Search PubMed⌕ Search

SEARCH · Search PubMed

Results for “fear conditioning”

Search indexed PubMed citations on genomics, clinical trials, systematic reviews and public health. Explore titles, authors and supplied subject terms, then open the PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 235 records · Page 13Linked to original sources
PubMed2001

Memory consolidation of Pavlovian fear conditioning: a cellular and molecular perspective.

Pavlovian fear conditioning has emerged as a leading behavioral paradigm for studying the neurobiological basis of learning and memory. Although considerable progress has been made in understanding the neural substrates of fear conditioning at the systems level, until recently little has been learned about the underlying cellular and molecular mechanisms. The success of systems-level work aimed at defining the neuroanatomical pathways underlying fear conditioning, combined with the knowledge accumulated by studies of long-term potentiation (LTP), has recently given way to new insights into the cellular and molecular mechanisms that underlie acquisition and consolidation of fear memories. Collectively, these findings suggest that fear memory consolidation in the amygdala shares essential biochemical features with LTP, and hold promise for understanding the relationship between memory consolidation and synaptic plasticity in the mammalian brain.

Animals↗
PubMed1998

Contextual learning and cue association in fear conditioning in mice: a strain comparison and a lesion study.

Fear conditioning with electric shock (unconditioned stimulus, US) paired with tone cue (conditioned stimulus, CS) has been extensively applied in recent molecular neurobiological analysis of hippocampal dysfunction in mice because the context-dependent test phase of this learning paradigm is claimed to detect hippocampal impairment in a specific manner, whereas the cue-dependent test serves as a control situation independent of hippocampal function. These claims are based on hippocampal lesion studies performed with rats and have not been conclusively confirmed with mice with specific hippocampal lesion. Therefore, I investigated how hippocampal ibotenic acid lesion affects conditioned fear in mice. I confirm that extensive lesions localized to the hippocampus impair context-dependent learning but also show that, unlike in the original rat studies, the behavioral impairment is only partial. Furthermore, studying two inbred strains of mice (C57BL/6 and DBA/2) with highly different hippocampal function, I show that the presence or absence of CS during training may influence the mouse's ability to learn complex multiple contextual stimuli in a genotype-dependent manner. I conclude that performance at the 'context' test may be based on complex configural (hippocampal) learning but it can also be based on a more simple elemental (non-hippocampal) learning thus leading to potentially false-negative findings in the analysis of hippocampal dysfunction.

Acoustic Stimulation↗
PubMed1995

Effects of novelty and conditioned fear on small intestinal and colonic motility and behaviour in the rat.

Novelty and conditioned fear were used to investigate the effects of psychological stress on fasting small intestinal and colonic myoelectric activity and their relation with behaviour in freely moving rats fitted with bipolar electrodes on proximal jejunum and colon. Rats in both novelty and conditioned fear groups spent a 15 min session in a novel box, where only rats in the fear group received unescapable, repeated foot shock (10 x 6 s, 0.5 mA). Behaviour in groups reexposed to the box on day 1 or day 7 indicated a profound difference in emotional state. Conditioned fear rats remained largely immobile, while novelty rats displayed active exploratory behaviour. Behaviour during conditioned fear did not differ significantly between rats reexposed to the box either 1 or 7 days after foot shock, while novelty animals appeared more aroused on day 7. Conditioned fear on day 1 caused a significant increase in colonic spike burst frequency compared to basal values in the home cage. A smaller but significant increase was found in novelty rats. In groups tested after 7 days, both novelty and conditioned fear resulted in small increases in colonic burst frequency that did not differ significantly from each other. No effects were found on the incidence of the fasting jejunal Migrating Motility Complex. Defecation was see only in conditioned fear rats, but did not differ quantitatively between day 1 and day 7. We conclude that, in the rat, colonic myoelectric spike burst activity is highly responsive to psychological stress, while the fasting pattern of small intestinal activity is more resistant.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed2004

Effects of ibotenic acid lesions of the dorsal hippocampus on contextual fear conditioning in mice: comparison with mammillary body lesions.

The goals of the present study were to determine if ibotenic acid lesions of the dorsal hippocampus (dHPC) or of mammillary body (MB) of the hypothalamus would induce similar contextual conditioning deficit in a fear-conditioning paradigm, previously developed in mice [Eur. J. Neurosci. 12 (2000) 2575]. Results showed that ibotenic acid lesions of the dHPC or of the MB both induced severe deficits on contextual conditioning but spared auditory conditioning, as compared to controls. This study provides direct evidence for an involvement of dHPC neurones in contextual fear conditioning and is first to demonstrate an involvement of the MB in the mediation of contextual fear conditioning.

Acoustic Stimulation↗
PubMed2002

Involvement of the human cerebellum in fear-conditioned potentiation of the acoustic startle response: a PET study.

Fear-conditioned potentiation of the startle response was used to study the role of the cerebellum in associative learning of non-specific aversive reactions in healthy human subjects using PET. Prior PET scanning initially neutral light stimuli were paired with painful electric shocks (fear-conditioning phase). Four PET-scans each were performed with presentation of acoustic startle stimuli (T), fear-conditioned light stimuli (L) or acoustic stimuli paired with light (LT, potentation phase). As a measure of fear-conditioning subtraction of condition T from LT revealed an increase of regional cerebellar blood flow (rCBF) in the left cerebellar hemisphere. Subtraction of condition L from LT, as a measure of fear-conditioned potentiation, revealed an increase of rCBF in the medial cerebellum. Different parts of the cerebellum appear to be involved in this form of motor associative learning.

Acoustic Stimulation↗
PubMed2006

Ketamine administration disturbs behavioural and distributed neural correlates of fear conditioning in the rat.

The neurotransmitter glutamate and its associated receptors perform an important role in the brain circuitry underlying normal fear processing. The glutamate NMDA receptor, in particular, is necessary for the acquisition and recollection of conditioned-fear responses. Here the authors examine how acute blockage of the NMDA receptor with sub-anaesthetic doses of ketamine affects behavioural assays of fear-conditioned stress (e.g. freezing) and cFos expression in a network of brain areas that have previously been implicated in fear processing. Fear-conditioned rats displayed significantly more freezing behaviour than non-conditioned controls. In fear-conditioned rats that also received ketamine, this conditioning effect was largely neutralised. Fear conditioning also led to increased cFos expression in various areas central to fear processing, including the basolateral nucleus of the amygdala, the paraventricular nucleus of the hypothalamus and the anterior cingulate. Ketamine abolished such increases in cFos expression in most brain areas investigated. The present study therefore demonstrates that systemic ketamine administration in rats interferes with fear conditioning on a behavioural level and in a network of brain regions associated with fear and anxiety. The combination of ketamine and fear conditioning may therefore provide a useful model of abnormal fear processing, as observed in certain psychiatric conditions.

Analysis of Variance↗
PubMed1997

Type II glucocorticoid receptor antagonists impair contextual but not auditory-cue fear conditioning in juvenile rats.

There is evidence that glucocorticoids may play a role in learning and memory. To further explore this possibility, we examined the effect of the Type II glucocorticoid antagonists on contextual fear conditioning. This conditioning task is dependent on the hippocampal formation, a brain structure known to be rich in glucocorticoid receptors. Rats systemically injected with a Type II antagonist either 1 h prior to conditioning (RU 38486 and RU 40555) or immediately after conditioning displayed less contextual fear conditioning than rats injected with vehicle. Although RU impaired contextual fear conditioning, it had no effect on auditory fear conditioning. These data are consistent with other reports that contextual fear conditioning and auditory-cue fear conditioning depend on different processes and with the hypothesis that glucocorticoid activity contributes to the processes involved in the consolidation of some forms of memory.

Animals↗
PubMedDate not supplied

Pavlovian fear conditioning in mice anesthetized with halothane.

Pavlovian fear conditioning was employed to investigate learning during general anesthesia. Mice were given three CS-UCS presentations while anesthetized with halothane. The CS was a 10-s tone and the UCS a 0.4-mA shock delivered intramuscularly to the hindlimbs via needle electrodes. Anesthetized control groups received either CS only, UCS only, or CS followed by a 3-min delayed UCS. Strength of fear conditioning was assessed by measuring duration of suppression of drinking induced by tone presentation in a test session conducted 24 h after training. Results showed that mice trained under anesthesia exhibited a significant amount of conditioned suppression relative to the anesthetized control groups. These results show that Pavlovian fear conditioning can occur under halothane anesthesia.

Acoustic Stimulation↗
PubMed2004

Memory enhancement of classical fear conditioning by post-training injections of corticosterone in rats.

There is extensive evidence that post-training administration of the adrenocortical hormone corticosterone facilitates memory consolidation processes in a variety of contextual and spatial-dependent learning situations. The present experiments examine whether corticosterone can modulate memory of auditory-cue classical fear conditioning, a learning task that is not contingent on contextual or spatial representations. Male Sprague-Dawley rats received three pairings of a single-frequency auditory stimulus and footshock, followed immediately by a post-training subcutaneous injection of either corticosterone (1.0 or 3.0mg/kg) or vehicle. Retention was tested 24h later in a novel test chamber and suppression of ongoing motor behavior served as the measure of conditioned fear. Corticosterone dose-dependently facilitated suppression of motor activity during the 10-s presentation of the auditory cue. As corticosterone administration did not alter responding after unpaired presentations of tone and shock, tone alone, shock alone or absence of tone/shock, the findings indicated that corticosterone selectively facilitated memory of the tone-shock association. Furthermore, injections of corticosterone given 3h after training did not alter motor activity during retention testing, demonstrating that corticosterone enhanced time-dependent memory consolidation processes. These findings provide evidence that corticosterone modulates the consolidation of memory for auditory-cue classical fear conditioning and are consistent with a wealth of data indicating that glucocorticoids can modulate a wide variety of emotionally influenced memories.

Animals↗
PubMed2005

Lesions of the dorsal hippocampus block trace fear conditioned potentiation of startle.

Several studies show that the hippocampus is critical for the memories mediating trace and contextual fear conditioning. This study investigates whether N-methyl-D-aspartate-induced lesions of the dorsal hippocampus made prior to training affect context fear conditioning and trace fear conditioning measured with the fear-potentiated startle. Pretraining excitotoxic lesions of the dorsal hippocampus blocked acquisition of trace fear conditioning to a tone stimulus but did not affect context fear conditioning. These data indicate that without a dorsal hippocampus rats are unable to acquire trace conditioning but can acquire contextual fear when fear is measured by potentiation of the startle response.

Acoustic Stimulation↗
PubMed2000

Effect of the dopamine D(1/5) antagonist SCH 23390 on the acquisition of conditioned fear.

The authors previously reported that typical and atypical antipsychotic drugs inhibited the acquisition but not expression of conditioned fear. The present study examined the effects of the selective dopamine D(1/5) agonist (SKF 38393) and antagonist (SCH 23390) on the acquisition and expression of conditioned fear. Drugs were administered subcutaneously to male Sprague-Dawley rats 30 min before foot shock (2.5 mA for 5 min). Twenty-four hours after foot shock, rats were again placed and observed in the shock chamber without shocks (conditioned fear). Freezing behavior induced by conditioned fear, an index of anxiety or fear, was recorded using a time-sampling procedure. SCH 23390 (0.1-1 mg/kg) inhibited the acquisition of conditioned freezing. The administration of SCH 23390 at a dose of 0.1 mg/kg 30 min after foot shock did not affect conditioned freezing. Taken together, it is concluded that D(1/5) antagonism inhibits the acquisition of conditioned fear. SKF 38393 (3-20 mg/kg) failed to change the acquisition of conditioned fear. SCH 23390 or SKF 38393 administered prior to testing did not reduce the expression of conditioned fear. These results suggest that D(1/5) receptors may play a role in the development of fear or anxiety.

Animals↗
PubMed2006

Neurophysiological theory of kamin blocking in fear conditioning.

Kamin blocking in fear conditioning is thought to reflect diminished processing of the unconditional stimulus (US) in the presence of a conditional stimulus (CS-super(+)) that was previously paired with this US. According to Fanselow's (1998) hypothesis, the CS-super(+) drives output from the amygdala that ultimately produces analgesia by causing opiate release onto afferent pain circuits. This hypothesis was explored quantitatively through neurophysiological simulations. The results suggest that opiate-mediated, negative-feedback control of US processing is too slow for efficient blocking of cue conditioning. The reason is that conditioning-produced synaptic modifications can be induced before the opiate-mediated inhibition has any substantial effect on US processing. The results suggest the existence of an additional, faster-acting, inhibitory neurotransmitter in the blocking circuit.

Action Potentials↗
PubMed2000

Neurosteroids ameliorate conditioned fear stress: an association with sigma receptors.

Mice exhibited a marked suppression of motility (conditioned fear stress) when placed in an environment in which they had previously received an electric footshock. This conditioned fear stress response was dose-dependently attenuated by neurosteroids such as dehydroepiandrosterone sulfate (DHEAS; 25 and 50 mg/kg, s.c.) and pregnenolone sulfate (PREGS; 10-50 mg/kg, s.c.), and by a putative sigma(1) receptor agonist, (+)-N-allylnormetazocine ((+)-SKF-10,047; 3 and 6 mg/kg, s.c.). However, progesterone (PROG; 10-50 mg/kg, s.c. ) and allopregnanolone (5 and 20 mg/kg, s.c.) had no effect on this stress response. The attenuating effects of DHEAS (50 mg/kg, s.c.), PREGS (50 mg/kg, s.c.), and (+)-SKF-10,047 (6 mg/kg, s.c.) were reversed by NE-100 (5 mg/kg, i.p.), a sigma(1) receptor antagonist and PROG (5 or 10 mg/kg, i.p.). When DHEAS (25 mg/kg) was co-administered with (+)-SKF-10,047 (3 mg/kg) at doses that do not affect the conditioned fear stress response by themselves, motor suppression was significantly attenuated. In mice showing the conditioned fear stress response, the serum concentration of DHEAS was lower than that in non-shocked mice. These results suggest that the attenuating effects of DHEAS and PREGS on the conditioned fear stress response are mediated via sigma(1) receptors and that PROG has a sigma(1) receptor antagonistic property. Further, the endogenous DHEAS may be involved in the expression of conditioned fear stress response in mice.

Animals↗
PubMed2005

Withdrawal from chronic nicotine administration impairs contextual fear conditioning in C57BL/6 mice.

The effects of acute nicotine administration (0.09 mg/kg nicotine), chronic nicotine administration (6.3 mg/kg/d nicotine for 14 d), and withdrawal from chronic nicotine administration on fear conditioning in C57BL/6 mice were examined. Mice were trained using two coterminating conditioned stimulus (30 s; 85 dB white noise)--unconditioned stimulus (2 s; 0.57 mA foot shock) pairings and tested 24 h later for contextual and cued fear conditioning. Acute nicotine administration enhanced contextual fear conditioning, chronic nicotine administration had no effect on contextual fear conditioning, and withdrawal from chronic nicotine administration impaired contextual fear conditioning. Plasma nicotine concentrations were similar after acute and chronic treatment and were within the range reported for smokers. During withdrawal, concentrations of nicotine were undetectable. An acute dose of nicotine (0.09 mg/kg) during withdrawal from chronic nicotine treatment reversed withdrawal-associated deficits in contextual fear conditioning. The results suggest that tolerance to the effects of nicotine on contextual fear conditioning develops with chronic nicotine treatment at a physiologically relevant dose, and withdrawal from this chronic nicotine treatment is associated with impairments in contextual fear conditioning. These findings provide a model of how the effects of nicotine on learning may contribute to the development and maintenance of nicotine addiction.

Animals↗
PubMed2005

The effects of DHBE and MLA on nicotine-induced enhancement of contextual fear conditioning in C57BL/6 mice.

RATIONALE: Previous research indicates that nicotine administration enhances hippocampus-dependent forms of learning, including contextual fear conditioning. This effect is blocked by mecamylamine, a noncompetitive, broad-spectrum nicotinic receptor antagonist. OBJECTIVES: The present study extends previous research by further characterizing the nicotinic acetylcholinergic receptor (nAChR) subtypes through which nicotine acts to enhance contextual fear conditioning. METHODS: C57BL/6J mice were trained with two conditioned stimulus (CS; 30 s, 85-dB white noise)-unconditioned stimulus (US; 2 s, 0.57-mA foot shock) pairings and tested 24 h later for contextual and cued fear conditioning. The effects of the alpha7 nAChR antagonist methyllycaconitine (MLA; 1.00, 10.00, and 20.00 mg/kg) and the effects of the alpha4beta2 nAChR antagonist dihydro-beta-erythroidine (DHBE; 1.00, 3.00, and 6.00 mg/kg) on cued and contextual fear conditioning and on the enhancement of contextual fear conditioning by nicotine (0.25 mg/kg) were examined. RESULTS: We demonstrate that DHBE (all doses) administration attenuates the enhancing effect of nicotine on contextual fear conditioning, and MLA administration has no significant effect on the enhancement of contextual fear conditioning by nicotine. CONCLUSIONS: The data suggest that non-alpha7 nAChRs (most likely alpha4beta2 nAChRs) underlie the enhancement of contextual fear conditioning by nicotine.

Aconitine↗
PubMed2003

Ethanol disrupts fear conditioning in C57BL/6 mice.

Ethanol has been demonstrated to disrupt numerous forms of learning. For example, ethanol disrupts fear conditioning in rats. Surprisingly, the opposite result was reported for mice. Because of the importance of mouse models in ethanol research and the predominance of transgenic mice generated on a C57BL/6 background, the present study examined the effects of acute ethanol administration on fear conditioning in C57BL/6 mice. Fear conditioning was chosen because of the apparent contradiction in results between mice and rats, because of its popularity in assessing forebrain-dependent learning and because the task examines two types of learning: (i) the hippocampus-dependent contextual learning and (ii) the hippocampus-independent conditioned stimulus-unconditioned stimulus learning. Dose-response curves were generated for ethanol (0.5, 1.0 and 1.5 g/kg) given on either training day, testing day, or both days. Ethanol, in a dose-dependent manner, disrupted fear conditioning when given on training day or given on both training and testing days. Ethanol given on testing day only did not disrupt fear conditioning. The present results demonstrate that ethanol disrupts fear conditioning in C57BL/6 mice.

Animals↗