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Jerry W. Rudy - One of the best experts on this subject based on the ideXlab platform.

  • amygdala regulation of immediate early gene expression in the hippocampus induced by Contextual Fear Conditioning
    The Journal of Neuroscience, 2006
    Co-Authors: Nicole C Huff, Matthew G Frank, Karli Wrighthardesty, David Sprunger, Patricia Matusamat, Emily A Higgins, Jerry W. Rudy
    Abstract:

    The basolateral nuclei of the amygdala (BLA) are thought to modulate memory storage in other brain regions (McGaugh, 2004). We reported that BLA modulates the memory for both an explored context and for Contextual Fear Conditioning. Both of these memories depend on the hippocampus. Here, we examined the hypothesis that the BLA exerts its modulatory effect by regulating the expression of immediate-early genes (IEGs) in the hippocampus. The main findings of these experiments were: (1) Arc activity-regulated cytoskeletal protein (Arc), an immediate-early gene (also termed Arg 3.1) and c-fos mRNA are induced in the hippocampus after a context exposure, or context plus shock experience, but not after an immediate shock; and (2) BLA inactivation with muscimol attenuated the increase in Arc and c-fos mRNA in the hippocampus associated with Contextual Fear Conditioning but did not influence Arc mRNA associated with context exploration. These results support the hypothesis that the amygdala modulates Contextual Fear memory by regulating expression of IEGs in the hippocampus.

  • Context pre-exposure obscures amygdala modulation of Contextual-Fear Conditioning.
    Learning & memory (Cold Spring Harbor N.Y.), 2005
    Co-Authors: Nicole C Huff, Emily A Higgins, Karli Wright-hardesty, Patricia Matus-amat, Jerry W. Rudy
    Abstract:

    We report that post-training inactivation of basolateral amygdala region (BLA) with muscimol impaired memory for Contextual-Fear Conditioning (as measured by freezing) and intra-BLA norepinephrine enhanced this memory. However, pre-exposure to the context eliminated both of these effects. These findings provide a likely explanation of why an earler study failed to observe that the BLA modulates Contextual Fear Conditioning-they pre-exposed their rats to the context. These results also suggest that the amygdala modulates the storage of the context Fear memory and may do so by influencing the storage of the representation of the context in which the shock occurred.

  • the ventral hippocampus supports a memory representation of context and Contextual Fear Conditioning implications for a unitary function of the hippocampus
    Behavioral Neuroscience, 2005
    Co-Authors: Jerry W. Rudy, Patricia Matusamat
    Abstract:

    The authors report that either inactivating the ventral hippocampus (VH) with muscimol prior to context preexposure or injecting anisomycin into the VH after preexposure significantly impaired rats' memory for context. Injecting anisomycin into the VH prior to Contextual Fear Conditioning also greatly reduced long-term memory (48-hr retention test) but had no effect on short-term memory (1-hr retention test) for Contextual Fear. Together with other results, these data suggest that the memory for a novel context is distributed throughout the longitudinal extent of the hippocampus and that this representation helps to support Contextual Fear Conditioning.

  • Understanding Contextual Fear Conditioning: insights from a two-process model.
    Neuroscience and biobehavioral reviews, 2004
    Co-Authors: Jerry W. Rudy, Nicole C Huff, Patricia Matus-amat
    Abstract:

    Contextual Fear Conditioning is an important behavioral paradigm for studying the neurobiology of learning and memory and the mnemonic function of the hippocampus. We suggest that research in this domain can profit by a better theoretical understanding of the processes that contribute to this phenomenon. To facilitate this understanding, we describe a theory which assumes that physical elements of a Conditioning context represented in the brain as either (a) a set of independent features or (b) features bound into a conjunctive representation by the hippocampus which supports pattern completion. Conditioning produced by shocking a rat in a particular context, in principle, can be produced by strengthening connections between the feature representations and/or the conjunctive representation and basolateral region of the amygdala. We illustrate how this theory clarifies some of the complexities associated with the existing literature and how it can be used to guide future empirical work. We also argue that the mechanisms (conjunctive representations and pattern completion) that mediate the contribution the hippocampus makes to Contextual Fear Conditioning are the same ones that enable the hippocampus to support declarative memory in humans.

  • Neonatal Handling Enhances Contextual Fear Conditioning and Alters Corticosterone Stress Responses in Young Rats
    Hormones and behavior, 2002
    Co-Authors: Melinda L. Beane, Michael Cole, Robert L. Spencer, Jerry W. Rudy
    Abstract:

    Abstract Previous studies have indicated that neonatal handling influences development of hypothalamic–pituitary–adrenal (HPA) control of corticosterone. In addition, corticosterone influences memory consolidation processes in Contextual Fear Conditioning. Therefore, neonatal handling may affect hippocampal-dependent memory processes present in Contextual Fear Conditioning by influencing the development of HPA control of corticosterone. To investigate the effects of neonatal handling on early learning, rat pups were either handled (15-min removal from home cage) on the first 15 days after birth or left undisturbed in their home cage. Handled rats and nonhandled rats were Fear conditioned at 18, 21, or 30 days of age and then tested at two time points—24 h following Conditioning and at postnatal day 45. Subsequently, at approximately postnatal day 60, rats were exposed to restraint stress and corticosterone levels were assessed during restraint and recovery. Handled and nonhandled rats did not differ significantly in their freezing response immediately following footshock on the Conditioning day. However, when tested for Contextual Fear Conditioning at 24 h following Conditioning and at postnatal day 45, handled rats showed more freezing behavior than nonhandled rats. When exposed to restraint stress, handled rats had a more rapid return of corticosterone to basal levels than nonhandled rats. These results indicate that neonatal handling enhances developmentally early memory processes involved in Contextual Fear Conditioning and confirms previously reported effects of neonatal handling on HPA control of corticosterone.

Thomas J. Gould - One of the best experts on this subject based on the ideXlab platform.

  • Stronger Learning Recruits Additional Cell-Signaling Cascades: c-Jun-N-Terminal Kinase 1 (JNK1) is Necessary for Expression of Stronger Contextual Fear Conditioning
    Neurobiology of learning and memory, 2014
    Co-Authors: Prescott T. Leach, Justin W. Kenney, Thomas J. Gould
    Abstract:

    Increased training often results in stronger memories but the neural changes responsible for these stronger memories are poorly understood. It is proposed here that higher levels of training that result in stronger memories recruit additional cell signaling cascades. This study specifically examined if c-Jun N-terminal kinase 1 (JNK1) is involved in the formation of stronger Fear Conditioning memories. Wildtype (WT), JNK1 heterozygous (Het), and JNK1 knockout (KO) mice were Fear conditioned with 1 trial, 2 trials, or 4 trials. All mice learned both Contextual (hippocampus-dependent) and cued (hippocampus-independent) Fear Conditioning but for Contextual Fear Conditioning only, the JNK1 KO mice did not show higher levels of learning with increased trials. That is, WT mice showed a significant linear increase in Contextual Fear Conditioning as training trials increased from 1 to 2 to 4 trials whereas KO mice showed the same level of Contextual Fear Conditioning as WT mice for 1 trial training but did not have increased levels of Contextual Fear Conditioning with additional trials. These data suggest that JNK1 may not be critical for learning but when higher levels of hippocampus-dependent learning occur, JNK1 signaling is recruited and is necessary for stronger hippocampus-dependent memory formation.

  • The effects of galantamine on nicotine withdrawal-induced deficits in Contextual Fear Conditioning in C57BL/6 mice.
    Behavioural brain research, 2011
    Co-Authors: Derek S. Wilkinson, Thomas J. Gould
    Abstract:

    Current smoking cessation are relatively ineffective at maintaining abstinence during withdrawal. Nicotine withdrawal is associated with a variety of symptoms including cognitive deficits and targeting these deficits may be a useful strategy for maintaining abstinence. Galantamine is an acetylcholinesterase inhibitor and allosteric modulator of nicotinic acetylcholine receptors (nAChRs) with cognitive enhancing effects that may alleviate cognitive deficits associated with nicotine withdrawal. The effects of galantamine on nicotine withdrawal-induced deficits in Contextual Fear Conditioning in C57BL/6 mice were examined. An initial acute dose-response experiment revealed that 0.5 and 1 mg/kg galantamine had no effect on Fear Conditioning. To determine if galantamine would reverse nicotine withdrawal-related deficits in Contextual Fear Conditioning, mice were implanted with osmotic mini-pumps that delivered chronic saline or 6.3 mg/kg/d nicotine for 12 days and then pumps were removed. Training and testing of Fear Conditioning occurred 24 and 48 hours later, respectively. Nicotine withdrawal disrupted Contextual Fear Conditioning, which was reversed with 1 but not 0.5 mg/kg galantamine. Across all conditions in both studies 2 mg/kg galantamine led to high levels of freezing that were likely due to nonspecific effects. The ability of galantamine to reverse nicotine withdrawal-deficits in Contextual Conditioning is likely mediated through enhanced levels of acetylcholine via inhibition of acetylcholinesterase, potentiation of hippocampal α4β2* nAChRs, or both. The present study suggests that acetylcholinesterase inhibitors and/or drugs that act as allosteric modulators of nAChRs might be targets for smoking cessation aids because they may alleviate withdrawal symptoms such as cognitive deficits that can lead to relapse.

  • The enhancement of Contextual Fear Conditioning by ABT-418.
    Behavioural pharmacology, 2010
    Co-Authors: Justin W. Kenney, Derek S. Wilkinson, Thomas J. Gould
    Abstract:

    Activation of nicotinic acetylcholine receptors (nAChRs) is known to modulate various forms of learning and memory, including Contextual Fear Conditioning. Although numerous studies have shown that high-affinity beta2-containing nAChRs are necessary for the nicotine-induced enhancement of Contextual Fear Conditioning, it is unknown whether other high-affinity nAChR agonists are capable of enhancing this learning. To examine this issue, ABT-418, a high-affinity nAChR agonist with greater selectivity for high-affinity receptors than nicotine, was administered before acquisition and/or recall of Contextual Fear memories. ABT-418 enhanced acquisition of Contextual Fear memories in a dose-dependent manner.

  • Hippocampal α4β2 Nicotinic Acetylcholine Receptor Involvement in the Enhancing Effect of Acute Nicotine on Contextual Fear Conditioning
    The Journal of neuroscience : the official journal of the Society for Neuroscience, 2007
    Co-Authors: Jennifer A. Davis, Justin W. Kenney, Thomas J. Gould
    Abstract:

    Nicotine is known to enhance learning and memory in hippocampus-dependent tasks such as Contextual Fear Conditioning. The present study was designed to directly examine whether the hippocampus plays a role in mediating this enhancement and which nicotinic acetylcholine receptor (nAChR) subtypes localized to the hippocampus are critical for enhanced learning. Contextual Fear Conditioning consisted of two white noise conditioned stimuli presentations, each coterminating with a 2 s, 0.57 mA footshock separated by a 120 s intertrial interval. Nicotine (0.09, 0.18, and 0.35 μg per side) was bilaterally infused into the dorsal hippocampus before training and testing. Infusions of nicotine into the dorsal hippocampus produced a dose-dependent enhancement of Contextual Fear Conditioning. To determine which nAChRs are critical to the enhancing effect of nicotine, the preferential α4β2 nAChR antagonist, dihydro-β-erythroidine (DHβE) (6.00 and 18.00 μg per side), or the preferential α7 nAChR antagonist, methyllycaconitine (MLA) (13.50 and 27.00 μg per side), was bilaterally infused into the dorsal hippocampus before systemic injections of nicotine (0.09 mg/kg). DHβE infusions dose-dependently blocked the enhancement of Contextual Fear Conditioning by nicotine, whereas MLA infusions yielded an intermediate effect. In addition, neither DHβE nor MLA had an effect on Contextual Fear Conditioning in the absence of systemic nicotine. The present results suggest a critical role for α4β2 nAChRs in the dorsal hippocampus for mediating the enhancing effect of nicotine on Contextual Fear Conditioning.

  • Bupropion dose-dependently reverses nicotine withdrawal deficits in Contextual Fear Conditioning.
    Pharmacology biochemistry and behavior, 2007
    Co-Authors: George S. Portugal, Thomas J. Gould
    Abstract:

    Bupropion, a norepinephrine and dopamine reuptake inhibitor and nicotinic acetylcholine receptor antagonist, facilitates smoking cessation and reduces some symptoms of nicotine withdrawal. However, the effects of bupropion on nicotine withdrawal-associated deficits in learning remain unclear. The present study investigated whether bupropion has effects on Contextual and cued Fear Conditioning following withdrawal from chronic nicotine or when administered alone. Bupropion was administered alone for a range of doses (2.5, 5, 10, 20 or 40 mg/kg), and dose-dependent impairments in Contextual and cued Fear Conditioning were observed (20 or 40 mg/kg). Follow-up studies investigated if bupropion disrupted acquisition or expression of Fear Conditioning. Bupropion (40 mg/kg) administration on training day only produced deficits in Contextual Fear Conditioning. Alternatively, bupropion (20 or 40 mg/kg) administration during testing dose-dependently produced deficits in Contextual and cued Fear Conditioning. To test the effect of bupropion on nicotine withdrawal, mice were withdrawn from 12 days of chronic nicotine (6.3 mg/kg/day) or saline treatment. Withdrawal from chronic nicotine disrupted Contextual Fear Conditioning; however, 5 mg/kg bupropion reversed this deficit. Overall, these results indicate that a low dose of bupropion can reverse nicotine withdrawal deficits in Contextual Fear Conditioning, but that high doses of bupropion produce deficits in Fear Conditioning.

Carmen Sandi - One of the best experts on this subject based on the ideXlab platform.

  • upregulation of polysialylated neural cell adhesion molecule in the dorsal hippocampus after Contextual Fear Conditioning is involved in long term memory formation
    The Journal of Neuroscience, 2007
    Co-Authors: Miguel A Lopezfernandez, César Venero, Mariefrancoise Montaron, Emilio Varea, Genevieve Rougon, Djoher Nora Abrous, Carmen Sandi
    Abstract:

    The role of the hippocampus in pavlovian Fear Conditioning is controversial. Although lesion and pharmacological inactivation studies have suggested a key role for the dorsal hippocampus in Contextual Fear Conditioning, the involvement of the ventral part is still uncertain. Likewise, the debate is open with regard to the putative implication of each hippocampal subdivision in Fear Conditioning to a discrete conditioned stimulus. We explored the potential existence of dissociations occurring in the dorsal versus ventral hippocampus at the cellular level while dealing with either Contextual or cued Fear Conditioning and focused in a molecular "signature" linked to structural plasticity, the polysialylated form of the neural cell adhesion molecule (PSA-NCAM). We found an upregulation of PSA-NCAM expression in the dorsal (but not ventral) dentate gyrus at 24 h after Contextual (but not tone) Fear Conditioning. Specific removal of PSA through microinfusion of the enzyme endoneuraminidase-N in the dorsal (but not ventral) hippocampus reduced freezing responses to the conditioned context. Therefore, we present evidence for a specific role of PSA-NCAM in the dorsal hippocampus in the plasticity processes occurring during consolidation of the context representation after "standard" Contextual Fear Conditioning. Interestingly, we also found that exposing animals just to the context induced an activation of PSA-NCAM in both dorsal and ventral dentate gyrus. Altogether, these findings highlighting the distinctive occurrence of these neuroplastic processes in the dorsal hippocampus during the standard Contextual Fear-Conditioning task enlighten the ongoing debate about the involvement of these hippocampal subdivisions in pavlovian Fear Conditioning.

  • Modulation of Contextual Fear Conditioning by chronic stress in rats is related to individual differences in behavioral reactivity to novelty.
    Brain research, 2003
    Co-Authors: M Isabel Cordero, Nyika D Kruyt, Carmen Sandi
    Abstract:

    We investigated whether Contextual Fear Conditioning could be related to the behavioral trait of locomotor reactivity to novelty in undisturbed and chronically stressed rats. Fear Conditioning was found to be specifically enhanced in low reactive-stressed animals, as compared to low reactive-undisturbed rats. The results suggest that individuals that display low reactivity to novelty are more susceptible to be influenced by stress exposure to subsequently exhibit potentiated Contextual Fear Conditioning.

  • Prior exposure to a single stress session facilitates subsequent Contextual Fear Conditioning in rats. Evidence for a role of corticosterone.
    Hormones and behavior, 2003
    Co-Authors: M Isabel Cordero, Nyika D Kruyt, César Venero, Carmen Sandi
    Abstract:

    Previous studies showed that exposure of rats to chronic restraint stress for 21 days enhances subsequent Contextual Fear Conditioning. Since recent evidence suggest that this effect is not dependent on stress-induced neurodegenerative processes, but to elevated training-elicited glucocorticoid release in chronically stressed animals, we aimed to explore here whether a single exposure to restraint stress, which is not expected to induce neuronal damage, would also affect Contextual Fear Conditioning. We also questioned whether post-training corticosterone levels might be associated with any potential effect of stress on Fear Conditioning. Adult male Wistar rats were exposed to acute restraint stress for 2 h and, two days later, trained in the Contextual Fear Conditioning task, under training conditions involving either moderate (0.4 mA shock) or high (1 mA shock) stress levels. The results showed that acute stress enhanced conditioned freezing at both training conditions, although data from the 1 mA shock intensity experiment only approached significance. Stressed animals were shown to display higher post-training corticosterone levels. Furthermore, the facilitating effect of prior stress was not evident when animals were trained in the hippocampal-independent auditory-cued Conditioning task. Therefore, these findings support the idea that stress experiences preceding exposure to new types of stressors facilitate the development of Contextual Fear Conditioning. They also indicate that not only repeated, but also a single exposure to aversive stimulation is sufficient to facilitate context-dependent Fear Conditioning, and suggest that increased glucocorticoid release at training might be implicated in the mechanisms mediating the memory facilitating effects induced by prior stress experiences.

  • a role for brain glucocorticoid receptors in Contextual Fear Conditioning dependence upon training intensity
    Brain Research, 1998
    Co-Authors: Isabel M Cordero, Carmen Sandi
    Abstract:

    We studied the possible involvement of corticosteroids in the establishment and long-term expression of Contextual Fear Conditioning and questioned whether a corticosteroid action might be dependent upon stimulus intensity at training. Experiments included: (i) the intracerebroventricular administration of specific antagonists for the two types of intracellular corticosteroid receptors to rats trained at either 1 mA or 0.4 mA shock intensity at Conditioning; and (ii) the administration of corticosterone after Conditioning rats to 0.2 mA shocks. The results showed that the administration of a type II glucocorticoid, but not a type I mineralocorticoid, receptor antagonist before Conditioning rats to the intermediate shock condition attenuated long-term expression of Contextual Fear Conditioning. However, treatment with the antagonists before Conditioning to the high shock intensity failed to influence the extent of Fear Conditioning. In addition, an intraperitoneal corticosterone injection, given immediately after training rats at the low shock intensity, enhanced long-term expression of the Fear response. The results support the view that post-training levels of circulating corticosterone, through an interaction with central type II glucocorticoid receptors, modulate the strength to which memory for Contextual Fear Conditioning is established and maintained.

  • Correlational relationship between shock intensity and corticosterone secretion on the establishment and subsequent expression of Contextual Fear Conditioning.
    Behavioral neuroscience, 1998
    Co-Authors: M Isabel Cordero, J. Joaquin Merino, Carmen Sandi
    Abstract:

    A role for corticosterone in the consolidation of Contextual Fear Conditioning has previously been proposed. In this study, physiological evidence was found to support this view. The extent of conditioned Fear and the levels of plasma corticosterone in rats, after context exposure at training and at different posttraining times (24 hr and 7 days), depended on the intensity of the unconditional stimulus (footshock). In each experimental session, a positive correlation was found between the magnitude of corticosterone levels and the Fear-related behavioral inhibition exhibited in the context. Results support the involvement of corticosterone on the processes that occur during consolidation in determining the strength at which the Contextual Fear Conditioning is stored as a long-term memory.

Maria Gabriela Menezes Oliveira - One of the best experts on this subject based on the ideXlab platform.

  • The dorsal subiculum is required for Contextual Fear Conditioning consolidation in rats.
    Behavioural brain research, 2020
    Co-Authors: Márcio Braga De Melo, Vanessa Manchim Favaro, Maria Gabriela Menezes Oliveira
    Abstract:

    The hippocampal formation has a well-known role in Contextual Fear Conditioning. The dorsal subiculum connects the hippocampus to the entorhinal cortex through pathways that seemingly rely on NMDA-dependent synaptic plasticity. The role of the dorsal subiculum in Contextual Fear Conditioning retrieval, but not acquisition, has been previously reported. However, most of the critical biological phenomena involved in memory formation occur in the consolidation phase. The present study aimed to assess the effects of intra-dorsal subiculum muscimol or AP5 infusion on Contextual Fear Conditioning consolidation. Our data show that dorsal subiculum integrity, as well as NMDA transmission in this region, seem to be necessary for Contextual Fear Conditioning consolidation.

  • Involvement of the prelimbic cortex in Contextual Fear Conditioning with temporal and spatial discontinuity.
    Neurobiology of learning and memory, 2017
    Co-Authors: Thays Brenner Santos, Vanessa Manchim Favaro, Juliana Carlota Kramer-soares, Maria Gabriela Menezes Oliveira
    Abstract:

    Time plays an important role in Conditioning, it is not only possible to associate stimuli with events that overlap, as in delay Fear Conditioning, but it is also possible to associate stimuli that are discontinuous in time, as shown in trace Conditioning for a discrete stimuli. The environment itself can be a powerful conditioned stimulus (CS) and be associated to unconditioned stimulus (US). Thus, the aim of the present study was to determine the parameters in which Contextual Fear Conditioning occurs by the maintenance of a Contextual representation over short and long time intervals. The results showed that a Contextual representation can be maintained and associated after 5s, even in the absence of a 15s re-exposure to the training context before US delivery. The same effect was not observed with a 24h interval of discontinuity. Furthermore, optimal conditioned response with a 5s interval is produced only when the contexts (of pre-exposure and shock) match. As the pre-limbic cortex (PL) is necessary for the maintenance of a continuous representation of a stimulus, the involvement of the PL in this temporal and Contextual processing was investigated. The reversible inactivation of the PL by muscimol infusion impaired the acquisition of Contextual Fear Conditioning with a 5s interval, but not with a 24h interval, and did not impair delay Fear Conditioning. The data provided evidence that short and long intervals of discontinuity have different mechanisms, thus contributing to a better understanding of PL involvement in Contextual Fear Conditioning and providing a model that considers both temporal and Contextual factors in Fear Conditioning.

  • Hippocampal NMDA receptor blockade impairs CREB phosphorylation in amygdala after Contextual Fear Conditioning.
    Hippocampus, 2013
    Co-Authors: Cesar A.o. Coelho, Tatiana L. Ferreira, Juliana Carlota Kramer Soares, Maria Gabriela Menezes Oliveira
    Abstract:

    In Contextual Fear Conditioning (CFC), hippocampus is thought to process environmental stimuli into a configural representation of the context and send it to amygdala nuclei, which current evidences point to be the site of CS-US association and Fear memory storage. If it is true, hippocampus should influence learning-induced plasticity in the amygdala nuclei after CFC acquisition. To test this, we infused wistar rats with saline or AP5, a NMDA receptor antagonist, in the dorsal hippocampus just before a CFC session, in which they were conditioned to a single shock, exposed to the context with no shocks or received an immediate shock. The rats were perfused, their brains harvested and immunohistochemically stained for cAMP element binding protein (CREB) phosphorylation ratio (pCREB/CREB) in lateral (LA), basal (B) and central (CeA) amygdala nuclei. CFC showed a learning-specific increase in pCREB ratio in B and CeA, in conditioned-saline rats compared to context and immediate shocked ones. Further, conditioned rats that received AP5 showed a decrease in pCREB ratio in LA, B and CeA. Our results support the current ideas that the role of hippocampus in Contextual Fear Conditioning occurs by sending Contextual information to amygdala to serve as conditioned stimulus.

  • Effects of dorsal striatum lesions in tone Fear Conditioning and Contextual Fear Conditioning.
    Brain research, 2003
    Co-Authors: Tatiana L. Ferreira, Karin M. Moreira, Daniela C. Ikeda, Orlando Francisco Amodeo Bueno, Maria Gabriela Menezes Oliveira
    Abstract:

    It has been suggested that the striatum mediates hippocampus-independent memory tasks. Classical Fear Conditioning to a discrete stimulus such as a tone is not affected by hippocampal lesion, whereas Contextual Fear Conditioning is an hippocampus dependent task. The purpose of the present study was to verify the effect of dorsal striatal lesions on tone and Contextual Fear Conditioning. The lesioned rats were not impaired in Contextual Fear Conditioning but in tone Fear Conditioning both electrolytically and neurotoxically lesioned animals showed less freezing compared with controls. The lesion effect was observed after a postoperative recovery period of 14 days but not after 2 months. The results support the hypothesis that the dorsal striatum is involved in hippocampus-independent memory tasks, but, in spite of this involvement, it does not seem to be a critical structure.

Stephen Maren - One of the best experts on this subject based on the ideXlab platform.

  • Nucleus reuniens mediates the extinction of Contextual Fear Conditioning.
    Behavioural brain research, 2019
    Co-Authors: Karthik R. Ramanathan, Stephen Maren
    Abstract:

    Abstract Learning and remembering the context in which events occur requires interactions between the hippocampus (HPC) and medial prefrontal cortex (mPFC). The nucleus reuniens (RE) is a ventral midline thalamic nucleus that coordinates activity in the mPFC and HPC and is involved in spatial and Contextual memory. We recently found that the RE is critical for Contextual Fear Conditioning in rats, a form of learning that involves interactions between the HPC and mPFC. Here we examined whether the RE mediates the extinction of Contextual Fear. After Contextual Fear Conditioning, rats underwent an extinction procedure in which they were merely exposed to the Conditioning context; freezing behavior during the extinction procedure and during a retrieval test 24 h later served as an index of conditioned Fear. Muscimol inactivation of the RE prior to extinction impaired the acquisition of both short- and long-term extinction memories. Similarly, inactivation of the RE prior to the extinction retrieval test also impaired the expression of extinction; this effect was not state-dependent. Taken together, these results reveal that the extinction of Contextual Fear memories requires the RE, which is consistent with a broader role for the RE in forms of learning that require HPC-mPFC interactions.

  • Estrogen modulates sexually dimorphic Contextual Fear Conditioning and hippocampal long-term potentiation (LTP) in rats
    Brain research, 2001
    Co-Authors: Rishi R. Gupta, Srijan Sen, Lisa L. Diepenhorst, Charles N. Rudick, Stephen Maren
    Abstract:

    The present study examined the role of ovarian steroids in Contextual Fear Conditioning and hippocampal synaptic plasticity in female rats. In experiment 1, adult female rats were ovariectomized and submitted to Contextual Fear Conditioning, a procedure in which rats received unsignaled footshock in a novel observation chamber; freezing behavior served as the measure of conditional Fear. Ovariectomized female rats froze at levels comparable to male rats, both of which froze significantly more than sham-operated female rats. In experiment 2, estrogen replacement in ovariectomized female rats reduced Fear Conditioning to a level comparable to that of sham-operated females in experiment 1. In experiment 3, the influence of estrogen on the induction of long-term potentiation (LTP) at perforant path-dentate granule cell synapses in ovariectomized female rats was examined. Estrogen decreased both population spike LTP and EPSP-spike potentiation at perforant path synapses. Taken together, these experiments indicate that ovarian steroids regulate both sexually dimorphic behavior and hippocampal plasticity in a Fear-Conditioning paradigm.

  • effects of 7 nitroindazole a neuronal nitric oxide synthase nnos inhibitor on locomotor activity and Contextual Fear Conditioning in rats
    Brain Research, 1998
    Co-Authors: Stephen Maren
    Abstract:

    The effect of 7-nitroindazole (7-NI), a selective neuronal nitric oxide synthase (nNOS) inhibitor, on Contextual Fear Conditioning in rats was examined. Systemic administration of 7-NI did not affect the acquisition of Contextual Fear (measured as freezing), but it did reduce locomotor activity and cause a corresponding increase in the expression of Contextual freezing. It is concluded that nNOS activity is not required for either the acquisition or expression of Contextual Fear Conditioning.

  • immediate early gene expression in the amygdala following footshock stress and Contextual Fear Conditioning
    Brain Research, 1998
    Co-Authors: Jeffrey B Rosen, Martina Sitcoske, Stacey L. Young, Michael S. Fanselow, Stephen Maren
    Abstract:

    This study investigated the increase in expression in the amygdala of 2 immediate-early genes, c-fos and NGFI-A, following Contextual Fear Conditioning. The immediate-shock freezing deficit paradigm was used to compare rats that received footshock after exploring a context to rats that received footshock immediately after placement in the chamber. The former procedure produces Contextual Fear Conditioning while the latter does not. Rats were either handled (handled group), placed in a test chamber without receiving footshock (context-no-footshock group), received footshock immediately upon being placed in the chamber (immediate-footshock group), or received footshock after a 1 min delay (delayed-footshock group). Only the delayed-footshock group displayed a Fear response (freezing behavior). Rats were sacrificed either 15 min after the experience or after a retention test 24 h later. The c-fos mRNA was increased in the medial nucleus of the amygdala in all of the groups that were placed in the test chamber. However, rats that received footshock (immediate- and delayed-footshock groups) had greater levels of c-fos mRNA expression than rats of the context-no-footshock group. The c-fos mRNA expression in the immediate- and delayed-footshock groups did not differ. However, after the retention test, the expression of c-fos mRNA in the medial nucleus of the amygdala did not differ between groups. In contrast to c-fos, NGFI-A mRNA expression in the lateral nucleus of the amygdala was greater in the delayed-footshock group than the handled and context-no-footshock groups 15 min after the footshock. This elevation in NGFI-A mRNA was not seen in the immediate-footshock group. This suggests that NGFI-A mRNA in the lateral nucleus of the amygdala may play a role in Contextual Fear Conditioning.

  • Scopolamine selectively disrupts the acquisition of Contextual Fear Conditioning in rats.
    Neurobiology of learning and memory, 1995
    Co-Authors: Stephan G. Anagnostaras, Stephen Maren, Michael S. Fanselow
    Abstract:

    Muscarinic cholinergic antagonism produces learning and memory deficits in a variety of hippocampal-dependent tasks. Hippocampal lesions produce both acquisition deficits and retrograde amnesia for Contextual Fear Conditioning, but do not impact Fear Conditioning to discrete cues. In order to examine the effects of muscarinic antagonism in this paradigm, rats were given scopolamine (1 mg/kg) either before or for 3 days after a Pavlovian Fear-Conditioning session in which tones were paired with aversive footshocks. Fear to the context and the tone was assessed by measuring freezing in separate tests. It was found that pretraining, but not posttraining, scopolamine severely impaired Contextual Fear Conditioning; tone Conditioning was not affected under either condition (cf., Young, Bohenek, & Fanselow,Neurobiology of Learning and Memory,63,174–180, 1995).