencing, or genetic deletion abrogated stimulation-induced Erk-recruitment to IEG promoters, gene expression and LTP generation in hippocampal CA3-CA1-connections. Moreover, a predominant binding of PARP1 to single-strand DNA breaks, occluding its Erk binding sites, suppressed IEG expression and prevented the generation of LTP. These findings outline a PARP1-dependent mechanism required for LTP generation, which may be implicated in long-term memory acquisition and in its deterioration in senescence.

Correlations between the Memory-Related Behavior and the Level of Oxidative Stress Biomarkers in the Mice Brain, Provoked by an Acute Administration of CB Receptor Ligands.

The endocannabinoid system, through cannabinoid (CB) receptors, is involved in memory-related responses, as well as in processes that may affect cognition, like oxidative stress processes. The purpose of the experiments was to investigate the impact of CB1 and CB2 receptor ligands on the long-term memory stages in male Swiss mice, using the passive avoidance (PA) test, as well as the influence of these compounds on the level of oxidative stress biomarkers in the mice brain. A single injection of a selective CB1 receptor antagonist, AM 251, improved long-term memory acquisition and consolidation in the PA test in mice, while a mixed CB1/CB2 receptor agonist WIN 55,212-2 impaired both stages of cognition. Additionally, JWH 133, a selective CB2 receptor agonist, and AM 630, a competitive CB2 receptor antagonist, significantly improved memory. Additionally, an acute administration of the highest used doses of JWH 133, WIN 55,212-2, and AM 630, but not AM 251, increased total antioxidant capacity (TAC) in the brain. In turn, the processes of lipids peroxidation, expressed as the concentration of malondialdehyde (MDA), were more advanced in case of AM 251. Thus, some changes in the PA performance may be connected with the level of oxidative stress in the brain.

Serotonin is a facilitatory neuromodulator of synaptic transmission and “reinforces” long-term potentiation induction in the vertical lobe of Octopus vulgaris

The modern cephalopod mollusks (coleoids) are considered the most behaviorally advanced invertebrate, yet little is known about the neurophysiological basis of their behaviors. Previous work suggested that the vertical lobe (VL) of cephalopods is a crucial site for the learning and memory components of these behaviors. We are therefore studying the neurophysiology of the VL in Octopus vulgaris and have discovered a robust activity-dependent long-term potentiation (LTP) of the synaptic input to the VL. Moreover, we have shown that the VL and its LTP are involved in behavioral long-term memory acquisition. To advance our understanding of the VL as a learning neural network we explore the possible involvement of neuromodulation in VL function. Here we examine whether the well studied serotonergic modulation in simple models of learning in gastropods mollusks is conserved in the octopus VL. We demonstrate histochemically that the VL is innervated by afferent terminals containing 5-HT immunoreactivity (5-HT-IR). Physiologically, 5-HT has a robust facilitatory effect on synaptic transmission and activity-dependent LTP induction. These results suggest that serotonergic neuromodulation is a part of a reinforcing/reward signaling system conserved in both simple and complex learning systems of mollusks. However, there are notable functional differences. First, the effective concentration of 5-HT in the VL is rather high (100 μM); secondly, only neuropilar regions but not cell bodies in the VL are innervated by terminals containing 5-HT-IR. Thirdly, repetitive or long exposures to 5-HT do not lead to a clear long-term facilitation. We propose that in the octopus VL, while the basic facilitatory properties of molluscan 5-HT system are conserved, the system has adapted to convey signals from other brain areas to reinforce the activity-dependent associations at specific sites in the large connections matrix in the VL.

Prefrontal and hippocampal coding during long-term memory formation in monkeys

Event Abstract Back to Event Prefrontal and hippocampal coding during long-term memory formation in monkeys Scott L. Brincat1* and Earl K. Miller1 1 MIT, Picower Institute for Learning & Memory, United States A number of convergent studies have implicated the hippocampus and prefrontal cortex (PFC) as two of the most critical brain areas for formation of new long-term declarative memories. However, their respective roles in memory encoding are still not well understood, particularly at the neural level. To address this question, we recorded spiking and local field potential activity simultaneously from multiple electrodes in the hippocampus and lateral PFC of monkeys learning novel associations between pairs of visual objects, an animal model of declarative memory formation. On each task trial, a cue object instructed recall from long-term memory of its learned associate object; the monkey then decided whether a subsequent test object matched the recalled associate, and was given feedback about the correctness of his response. Each day, four novel object-pair associations were learned through trial and error to a high level of performance, so neural activity could be tracked though the full course of long-term memory acquisition and analytically partitioned into factors reflecting perceptual, mnemonic, and response processes. We found that, in parallel with the monkeys’ behavioral learning, prefrontal neurons acquired two types of specific information reflecting the contents of the newly-formed long-term memories-information about the recalled associate object and about the associative match/non-match decision. Hippocampal neurons, in contrast, showed very little information reflecting memory content, but strongly represented trial outcome-whether the monkey’s response on each trial was correct or not. Hippocampal outcome information was strongest during the initial stages of learning, when it might be used as a "teaching signal" instructing PFC and other neocortical structures what should be encoded into memory, and subsided as associations became well-learned. Robust trial outcome information was also conveyed in the strength of phase-synchrony between hippocampal spikes and PFC local field potentials, consistent with the idea of a hippocampal teaching signal being communicated to PFC. Interestingly, positive and negative trial outcomes were represented in distinct beta (~12-32 Hz) and theta (~4-8 Hz) frequency bands, respectively, perhaps reflecting their putatively opposing effects on target structures. These results suggest prefrontal cortex plays a central role in long-term memory formation and storage, while the hippocampus-contrary to many accounts-may function primarily in driving memory encoding and/or consolidation in other structures. Conference: Computational and Systems Neuroscience 2010, Salt Lake City, UT, United States, 25 Feb - 2 Mar, 2010. Presentation Type: Poster Presentation Topic: Poster session II Citation: Brincat SL and Miller EK (2010). Prefrontal and hippocampal coding during long-term memory formation in monkeys. Front. Neurosci. Conference Abstract: Computational and Systems Neuroscience 2010. doi: 10.3389/conf.fnins.2010.03.00216 Copyright: The abstracts in this collection have not been subject to any Frontiers peer review or checks, and are not endorsed by Frontiers. They are made available through the Frontiers publishing platform as a service to conference organizers and presenters. The copyright in the individual abstracts is owned by the author of each abstract or his/her employer unless otherwise stated. Each abstract, as well as the collection of abstracts, are published under a Creative Commons CC-BY 4.0 (attribution) licence (https://creativecommons.org/licenses/by/4.0/) and may thus be reproduced, translated, adapted and be the subject of derivative works provided the authors and Frontiers are attributed. For Frontiers’ terms and conditions please see https://www.frontiersin.org/legal/terms-and-conditions. Received: 04 Mar 2010; Published Online: 04 Mar 2010. * Correspondence: Scott L Brincat, MIT, Picower Institute for Learning & Memory, Paris, United States, sbrincat@mit.edu Login Required This action requires you to be registered with Frontiers and logged in. To register or login click here. Abstract Info Abstract The Authors in Frontiers Scott L Brincat Earl K Miller Google Scott L Brincat Earl K Miller Google Scholar Scott L Brincat Earl K Miller PubMed Scott L Brincat Earl K Miller Related Article in Frontiers Google Scholar PubMed Abstract Close Back to top Javascript is disabled. Please enable Javascript in your browser settings in order to see all the content on this page.

The Octopus Vertical Lobe Modulates Short-Term Learning Rate and Uses LTP to Acquire Long-Term Memory

Analyzing the processes and neuronal circuitry involved in complex behaviors in phylogenetically remote species can help us understand the evolution and function of these systems. Cephalopods, with their vertebrate-like behaviors but much simpler brains, are ideal for such an analysis. The vertical lobe (VL) of Octopus vulgaris is a pivotal brain station in its learning and memory system. To examine the organization of the learning and memory circuitry and to test whether the LTP that we discovered in the VL is involved in behavioral learning, we tetanized the VL to induce a global synaptic enhancement of the VL pathway. The effects of tetanization on learning and memory of a passive avoidance task were compared to those of transecting the same pathway. Tetanization accelerated and transection slowed short-term learning to avoid attacking a negatively reinforced object. However, both treatments impaired long-term recall the next day. Our results suggest that the learning and memory system in the octopus, as in mammals [9], is separated into short- and long-term memory sites. In the octopus, the two memory sites are not independent; the VL, which mediates long-term memory acquisition through LTP, also modulates the circuitry controlling behavior and short-term learning.

Species-specific acquisition and consolidation of long-term memory in parasitic wasps

Long-term memory (LTM) formation usually requires repeated, spaced learning events and is achieved by the synthesis of specific proteins. Other memory forms require a single learning experience and are independent of protein synthesis. We investigated in two closely related parasitic wasp species, Cotesia glomerata and Cotesia rubecula, whether natural differences in foraging behaviour are correlated with differences in LTM acquisition and formation. These parasitic wasp species lay their eggs in young caterpillars of pierid butterflies and can learn to associate plant odours with a successful egg laying experience on caterpillars on the odour-producing plant. We used a classical conditioning set-up, while interfering with LTM formation through translation or transcription inhibitors. We show here that C. rubecula formed LTM after three spaced learning trials, whereas C. glomerata required only a single trial for LTM formation. After three spaced learning trials, LTM formation was complete within 4 h in C. glomerata, whereas in C. rubecula, LTM formation took 3 days. Linking neurobiology with ecology, we argue that this species-specific difference in LTM acquisition and formation is adaptive given the extreme differences in both the number of foraging decisions of the two wasp species and in the spatial distributions of their respective hosts in nature.

One-trial conditioned taste aversion inLymnaea: good and poor performers in long-term memory acquisition

In the majority of studies designed to elucidate the causal mechanisms of memory formation, certain members of the experimental cohort, even though subjected to exactly the same conditioning procedures, remember significantly better than others, whereas others show little or no long-term memory (LTM) formation. To begin to address the question of why this phenomenon occurs and thereby help clarify the causal mechanism of LTM formation, we used a conditioned taste aversion (CTA) procedure on individuals of the pond snail Lymnaea stagnalis and analyzed their subsequent behavior. Using sucrose as an appetitive stimulus and KCl as an aversive stimulus, we obtained a constant ratio of ;poor' to ;good' performers for CTA-LTM. We found that approximately 40% of trained snails possessed LTM following a one-trial conditioning procedure. When we examined the time-window necessary for the memory consolidation, we found that if we cooled snails to 4 degrees C for 30 min within 10 min after the one-trial conditioning, LTM was blocked. However, with delayed cooling (i.e. longer than 10 min), LTM was present. We could further interfere with LTM formation by inducing inhibitory learning (i.e. backward conditioning) after the one-trial conditioning. Finally, we examined whether we could motivate snails to acquire LTM by depriving them of food for 5 days before the one-trial conditioning. Food-deprived snails, however, failed to exhibit LTM following the one-trial conditioning. These results will help us begin to clarify why some individuals are better at learning and forming memory for specific tasks at the neuronal level.