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PubMed1989

Sensory preconditioning and UCS inflation in human 'fear' conditioning.

This study describes a human electrodermal conditioning experiment involving processes of sensory preconditioning and UCS inflation. In stage 1 of the experiment Ss received six presentations of a CS+ paired with an innocuous 65 dB tone (UCS) and six presentations of an unpaired CS-. In stage 2, Ss in the experimental group had the aversiveness of the UCS inflated as the intensity of the 65 dB tone was increased to 115 dB. In stage 3, Ss were given test presentations of CS+ and CS-. A differential CR to CS+ was found only in stage 3 of the experiment and only in Ss who had experienced the UCS inflation procedure. These results suggest that (i) sensory preconditioning had occurred in stage 1 despite the failure to observe a differential CR in this stage, and (ii) the differential CR observed in stage 3 was mediated by an internal representation of the UCS whose aversiveness had been inflated in stage 2. As well as confirming that processes of sensory preconditioning and UCS inflation can be observed in human as well as animal Ss, these findings have important implications for contemporary conditioning models of clinical fears. In particular, they suggest that a contemporary conditioning model of acquired fears is not bound by the need to discover contiguous stimulus-trauma experiences in the histories of clinical phobias since, in humans at least, processes of stimulus association and UCS revaluation appear to be relatively independent.

Adolescent↗
PubMedDate not supplied

Cardiac arrhythmias in the monkey during classically conditioned fear and excitement.

Rhesus monkeys (Macaca mulatta) were tested in classic aversive and appetitive conditioning paradigms following complete coronary artery occlusion (CO) to test the hypothesis that "emotional stress" induces ventricular arrhythmias. Findings were based upon conditioning trials conducted for one or more weeks after occlusion in 13 animals. When all data from each animal for the week following CO were considered, there was no demonstrable tendency for arrhythmias to increase during "fear" conditioned to unavoidable electric shock or during "excitement" in anticipation of food. However, selected trials from six monkeys did reveal instances when changes in the frequency of occurrence of arrhythmias were coupled with behavioural conditioning. While analysis of these trials did not reveal any simple relationship between emotional stress and the development of ventricular arrhythmias after myocardial infarction, certain of the behavioral situations may be more potentially arrhythmogenic than others. For these selected trials, with respect to control, the number of arrhythmias may have increased or decreased upon presentation of the conditional stimulus; the exact response appears to depend upon the immediate physiologic status of the animal as well as on the behavioral condition. "More stressful" situations, such as aversive conditioning, are not necessarily associated with greater numbers of arrhythmias than were "less stressful" situations, such as appetitive conditioning. Arrhythmias appear to occur more frequently when an animal's heart rate is within a given range; this may reflect underlying cardiac sympathetic and parasympathetic nerve activity.

Animals↗
PubMedDate not supplied

Effects of conditioned fear stress on 5-HT release in the rat prefrontal cortex.

The effects of conditioned fear stress (CFS) on 5-HT release in the medial prefrontal cortex were studied by in vivo microdialysis. CFS (exposure to an environment in which foot-shock had been delivered previously) induced a marked suppression of motility-that is, freezing behavior. The extracellular concentration of 5-HT in the medial prefrontal cortex increased during this freezing behavior, but no significant changes were observed in the concentration of its metabolite, 5-HIAA. The increased 5-HT concentration returned to pretreatment levels when the animals were returned to their home cages. Diazepam (0.5 mg/kg, intraperitoneally) reduced the CFS-induced freezing behavior and prevented the increases in extracellular 5-HT levels. A 5-HT3 receptor antagonist, tropisetron (10 and 100 micrograms/kg), also inhibited both the CFS-induced increase in 5-HT release and the freezing behavior. These findings suggest that there is a relationship between anxiety and 5-HT release in the prefrontal cortex and that the 5-HT3 receptor antagonist tropisetron might have anxiolytic properties.

Animals↗
PubMed1996

Effect of conditioned fear stress on dopamine release in the rat prefrontal cortex.

The effects of conditioned fear stress (CFS) on dopamine release in the medial prefrontal cortex were studied by in vivo microdialysis in the rat. CFS (exposure to an environment in which foot-shock had been delivered previously) induced a marked suppression of motility, i.e., freezing behavior. Extracellular concentrations of dopamine in the medial prefrontal cortex were increased by CFS. The increase of dopamine returned to the pretreatment levels when rats were returned to the home cages. Diazepam (0.5 mg/kg, i.p.) suppressed both the CFS-induced freezing behavior and extracellular dopamine levels in the medial prefrontal cortex. These findings suggest that anxiety and dopamine release in the prefrontal cortex might be related.

Animals↗
PubMed1995

Effects of benzodiazepine microinjection into the amygdala or periaqueductal gray on the expression of conditioned fear and hypoalgesia in rats.

Four experiments studied the effects of an intracranial microinjection of a benzodiazepine (midazolam) on the expression of conditioned fear (measured as passive avoidance) and conditioned hypoalgesia in rats. Unilateral microinjection of midazolam into the basolateral amygdala reduced both hypoalgesic and avoidance responses, whereas unilateral microinjection of midazolam into the ventrolateral region of the periaqueductal gray (vlPAG) reduced the hypoalgesic response but not the avoidance response. The results are discussed in terms of gamma-aminobutyric acid-ergic inhibition of antinociceptive mechanisms in the vlPAG and of the activation of these mechanisms by amygdala-based fear processes.

Amygdala↗
PubMed2005

Effects of inactivation of serotonergic neurons of the median raphe nucleus on learning and performance of contextual fear conditioning.

Several studies have shown that the median raphe nucleus (MRN) is involved in anxiety. However, no study assessed the role of 5-HT mechanisms of MRN in both freezing and fear-potentiated startle (FPS) within a single form of conditioned learning. In this work we examined the effects of neurotoxic lesions of the MRN with NMDA on freezing and FPS of rats submitted to a contextual fear conditioning paradigm, in which they were tested in the same chamber where they received foot-shocks 24 h before. Compared to controls NMDA-injected rats showed a reduction of freezing and FPS in response to contextual cues. Next, we examined the effects of stimulation of 5-HT1A somatodendritic autoreceptors of the MRN with local injections of 8-OH-DPAT either before training or testing sessions conducted 2 or 24 h post-conditioning. Pre-training injections of 8-OH-DPAT intra-MRN reduced both freezing and FPS whereas post-training injections reduced only freezing to the aversive context without changing the FPS. Thus, freezing is easily disrupted by post-training MRN injections of 8-OH-DPAT while memory for FPS remained unchanged. It is proposed that the consolidation of contextual conditioned fear promoting freezing takes place through a slow mechanism of transference of information through 5-HT mechanisms of the MRN-hippocampus pathway. On the other hand, a rapid fear conditioning process operates for FPS, probably through other pathways.

8-Hydroxy-2-(di-n-propylamino)tetralin↗
PubMed2006

Prefrontal mechanisms in extinction of conditioned fear.

Interest in the medial prefrontal cortex (mPFC) as a source of behavioral inhibition has increased with the mounting evidence for a functional role of the mPFC in extinction of conditioned fear. In fear extinction, a tone-conditioned stimulus (CS) previously paired with a footshock is presented repeatedly in the absence of footshock, causing fear responses to diminish. Here, we review converging evidence from different laboratories implicating the mPFC in memory circuits for fear extinction: (1) lesions of mPFC impair recall of extinction under various conditions, (2) extinction potentiates mPFC physiological responses to the CS, (3) mPFC potentiation is correlated with extinction behavior, and (4) stimulation of mPFC strengthens extinction memory. These findings support Pavlov's original notion that extinction is new learning, rather than erasure of conditioning. In people suffering from posttraumatic stress disorder (PTSD), homologous areas of ventral mPFC show morphological and functional abnormalities, suggesting that extinction circuits are compromised in PTSD. Strategies for augmenting prefrontal function for clinical benefit are discussed.

Animals↗
PubMed2004

Footshock intensity and generalization in contextual and auditory-cued fear conditioning in the rat.

The relationship between US (footshock) intensity and the two conditioned freezing responses (to acoustic CS and to "context") was investigated in fear conditioning. Administered footshock intensity was 0.00, 0.15, 0.30, 0.60, 0.90, and 1.20 mA to six different groups of 70-day-old male Albino Wistar rats. To measure contextual freezing, the animals were again placed inside the conditioning apparatus without acoustic CS and US presentation. To measure acoustic CS freezing, the animals were placed in a totally different apparatus and only the acoustic CS was presented. The 0.15 mA footshock intensity was not sufficient to condition the animals, in fact no freezing was exhibited as in the non-shocked control group. The 0.30 mA footshock intensity was sufficient only to condition the animals to the acoustic CS, whereas the 0.60 mA was sufficient to condition the animals both to acoustic CS and to context. Footshock intensities (0.90 and 1.20 mA) did not elicit any significant increase in conditioned freezing for either acoustic CS or context but at the highest one the generalization phenomenon appeared (freezing in the different context before presentation of acoustic CS). Acoustic CS freezing to all over-threshold intensities was longer than that to context. In conclusion, freezing responses to acoustic CS and context after increasing footshock intensities follow distinct patterns, and intermediate footshock intensities (0.60 and 0.90 mA) appear to be the most useful for eliciting conditioned freezing responses to acoustic CS and to context without inducing a generalized fear status contamination.

Acoustic Stimulation↗
PubMed2006

Pharmacological dissociation of trace and long-delay fear conditioning in young rats.

In most studies comparing trace and delay conditioning, CS duration is kept constant across training conditions but the interstimulus interval (ISI), the time from CS onset to US onset, is confounded. In the infrequently used long-delay condition, however, ISI is kept constant across the trace and delay conditions but CS duration varies. A recent study reported that trace and long-delay fear conditioning have the same developmental trajectory, with both emerging later in development than standard-delay conditioning (). Past studies have shown that trace conditioning is mediated by the cholinergic system; given the parallel developmental emergence of trace and long-delay conditioning, the present study examined whether the cholinergic system also mediates long-delay conditioning. Two experiments, both involving Sprague-Dawley-derived rats and using freezing as a measure of learned fear, showed that the cholinergic system is critically involved in trace conditioning but is not involved in long-delay conditioning. Specifically, pre-training injections of the muscarinic receptor antagonist scopolamine impaired acquisition of a CS-US association in 32-day-old rats trained with a trace procedure but had no effect on rats this age trained with a long-delay procedure (Experiment 1). Similarly, pre-training injections of physostigmine, a cholinesterase inhibitor, enhanced acquisition of trace conditioning in 25-day-old rats but had no effect on long-delay conditioning in rats this age (Experiment 2). Taken together, the results indicate that despite the similarities between trace and long-delay conditioning in terms of developmental emergence and level of conditioned responding, they are mediated by different physiological systems.

Age Factors↗
PubMed2005

The cerebellum: synaptic changes and fear conditioning.

In addition to coordinating movement, the cerebellum participates in motor learning, emotional behavior, and fear memory. Fear learning is reflected in a change of autonomic and somatic responses, such as heart rate and freezing, elicited by a neutral stimulus that has been previously paired with a painful one. Manipulation of the vermis affects these responses, and its reversible inactivation during the consolidation period impairs fear memory. The neural correlate of cerebellar involvement in fear consolidation is provided by a behaviorally induced long-term increase of synaptic efficacy between parallel fibers and a Purkinje cell. Similar synaptic changes after fear conditioning are well documented in the amygdala and hippocampus, providing a link between emotional experiences and changes in neural activity. In addition, in hotfoot mice, with a primary deficiency of parallel fiber to Purkinje cell synapse, short- and long-term fear memories are affected. All these data support the idea that the cerebellum participates in fear learning. The functional interconnection of the vermis with hypothalamus, amygdala, and hippocampus suggests a more complex role of the cerebellum as part of an integrated network regulating emotional behavior.

Animals↗
PubMed1996

A comparison of contextual and generalized auditory-cue fear conditioning: evidence for similar memory processes.

A number of variables influence contextual, but not auditory-cue, fear conditioning. However, several of these variables (isolation, stimulus preexposure, retention interval, and age) affect generalized auditory-cue fear. More generalized fear was found when (a) rats were isolated in a novel environment than when returned to their home cages, (b) the retention interval was 3 hr rather than 24 hr, and (c) in 18-day-old compared with 25-day-old rats. Moreover, preexposure to the auditory cue eliminated the isolation effect. At a behavioral-psychological level, these variables may exert their effects by influencing the processes that construct a memory representation of the stimulus. At a neural systems level, they may influence processing carried out in the thalamo-corticoamygdaloid auditory pathway.

Age Factors↗
PubMed2003

Working memory and fear conditioning.

Previous studies of associative learning implicate higher-level cognitive processes in some forms of classical conditioning. An ongoing debate is concerned with the extent to which attention and awareness are necessary for trace but not delay eye-blink conditioning [Clark, R. E. & Squire, L. R. (1998) Science 280, 77-81; Lovibond, P. F. & Shanks, D. (2002) J. Exp. Psychol. Anim. Behav. Processes 28, 38-42]. In trace conditioning, a short interval is interposed between the termination of the conditioned stimulus (CS) and the onset of the unconditioned stimulus (US). In delay conditioning, the CS and US overlap. We here investigate the extent to which human classical fear conditioning depends on working memory. Subjects had to carry out an n-back task, requiring tracking an item 1 or 2 back in a sequentially presented list of numbers, while simultaneously being tested for their ability to associate auditory cues with shocks under a variety of conditions (single-cue versus differential; delay versus trace; no task versus 0-, 1-, and 2-back). Differential delay conditioning proved to be more resilient than differential trace conditioning but does show a reduction due to task interference similar in slope to that found in trace conditioning. Explicit knowledge of the stimulus contingency facilitates but does not guarantee trace conditioning. Only the single-cue delay protocol shows conditioning during the more difficult working memory task. Our findings suggest that the larger the cognitive demands on the system, the less likely conditioning occurs. A postexperimental questionnaire showed a positive correlation between conditioning and awareness for differential trace conditioning extinction.

Adolescent↗
PubMed2002

Fear conditioning in humans: the influence of awareness and autonomic arousal on functional neuroanatomy.

The degree to which perceptual awareness of threat stimuli and bodily states of arousal modulates neural activity associated with fear conditioning is unknown. We used functional magnetic neuroimaging (fMRI) to study healthy subjects and patients with peripheral autonomic denervation to examine how the expression of conditioning-related activity is modulated by stimulus awareness and autonomic arousal. In controls, enhanced amygdala activity was evident during conditioning to both "seen" (unmasked) and "unseen" (backward masked) stimuli, whereas insula activity was modulated by perceptual awareness of a threat stimulus. Absent peripheral autonomic arousal, in patients with autonomic denervation, was associated with decreased conditioning-related activity in insula and amygdala. The findings indicate that the expression of conditioning-related neural activity is modulated by both awareness and representations of bodily states of autonomic arousal.

Aged↗
PubMedDate not supplied

[C-fos topography in neocortical neurons of mice during fear conditioning].

Patterns of expression of c-Fos transcription factor in the motor (M1 and M2) and cingulate cortex (dorsal part, Cg1, RSA, and ventral part, PrL, Cg2, RSG) were analyzed after fear conditioning in 129 sv mice. Mice were exposed to the context and tone followed by electric footshock (footshock group, FG) or to context only (context group, CG). Control mice were taken from a home cage (HG). In the rostral part of the motor cortex the number of c-Fos-labeled neurons was the same in all the groups. It was increased in the rostrocaudal direction in FG and CG but not in HG mice. A higher level of c-Fos expression in FG (as compared to CG) was observed in the medial parts of the M1, in the caudal and medial parts of the M2, and in the dorsal but not ventral regions of the cingulate cortex. Thus, the rostrocaudal gradient of c-Fos expression was originally demonstrated in motor cortex of mice during learning.

Animals↗
PubMed2001

Nonconscious fear conditioning, visceral perception, and the development of gut feelings.

When people are presented with backward-masked images of fear-relevant stimuli and only some of these images are paired consistently with electric shocks, they can predict the occurrence of shocks even though they do not consciously know which images they have seen. We postulated that they may use the perception of visceral cues from the conditional fear response to facilitate the prediction of shocks. In this study, ability to detect heartbeats was used to index sensitivity to visceral cues. The results showed that subjects who could detect their heartbeats performed better than chance in predicting whether or not they would receive a shock during the conditioning task. The findings support the notion that hunches, or "gut feelings," are based in part on the perception of visceral cues.

Adolescent↗
PubMed2005

Trace fear conditioning depends on NMDA receptor activation and protein synthesis within the dorsal hippocampus of mice.

Various lesion studies demonstrated that trace but not delay fear conditioning requires an intact hippocampal formation. Our present study examined the role of NMDA receptor activation and protein synthesis within the dorsal hippocampus for acquisition of fear memories following trace (5-s trace) and delay conditioning. To this end male C57BL/6JOlaHsd mice were chronically implanted with guide cannulae targeting the dorsal hippocampus. Fifteen minutes before conditioning mice received a bilateral intrahippocampal injection of either the NMDA receptor antagonist AP5 (0.5 or 1 microg per 0.5 microl per side) or of anisomycin, an inhibitor of protein synthesis (62.5 microg per 0.5 microl per side). Control mice were treated with vehicle (Ringer's solution). Blocking NMDA receptors before trace but not delay conditioning dose-dependently attenuated the freezing response to the tone as assessed 24 h after conditioning. The same findings were obtained after blocking protein synthesis within the dorsal hippocampus. These data indicate that the hippocampus shows synaptic plasticity during trace conditioning that requires an activation of NMDA receptors and protein synthesis as prerequisites for the acquisition of fear memory.

Analysis of Variance↗
PubMed2000

Contextual fear conditioning is associated with an increase of acetylcholine release in the hippocampus of rat.

The effects of contextual fear conditioning on the release of acetylcholine (ACh) in the hippocampus of freely moving rats was assessed using microdialysis. Measures were carried out during both acquisition and retention testing (re-exposure to the conditioning chamber) and compared between animals that either received foot-shocks as unconditioned stimulus (conditioned group) or no foot-shocks (control group) during acquisition. Results showed that during acquisition, hippocampal ACh extracellular level was increased with respect to baseline but that this increase was of similar magnitude in both groups. By contrast, re-exposure to the conditioning chamber the day after (retention testing) produced a significantly greater increase in ACh extracellular level in the conditioned (that, otherwise, displayed conditioned freezing behavior to contextual cues), than in the control group (which displayed virtually no freezing). This enhanced hippocampal ACh release seems to result from the greater hippocampal processing of contextual stimuli in conditioned animals with respect to controls.

Acetylcholine↗
PubMed1992

N-methyl-D-aspartate receptor antagonist MK-801 impairs learning but not memory fixation or expression of classical fear conditioning in goldfish (Carassius auratus).

The amnestic effects of the noncompetitive antagonist MK-801 on visually mediated, classic fear conditioning in goldfish (Carassius auratus) was examined in 5 experiments. MK-801 was administered 30 min before the training session on Day 1 to look for anterograde amnestic effects, immediately after training to look for retrograde amnestic effects, and before the training or test session, or both, to look for state-dependence effects. The results showed that MK-801 produced anterograde amnesia at doses that did not produce retrograde amnesia or state dependency and did not impair the expression of conditioned or unconditioned branchial suppression responses (BSRs) to the conditioned stimulus. The results indicate that MK-801 disrupts the mechanism of learning of the conditioned stimulus-unconditioned stimulus relation. Evidence is also presented that the learning processes that are disrupted by MK-801 occur during the initial stage of BSR conditioning.

Animals↗