The Experts below are selected from a list of 23463 Experts worldwide ranked by ideXlab platform
Thomas J. Gould - One of the best experts on this subject based on the ideXlab platform.
-
The role of nicotinic acetylcholine receptors in the medial prefrontal cortex and hippocampus in trace Fear Conditioning.
Neurobiology of learning and memory, 2010Co-Authors: Jonathan D. Raybuck, Thomas J. GouldAbstract:Acute nicotine enhances multiple types of learning including trace Fear Conditioning but the underlying neural substrates of these effects are not well understood. Trace Fear Conditioning critically involves the medial prefrontal cortex and hippocampus, which both express nicotinic acetylcholine receptors (nAChRs). Therefore, nicotine could act in either or both areas to enhance trace Fear Conditioning. To identify the underlying neural areas and nAChR subtypes, we examined the effects of infusion of nicotine, or nicotinic antagonists dihydro-beta-erythroidine (DHβE: high-affinity nAChRs) or methyllycaconitine (MLA: low-affinity nAChRs) into the dorsal hippocampus, ventral hippocampus, and medial prefrontal cortex (mPFC) on trace and contextual Fear Conditioning. We found that the effects of nicotine on trace and contextual Fear Conditioning vary by brain region and nAChR subtype. The dorsal hippocampus was involved in the effects of nicotine on both trace and contextual Fear Conditioning but each task was sensitive to different doses of nicotine. Additionally, dorsal hippocampal infusion of the antagonist DHβE produced deficits in trace but not contextual Fear Conditioning. Nicotine infusion into the ventral hippocampus produced deficits in both trace and contextual Fear Conditioning. In the mPFC, nicotine enhanced trace but not contextual Fear Conditioning. Interestingly, infusion of the antagonists MLA or DHβE in the mPFC also enhanced trace Fear Conditioning. These findings suggest that nicotine acts on different substrates to enhance trace versus contextual Fear Conditioning, and that nicotine-induced desensitization of nAChRs in the mPFC may contribute to the effects of nicotine on trace Fear Conditioning.
-
Bupropion dose-dependently reverses nicotine withdrawal deficits in contextual Fear Conditioning.
Pharmacology biochemistry and behavior, 2007Co-Authors: George S. Portugal, Thomas J. GouldAbstract: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.
-
Coantagonism of Glutamate Receptors and Nicotinic Acetylcholinergic Receptors Disrupts Fear Conditioning and Latent Inhibition of Fear Conditioning.
Learning & memory (Cold Spring Harbor N.Y.), 2005Co-Authors: Thomas J. Gould, Michael C. LewisAbstract:The present study investigated the hypothesis that both nicotinic acetylcholinergic receptors (nAChRs) and glutamate receptors (alpha-amino-3-hydroxy-5-methyl-4-isoxazole propionate receptors (AMPARs) and N-methyl-d-aspartate glutamate receptors (NMDARs)) are involved in Fear Conditioning, and may modulate similar processes. The effects of the nAChR antagonist mecamylamine administered alone, the AMPAR antagonist NBQX administered alone, and the NMDAR antagonist MK-801 administered alone on cued Fear Conditioning, contextual Fear Conditioning, and latent inhibition of cued Fear Conditioning were examined. In addition, the effects of coadministration of either mecamylamine and NBQX or mecamylamine and MK-801 on these behaviors were examined. Consistent with previous studies, neither mecamylamine nor NBQX administered alone disrupted any of the tasks. However, coadministration of mecamylamine and NBQX disrupted both contextual Fear Conditioning and latent inhibition of cued Fear Conditioning. In addition, coadministration of mecamylamine with a dose of MK-801 subthreshold for disrupting either task disrupted both contextual Fear Conditioning and latent inhibition of cued Fear Conditioning. Coadministration of mecamylamine and NBQX, and coadministration of mecamylamine with a dose of MK-801 subthreshold for disrupting Fear Conditioning had little effect on cued Fear Conditioning. These results suggest that nAChRs and glutamate receptors may support similar processes mediating acquisition of contextual Fear Conditioning and latent inhibition of Fear Conditioning.
-
Nicotine enhances trace cued Fear Conditioning but not delay cued Fear Conditioning in C57BL/6 mice.
Behavioural brain research, 2004Co-Authors: Thomas J. Gould, Olivia Feiro, Dan MooreAbstract:Nicotine facilitates hippocampus-dependent contextual but not hippocampus-independent cued delay Fear Conditioning. To test if the effects of nicotine are specific to contextual Fear Conditioning or would extend to another hippocampus-dependent version of Fear Conditioning, we compared the effects of nicotine on cued delay and cued trace Fear Conditioning in male and female C57BL/6 mice. Unlike cued delay Fear Conditioning, cued trace Fear Conditioning is hippocampus dependent. Thus, if nicotine enhances hippocampus-dependent Fear Conditioning, nicotine should enhance trace Fear Conditioning. For both trace and delay Conditioning, five 30 s, 85 dB white noise conditioned stimuli (CS) were paired with five 2 s, 0.5 mA footshock unconditioned stimuli (US). In the trace paradigm, a 30-s period was inserted between CS offset and US onset. The CS and US co-terminated in the delay paradigm. Testing occurred 24 h later. The data indicate that nicotine (given on training and testing day) enhances trace but not delay cued Fear Conditioning. No sex differences were found. For delay cued Fear Conditioning a high level of freezing to the CS was found. Thus, a second experiment examined if the lack of enhancement of delay cued Fear Conditioning by nicotine was due to a ceiling effect. The CS duration was decreased to 15 s and only one CS-US pairing was used for delay and trace cued Fear Conditioning. Although overall levels of freezing to the cue were lower in the second experiment, nicotine still enhanced trace Fear Conditioning but did not enhance delay Fear Conditioning. Taken together, the results of the present experiments suggest that nicotine enhances hippocampus-dependent versions of Fear Conditioning.
-
Nicotine enhances contextual Fear Conditioning and ameliorates ethanol-induced deficits in contextual Fear Conditioning.
Behavioral neuroscience, 2003Co-Authors: Thomas J. Gould, Joel A. LommockAbstract:Nicotine and ethanol are 2 commonly used and abused drugs that have divergent effects on learning. The present study examined the effects of acute nicotine (0.25 mg/kg), ethanol (1.0 g/kg), and ethanol-nicotine coadministration on Fear Conditioning in C57BL/6 mice. Mice were assessed for contextual and cued Fear Conditioning at 1 day and 1 week posttraining. Ethanol disrupted acquisition but not consolidation of contextual Fear Conditioning; nicotine enhanced contextual Fear Conditioning and ameliorated ethanol-associated deficits in contextual Fear Conditioning. Mecamylamine antagonized this effect. Fear Conditioning was reassessed 1 week after initial testing with no drug administered. At the 1-week retest, mice previously treated with nicotine continued to show enhanced contextual Fear, and mice previously treated with ethanol continued to show contextual Fear deficits. Thus, nicotine both produces a long-lasting enhancement of contextual Fear Conditioning and protects against ethanol-associated deficits.
Ted Abel - One of the best experts on this subject based on the ideXlab platform.
-
Fear Conditioning increases NREM sleep.
Behavioral neuroscience, 2007Co-Authors: Kevin M. Hellman, Ted AbelAbstract:To understand the role that sleep may play in memory storage, the authors investigated how Fear Conditioning affects sleep-wake states by performing electroencephalographic (EEG) and electromyographic recordings of C57BL/6J mice receiving Fear Conditioning, exposure to Conditioning stimuli, or immediate shock treatment. This experimental design allowed us to examine the effects of associative learning, presentation of the Conditioning stimuli, and presentation of the unconditioned stimuli on sleep-wake states. During the 24 hr after training, Fear-conditioned mice had approximately 1 hr more of nonrapid-eye-movement (NREM) sleep and less wakefulness than mice receiving exposure to Conditioning stimuli or immediate shock treatment. Mice receiving Conditioning stimuli had more delta power during NREM sleep, whereas mice receiving Fear Conditioning had less theta power during rapid-eye-movement sleep. These results demonstrate that a single trial of Fear Conditioning alters sleep-wake states and EEG oscillations over a 24-hr period, supporting the idea that sleep is modified by experience and that such changes in sleep-wake states and EEG oscillations may play a role in memory consolidation.
-
sleep deprivation selectively impairs memory consolidation for contextual Fear Conditioning
Learning & Memory, 2003Co-Authors: Laurel A Graves, Elizabeth A Heller, Allan I Pack, Ted AbelAbstract:Many behavioral and electrophysiological studies in animals and humans have suggested that sleep and circadian rhythms influence memory consolidation. In rodents, hippocampus-dependent memory may be particularly sensitive to sleep deprivation after training, as spatial memory in the Morris water maze is impaired by rapid eye movement sleep deprivation following training. Spatial learning in the Morris water maze, however, requires multiple training trials and performance, as measured by time to reach the hidden platform is influenced by not only spatial learning but also procedural learning. To determine if sleep is important for the consolidation of a single-trial, hippocampus-dependent task, we sleep deprived animals for 0–5 and 5–10 h after training for contextual and cued Fear Conditioning. We found that sleep deprivation from 0–5 h after training for this task impaired memory consolidation for contextual Fear Conditioning whereas sleep deprivation from 5–10 h after training had no effect. Sleep deprivation at either time point had no effect on cued Fear Conditioning, a hippocampus-independent task. Previous studies have determined that memory consolidation for Fear Conditioning is impaired when protein kinase A and protein synthesis inhibitors are administered at the same time as when sleep deprivation is effective, suggesting that sleep deprivation may act by modifying these molecular mechanisms of memory storage.
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, 2020Co-Authors: Márcio Braga De Melo, Vanessa Manchim Favaro, Maria Gabriela Menezes OliveiraAbstract: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.
-
Effects of pre- or post-training entorhinal cortex AP5 injection on Fear Conditioning
Physiology & behavior, 2005Co-Authors: Eduardo Ekman Schenberg, Juliana Carlota Kramer Soares, Maria Gabriela Menezes OliveiraAbstract:Abstract Fear Conditioning is one of the most studied paradigms to assess the neural basis of emotional memory. The circuitry involves NMDA receptor activation in the amygdala and, in the case of contextual Conditioning, in the hippocampus. Entorhinal cortex is one of the major input/output structures to the hippocampus and also projects to the amygdala, both through glutamatergic transmission. Other learning tasks involving hippocampus and amygdala, such as inhibitory avoidance, require entorhinal cortex during acquisition and consolidation. However, the involvement of NMDA receptors mediated transmission in entorhinal cortex in Fear Conditioning acquisition and consolidation is not clear. To investigate that issue, rats were trained in Fear Conditioning to both contextual and tone conditioned stimulus. Immediately before, immediately, 30 or 90 min after training they received NMDA antagonist AP5 or saline injections bilaterally in the entorhinal cortex (AP—6.8 mm, L ± 5.0 mm DV—6.8 mm). Contextual Fear Conditioning was measured 24 h after training, and tone Fear Conditioning 48 h after training. AP5 injections selectively impaired contextual Fear Conditioning only when injected pre-training. Post-training injections had no effect. These findings suggest that entorhinal cortex NMDA receptors are necessary for acquisition, but not for consolidation, of contextual Fear Conditioning. On the other hand, both acquisition and consolidation of tone Fear Conditioning seem to be independent of NMDA receptors in the entorhinal cortex.
-
Effects of dorsal striatum lesions in tone Fear Conditioning and contextual Fear Conditioning.
Brain research, 2003Co-Authors: Tatiana L. Ferreira, Karin M. Moreira, Daniela C. Ikeda, Orlando Francisco Amodeo Bueno, Maria Gabriela Menezes OliveiraAbstract: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.
-
pavlovian Fear Conditioning as a behavioral assay for hippocampus and amygdala function cautions and caveats
European Journal of Neuroscience, 2008Co-Authors: Stephen MarenAbstract:Pavlovian Fear Conditioning has become an important model for investigating the neural substrates of learning and memory in rats, mice and humans. The hippocampus and amygdala are widely believed to be essential for Fear Conditioning to contexts and discrete cues, respectively. Indeed, this parsing of function within the Fear circuit has been used to leverage Fear Conditioning as a behavioral assay of hippocampal and amygdala function, particularly in transgenic mouse models. Recent work, however, blurs the anatomical segregation of cue and context Conditioning and challenges the necessity for the hippocampus and amygdala in Fear learning. Moreover, nonassociative factors may influence the performance of Fear responses under a variety of conditions. Caution must therefore be exercised when using Fear Conditioning as a behavioral assay for hippocampal- and amygdala-dependent learning. When Estes and Skinner described the Conditioning of ‘anxiety’ in rats in 1941 (Estes & Skinner, 1941), they did not foresee that rodent models of aversive Conditioning would become one of the most ubiquitous behavioral paradigms to explore the neural substrates of learning and memory. Indeed, Pavlovian Fear Conditioning has become part of the standard arsenal of behavioral tasks used to interrogate the mnemonic capacities of rats, mice and humans. In Fear Conditioning, neutral stimuli (conditional stimuli or CSs) such as tones, lights, or places (contexts) are arranged to predict aversive outcomes such as footshock (an unconditional stimulus or US). After Conditioning, CSs come to evoke learned Fear responses (conditional responses or CRs) such as conditioned suppression, freezing and tachycardia. The explosion of scientific papers on this topic indexes the popularity of Fear Conditioning. A search of the Institute for Scientific Information Web of Science database reveals an enormous and exponential growth in publications on Fear Conditioning from a total of 17 papers in 1977, 12 papers in 1987, 138 papers in 1997 and 381 papers in 2007. The search terms were ‘Fear Conditioning’, ‘conditioned Fear’, ‘conditioned suppression’, ‘conditioned freezing’, or ‘Fear-potentiated startle’. The search revealed a total of 4207 hits over the history of the database
-
neurobiology of pavlovian Fear Conditioning
Annual Review of Neuroscience, 2001Co-Authors: Stephen MarenAbstract:▪ Abstract Learning the relationships between aversive events and the environmental stimuli that predict such events is essential to the survival of organisms throughout the animal kingdom. Pavlovian Fear Conditioning is an exemplar of this form of learning that is exhibited by both rats and humans. Recent years have seen an incredible surge in interest in the neurobiology of Fear Conditioning. Neural circuits underlying Fear Conditioning have been mapped, synaptic plasticity in these circuits has been identified, and biochemical and genetic manipulations are beginning to unravel the molecular machinery responsible for the storage of Fear memories. These advances represent an important step in understanding the neural substrates of a rapidly acquired and adaptive form of associative learning and memory in mammals.
-
scopolamine and pavlovian Fear Conditioning in rats dose effect analysis
Neuropsychopharmacology, 1999Co-Authors: Stephan G. Anagnostaras, Jennifer R Sage, Stacy Goodrich, Stephen Maren, Michael S. FanselowAbstract:Muscarinic-cholinergic antagonism produces learning and memory deficits in a wide variety of hippocampal-dependent tasks. Hippocampal lesions produce both acquisition deficits and retrograde amnesia of contextual Fear (Fear of the place of Conditioning), but do not impact Fear Conditioning to discrete cues (such as a tone). In order to examine the effects of muscarinic antagonism in this paradigm, rats were given 0.01 to 100 mg/kg of scopolamine (or methylscopolamine) either before or after a Fear Conditioning session in which tones were paired with aversive footshocks. Fear to the context and the tone were assessed by measuring freezing in separate tests. It was found that pretraining, but not post-training, scopolamine severely impaired Fear Conditioning; methylscopolamine was ineffective in disrupting Conditioning. Although contextual Fear Conditioning was more sensitive to cholinergic disruption, high doses of scopolamine also disrupted tone Conditioning. Scopolamine did not affect footshock reactivity, but did produce high levels of activity. However, hyperactivity was not directly responsible for deficits in Conditioning. It was concluded that scopolamine disrupts CS-US association formation or CS processing, perhaps through an attenuation of hippocampal theta rhythm.
-
Scopolamine selectively disrupts the acquisition of contextual Fear Conditioning in rats.
Neurobiology of learning and memory, 1995Co-Authors: Stephan G. Anagnostaras, Stephen Maren, Michael S. FanselowAbstract: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).
Michael S. Fanselow - One of the best experts on this subject based on the ideXlab platform.
-
The place of the hippocampus in Fear Conditioning.
European journal of pharmacology, 2003Co-Authors: Matthew J Sanders, Brian J Wiltgen, Michael S. FanselowAbstract:Pavlovian Fear Conditioning is a phenomenon amenable to laboratory analysis of the neurobiology of Fear and the investigation of neural mechanisms of learning and memory. Investigators have made much progress in delineating the neurocircuitry and neurochemistry of Fear Conditioning. The place of the hippocampus in context Fear remains a controversial issue. In this review, we examine the evidence that the hippocampus plays a role in Fear Conditioning. We then critically examine hypotheses concerning its exact role in learning and memory for cued and context Fear Conditioning.
-
scopolamine and pavlovian Fear Conditioning in rats dose effect analysis
Neuropsychopharmacology, 1999Co-Authors: Stephan G. Anagnostaras, Jennifer R Sage, Stacy Goodrich, Stephen Maren, Michael S. FanselowAbstract:Muscarinic-cholinergic antagonism produces learning and memory deficits in a wide variety of hippocampal-dependent tasks. Hippocampal lesions produce both acquisition deficits and retrograde amnesia of contextual Fear (Fear of the place of Conditioning), but do not impact Fear Conditioning to discrete cues (such as a tone). In order to examine the effects of muscarinic antagonism in this paradigm, rats were given 0.01 to 100 mg/kg of scopolamine (or methylscopolamine) either before or after a Fear Conditioning session in which tones were paired with aversive footshocks. Fear to the context and the tone were assessed by measuring freezing in separate tests. It was found that pretraining, but not post-training, scopolamine severely impaired Fear Conditioning; methylscopolamine was ineffective in disrupting Conditioning. Although contextual Fear Conditioning was more sensitive to cholinergic disruption, high doses of scopolamine also disrupted tone Conditioning. Scopolamine did not affect footshock reactivity, but did produce high levels of activity. However, hyperactivity was not directly responsible for deficits in Conditioning. It was concluded that scopolamine disrupts CS-US association formation or CS processing, perhaps through an attenuation of hippocampal theta rhythm.
-
Scopolamine selectively disrupts the acquisition of contextual Fear Conditioning in rats.
Neurobiology of learning and memory, 1995Co-Authors: Stephan G. Anagnostaras, Stephen Maren, Michael S. FanselowAbstract: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).
