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Results for “fear conditioning”

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At least 793 records · Page 44Linked to original sources
PubMed1989

Delta opioid antagonist, 16-Me cyprenorphine, selectively attenuates conditional fear- and DPDPE-induced analgesia on the formalin test.

The effects of 16-Me cyprenorphine (M80) on the antinociception produced by reexposing rats to a chamber associated with footshock (1 mA, 0.75 sec) 24 hr earlier was assessed with the formalin test. In Experiment 1, intracerebroventricular administration of M80 dose-dependently (0.5-8 micrograms) reversed conditional analgesia. Experiment 2 demonstrated that M80 (5 micrograms) had no effect on baseline pain sensitivity, but completely reversed conditional analgesia. Experiment 3 demonstrated that 0.25 micrograms DAGO, 3.5 micrograms DPDPE, and 28 micrograms U50,488H all produced equivalent levels of antinociception on the formalin test. The 5 micrograms dose of M80 completely reversed the antinociception produced by DPDPE but did not influence that produced by DAGO or U50,488H. These data suggest, that at the doses employed, M80 is a selective delta-opioid receptor antagonist and that delta-receptors are involved in conditional fear-induced analgesia.

3,4-Dichloro-N-methyl-N-(2-(1-pyrrolidinyl)-cycloh↗
PubMed1996

Effects of typical and atypical antipsychotic drugs on freezing behavior induced by conditioned fear.

A typical antipsychotic drugs (atypical APDs), such as clozapine, ORG5222, and olanzapine, have been suggested to possess anxiolytic activity in the conflict test and elevated plus-maze test, while several studies have suggested that typical APDs are not anxiolytic in several models of anxiety. We investigated the effects of typical and atypical APDs on the acquisition and expression of conditioned fear-induced freezing. Drugs were administered subcutaneously to male Sprague-Dawley rats 30 min before foot shock stress (the VI60s schedule, 2.5 mA for 30 min). Twenty-four hours after foot shock, freezing behavior of rats was observed in the shock chamber without shocks. The atypical APD clozapine (0.3-10 mg/kg) dose-dependently inhibited the acquisition of conditioned freezing. Candidates for atypical APDs, ORG5222 (0.1-1 mg/kg), olanzapine (1-10 mg/kg), and raclopride (3-30 mg/kg), also reduced the acquisition of conditioned freezing in a dose-dependent manner. Typical APDs, haloperidol (3 mg/kg), spiperone (0.1-1 mg/kg) and nemonapride (1 mg/kg) had significant inhibitory effects on the acquisition of conditioned freezing, but their effects were reduced at higher doses. Chlorpromazine, a typical APD, showed about 50% inhibition of the acquisition of conditioned freezing at the dose of 10 mg/kg, but did not reveal significant inhibition at any of the doses (3-30 mg/kg). The ED50S (mg/kg) for inhibiting the acquisition of conditioned freezing significantly correlated with the Ki values for D4 dopaminergic receptors, but not with the Ki values for other monoamine and acetylcholine receptors. On the other hand, clozapine or haloperidol did not change the expression of conditioned freezing. These results suggest that protective effects of clozapine and other antipsychotic drugs on the acquisition of conditioned freezing may be mediated by blockade of D4 receptors.

Animals↗
PubMed2000

Impairment of conditioned contextual fear of C57BL/6J mice by intracerebral injections of the NMDA receptor antagonist APV.

The effects of acute injections of the NMDA receptor antagonist APV on one-trial fear conditioning of C57BL/6J mice were investigated in a time, dose (0.4-3.2 microg) and region-specific manner. Conditioned fear was determined by the assessment of freezing and the computer-controlled measurement of inactivity. Additionally, conditioned heart rate responses were evaluated in the tone-dependent memory test performed in the home cage with the help of implanted ECG transmitters. Injections of APV into the dorsal hippocampus (i.h.) 15 min before training, impaired dose-dependent contextual fear conditioning without discrimination between contextual foreground (unsignaled shock) and background (signaled shock) conditioning as tested 24 h after training. Short-term memory analyzed 1 h after training was also impaired. The observation that a smaller dose of APV was required for intracerebroventricular than for i.h. injection to achieve a similar memory impairment, pointed to the involvement of extrahippocampal NMDA receptors. APV treatment did not affect conditioned tone-dependent fear as indicated by unchanged freezing and heart rate responses of the freely moving mice. The results indicated the contribution of hippocampal and extrahippocampal NMDA receptors to multisensory contextual information processing during acquisition.

Animals↗
PubMed2003

Inhibition of mRNA and protein synthesis in the CA1 region of the dorsal hippocampus blocks reinstallment of an extinguished conditioned fear response.

Memories are extinguished by the repeated presentation of a conditioned stimulus in the absence of an unconditioned stimulus to which it has been associated. It is believed that extinction establishes a new hierarchy of responses rather than an actual forgetting of the original response, which can usually reappear spontaneously after interruption of the extinction process. In this study, our aim was to analyze how profound extinction can be. Rats were trained in a one-trial, step-down inhibitory avoidance paradigm and then were exposed to several extinction sessions in which they were allowed to freely explore the apparatus for 30 sec after having stepped down. Extinction was complete enough so that there was no spontaneous recovery, and test session performance could not be enhanced by pharmacological agents with well known facilitative actions on retrieval. After being submitted to a new training session, control animals reacquired the avoidance response; however, animals failed to do so after receiving bilateral intra-CA1 infusions of either the protein synthesis inhibitor anisomycin or the mRNA synthesis blocker 5,6-dichloro-1-beta-d-ribofuranosyl benzimidazole 15 min before the retraining session. Our results indicate that extinction can be carried to a point at which reinstallment of the conditioned response requires, like the original learning, de novo gene expression and protein synthesis in the CA1 region of the dorsal hippocampus.

Animals↗
PubMed2006

Reinstatement of conditioned fear and the hippocampus: an attentional-associative model.

An existing attentional-associative model of classical conditioning [Schmajuk N, Lam Y, Gray JA. Latent inhibition: a neural network approach. J Exp Psychol: Anim Behav Process 1996;22:321-49] is applied to the description of reinstatement in animals and humans. According to the model, inhibitory associations between the context (CX) and unconditioned stimulus (US) are formed during extinction, which help preserve the association between the conditioned stimulus (CS) and the US. However, summation and retardation tests fail to reveal these associations because (a) the CX is not attended or (b) a CX-CS configural stimulus formed during extinction is both poorly attended and weakly active during testing. When US presentations and testing occur in the same context, reinstatement is the consequence of a decreased CX inhibition and the increased attention to the CS, which activates the remaining CS-US association. When US presentations occur in the context of extinction but the CS is tested in a different context, reinstatement results from an increased attention to the CS and the combination of CS-CX and CX-US excitatory associations. The assumption that associations between CSs are impaired following neurotoxic hippocampal lesions or in amnesia, is sufficient to describe absence of reinstatement in those cases. However, additional assumptions might be needed to describe the effect of hippocampal lesions on other postextinction manipulations.

Animals↗
PubMed2003

Isoflurane antagonizes the capacity of flurothyl or 1,2-dichlorohexafluorocyclobutane to impair fear conditioning to context and tone.

UNLABELLED: In animals, the conventional inhaled anesthetic, isoflurane, impairs learning fear to context and fear to tone, doing so at concentrations that produce amnesia in humans. Nonimmobilizers are inhaled compounds that do not produce immobility in response to noxious stimulation, nor do they decrease the requirement for conventional inhaled anesthetics. Like isoflurane, the nonimmobilizer 1,2-dichlorohexafluorocyclobutane (2N) impairs learning at concentrations less than those predicted from its lipophilicity to produce anesthesia. The capacity of the nonimmobilizer di-(2,2,2,-trifluoroethyl) ether (flurothyl) to affect learning and memory has not been studied. Both nonimmobilizers can cause convulsions. We hypothesized that if isoflurane, 2N, and flurothyl act by the same mechanism to impair learning and memory, their effects should be additive. We found that isoflurane, 2N, and flurothyl (each, alone) impaired learning fear to context and fear to tone in rats, with the nonimmobilizers doing so at concentrations less than those that cause convulsions. (Fear was defined by freezing [volitional immobility] in the presence of the conditioned stimulus [context or tone].) However, the combination of isoflurane and 2N or flurothyl produced an antagonistic rather than an additive effect on learning, a finding in conflict with our hypothesis. And flurothyl was no less potent than 2N (at least no less potent relative to the concentration of each that produced convulsions) in its capacity to impair learning. We conclude that conventional inhaled anesthetics and nonimmobilizers impair learning and memory by different mechanisms. The basis for this impairment remains unknown. IMPLICATIONS: Conventional inhaled anesthetics and nonimmobilizers are antagonistic in their effects on learning and memory, and this finding suggests that they impair learning and memory, at least in part, by different mechanisms.

Acoustic Stimulation↗
PubMed2001

Hippocampus and contextual fear conditioning: recent controversies and advances.

Dorsal hippocampal (DH) lesions produce a severe deficit in recently, but not remotely, acquired contextual fear without impairing memory of discrete training stimuli, i.e., DH lesions produce an anterograde and time-limited retrograde amnesia specific to contextual memory. These data are consistent with the standard model which posits temporary involvement of the hippocampus in recent memory maintenance. However, three recent controversies apparently weaken the case for a selective mnemonic role for the hippocampus in contextual fear. First, although retrograde amnesia (from posttraining lesions) is severe, anterograde amnesia (from pretraining lesions) may be mild or nonexistent. Second, a performance, rather than mnemonic, account of contextual freezing deficits in hippocampal-lesioned animals has been offered. Third, damage to the entire hippocampus, including the ventral hippocampus, can produce a dramatic and temporally stable disruption of context and tone fear. These data are reviewed and explanations are offered as to why they do not necessarily challenge the standard model of hippocampal memory function in contextual fear. Finally, a more complete description of the hippocampus' proposed role in contextual fear is offered, along with new data supporting this view. In summary, the data support a specific mnemonic role for the DH in the acquisition and consolidation of contextual representations.

Amnesia↗
PubMed2003

Opioid receptors regulate the extinction of Pavlovian fear conditioning.

Rats received a single pairing of an auditory conditioned stimulus (CS) with a footshock unconditioned stimulus (US). The fear (freezing) that had accrued to the CS was then extinguished. Injection of naloxone prior to this extinction significantly impaired the development of extinction. This impairment was mediated by opioid receptors in the brain and was not observed when naloxone was injected after extinction training. Finally, an injection of naloxone on test failed to reinstate extinguished responding that had already accrued to the CS. These experiments show that opioid receptors regulate the development, but not the expression, of fear extinction and are discussed with reference to the roles of opioid receptors in US processing, memory, and appetitive motivation.

Acoustic Stimulation↗