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Results for “fear conditioning”

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PubMed2005

Deficient fear conditioning in psychopathy: a functional magnetic resonance imaging study.

CONTEXT: Psychopaths belong to a larger group of persons with antisocial personality disorder and are characterized by an inability to have emotional involvement and by the repeated violation of the rights of others. It was hypothesized that this behavior might be the consequence of deficient fear conditioning. OBJECTIVE: To study the cerebral, peripheral, and subjective correlates of fear conditioning in criminal psychopaths and healthy control subjects. DESIGN: An aversive differential pavlovian delay conditioning paradigm with slides of neutral faces serving as conditioned and painful pressure as unconditioned stimuli. SETTING: The Department of Medical Psychology at the University of Tübingen, Tübingen, Germany. PARTICIPANTS: Ten male psychopaths as defined by the Hare Psychopathy Checklist-Revised and 10 age- and education-matched healthy male controls. The psychopaths were criminal offenders on bail and waiting for their trial or were on parole. The healthy controls were recruited from the community. MAIN OUTCOME MEASURES: Brain activation based on functional magnetic resonance imaging, electrodermal responses, emotional valence, arousal, and contingency ratings. RESULTS: The healthy controls showed enhanced differential activation in the limbic-prefrontal circuit (amygdala, orbitofrontal cortex, insula, and anterior cingulate) during the acquisition of fear and successful verbal and autonomic conditioning. The psychopaths displayed no significant activity in this circuit and failed to show conditioned skin conductance and emotional valence ratings, although contingency and arousal ratings were normal. CONCLUSION: This dissociation of emotional and cognitive processing may be the neural basis of the lack of anticipation of aversive events in criminal psychopaths.

Adult↗
PubMed2000

Pretraining exposure to physiologically patterned electromagnetic stimulation attenuates fear-conditioned analgesia.

The effect of weak electromagnetic stimulation on the emergence of conditioned analgesia was examined in the adult rat. Subjects were conditioned to associate a continuous 20 kHz ultrasonic tone (CS) with 0.2 mA footshock (UCS-) over five successive days. For 30 min either before or after conditioning sessions, rats were exposed to sham or pulsed (primed burst potentiation) magnetic fields (500 nT). At the end of the conditioning phase, all animals were evaluated for anticipatory analgesia following CS presentation using a hotplate analgesiometer. Data analysis suggested a statistically significant attenuation of fear-conditioned analgesia in rats exposed to electromagnetic stimulation prior to conditioning, whereas post-conditioning exposure potentiated the reduction in pain sensitivity compared to baseline measures. The present results suggest that the emergence of fear-conditioned responses is sensitive to whole body exposure to a magnetic field pattern that has been shown to induce long-term potentiation in hippocampal slices.

Analgesia↗
PubMed1998

Human amygdala activation during conditioned fear acquisition and extinction: a mixed-trial fMRI study.

Echoplanar functional magnetic resonance imaging (fMRI) was used in normal human subjects to investigate the role of the amygdala in conditioned fear acquisition and extinction. A simple discrimination procedure was employed in which activation to a visual cue predicting shock (CS+) was compared with activation to another cue presented alone (CS-). CS+ and CS- trial types were intermixed in a pseudorandom order. Functional images were acquired with an asymmetric spin echo pulse sequence from three coronal slices centered on the amygdala. Activation of the amygdala/periamygdaloid cortex was observed during conditioned fear acquisition and extinction. The extent of activation during acquisition was significantly correlated with autonomic indices of conditioning in individual subjects. Consistent with a recent electrophysiological recording study in the rat (Quirk et al., 1997), the profile of the amygdala response was temporally graded, although this dynamic was only statistically reliable during extinction. These results provide further evidence for the conservation of amygdala function across species and implicate an amygdalar contribution to both acquisition and extinction processes during associative emotional learning tasks.

Adolescent↗
PubMed2000

Acquisition deficit and time-dependent retrograde amnesia for contextual fear conditioning in agmatine-treated rats.

Cumulative evidence indicates that the hippocampus plays a time-limited role in contextual learning paradigms. Pharmacological studies have indicated that acquisition of background contextual cues during Pavlovian fear conditioning is dependent upon hippocampal function, whereas early inactivation of the hippocampus after training produces retrograde amnesia. When administered prior to contextual fear conditioning, agmatine (5 and 10 mg/kg, i.p.), an endogenous polyamine and N-methyl-D-aspartate (NMDA) receptor ligand found at excitatory synapses in the hippocampus, impaired the acquisition of contextual fear (measured as defensive freezing 26 hours later) without a reduction in baseline motor activity during training. Furthermore, ascending doses of agmatine were found not to exert analgesic effects on response thresholds to peripheral shock. This negated the possibility that the observed learning deficit resulted from a difference in perceived shock intensity. Post-training agmatine treatment produced a time-dependent impairment of consolidation, with subjects approaching a level of fear equivalent to that of a reference group as the delay of treatment increased (up to 6 hours). Since physiologically high levels of agmatine are able to inhibit NMDA receptor activity, these results suggest that polyamine modulation of NMDA receptors, most likely within the hippocampus, is required for the acquisition and consolidation of contextual fear stimuli.

Agmatine↗
PubMed2006

Fear but not awareness predicts enhanced sensory processing in fear conditioning.

It is not clear whether enhanced cortical processing of reinforced stimuli as reported by neuroimaging studies is due to expectancy of an aversive event alone or to activation of the fear system. The present study investigated cortical and autonomic responses of aware participants using an instructed fear conditioning design. Steady-state visual evoked fields (ssVEF) and heart rate change were recorded to assess sensory processing and activation of the fear system by reinforced (CS+) and nonreinforced stimuli (CS-). Participants who showed heart rate acceleration demonstrated increased ssVEFs in visual and parietal cortex during CS+ in acquisition trials. Heart rate decelerators did not show enhanced cortical activation with respect to the CS+. Participants in both groups reported awareness of CS-US contingencies. Awareness of stimulus contingency in fear conditioning seems not to be sufficient to elicit enhanced visual cortical processing.

Adult↗
PubMed2003

An 8-day extensive elemental, but not contextual, fear conditioning potentiates hippocampal-lateral septal synaptic efficacy in mice.

Previous findings have suggested a critical role for hippocampal-lateral septal (HPC-LS) synaptic transmission in the modulation of elemental vs. contextual fear conditioning. Pharmacologically- or electrophysiologically-induced increases in HPC-LS neurotransmission were shown to be associated with both an increase in elemental and a decrease in contextual fear conditioning. However, elemental conditioning, induced by an unconditional stimulus (US) that was explicitly paired with a simple conditional stimulus (CS), did not result in any change in this neurotransmission when two tone CS-footshock US pairings were provided. The present experiment was thus designed to investigate directly, in mice, whether extensive elemental conditioning (repeated CS-US pairings) could induce an increase in HPC-LS neurotransmission. For that purpose, over 8 days, an elemental conditioning group was repeatedly submitted to CS-US pairings in either one context (A) or another (B) depending on the training day. Hence, whichever the context, the tone CS was the relevant predictive stimulus for the occurrence of the footshock US. In contrast, a contextual conditioning group was submitted to the same regimen except that the US was delivered only in context A and was never paired with the CS, making, thereby, the context A the relevant predictor for the US regardless of the occurrence of the tone CS. Results show that during re-exposure of the animals to either context A or B, a significant increase in HPC-LS neurotransmission was selectively associated with the repeated elemental conditioning. This study supports the idea that changes in HPC-LS neurotransmission may modulate the strength of simple CS-US associations, and suggests that alterations of hippocampal functioning might be involved.

Animals↗
PubMed1992

Associative regulation of Pavlovian fear conditioning: unconditional stimulus intensity, incentive shifts, and latent inhibition.

Conditional stimuli (CS) associated with painful unconditional stimuli (US) produce a naloxone-reversible analgesia. The analgesia serves as a negative-feedback regulation of fear conditioning that can account for the impact of US intensity and CS predictiveness on Pavlovian fear conditioning. In Experiment 1 training under naloxone produced learning curves that approached the same high asymptote despite US intensity. Shifting drug treatment during acquisition had effects that paralleled US intensity shifts. In Experiment 3 naloxone reversed Hall-Pearce (1979) negative transfer using a contextual CS, indicating that conditional analgesia acquired during the CS-weak-footshock phase retards acquisition in the CS-strong-footshock phase. Experiment 5 used a tone CS in both a latent-inhibition and a negative-transfer procedure. Only negative transfer was blocked by naloxone. Therefore, negative transfer but not latent inhibition is mediated by a reduction of US processing.

Animals↗
PubMed1997

Functional inactivation of the lateral and basal nuclei of the amygdala by muscimol infusion prevents fear conditioning to an explicit conditioned stimulus and to contextual stimuli.

The GABAa agonist, muscimol (0.5 microgram in 0.5 microliter saline), or vehicle was infused into the lateral and basal amygdala nuclei prior to fear conditioning or testing in rats. Rats given muscimol before conditioning and saline before testing showed much less freezing to the conditioned stimulus (CS) and the context than did controls given saline before training and testing. Rats given saline before training and muscimol prior to testing also showed low levels of freezing to the CS and the context. In follow-up procedures, rats with acquisition initially blocked by pretraining muscimol infusions froze in a manner similar to that of controls when retrained and retested with saline infusions. Rats trained with saline but tested with muscimol presumably became conditioned but could express the learning. When retested with saline, they froze in the same manner as controls. Thus, activity in the lateral and basal amygdala appears to play an essential role in the acquisition and expression of fear conditioning.

Amygdala↗
PubMed2004

Long-term synaptic changes induced in the cerebellar cortex by fear conditioning.

To better understand learning mechanisms, one needs to study synaptic plasticity induced by behavioral training. Recently, it has been demonstrated that the cerebellum is involved in the consolidation of fear memory. Nevertheless, how the cerebellum contributes to emotional behavior is far from known. In cerebellar slices at 10 min and 24 hr following fear conditioning, we found a long-lasting potentiation of the synapse between parallel fibers and Purkinje cells in vermal lobules V-VI, but not in the climbing fiber synapses. The mechanism is postsynaptic, due to an increased AMPA response. In addition, in hotfoot mice with a primary deficiency of the parallel fiber to Purkinje cell synapse, cued (but not contextual) fear conditioning is affected. We propose that this synapse plays an important role in the learned fear and that its long-term potentiation may represent a contribution to the neural substrate of fear memory.

Animals↗
PubMedDate not supplied

Prenatal cocaine effects on fear conditioning: exaggeration of sex-dependent context extinction.

Prenatal cocaine exposure results in deficits in sensory preconditioning, discrimination reversal, and spatial navigation, tasks that require input from the hippocampus. However, there are no previous studies concerning prenatal cocaine effects on contextual fear conditioning, another hippocampal-dependent task. The present experiments tested whether chronic subcutaneous administration of 40 mg/kg of cocaine HCl to pregnant rats, from gestational day (GD) 8 through 20 would lead to disruption of contextual fear conditioning in adult male and female offspring. Offspring of saline-injected/pair-fed and untreated dams served as controls. Experiment 1 used a one-trial context conditioning preparation. Rats received a 2-s, 1-mA footshock in either the test context or a novel context, or received no shock on the day prior to the no-shock test. Defecation and freezing were measures of fear. Experiment 2 used a multiple measures protocol to optimize detection of prenatal treatment effects and was preceded by an open-field test. Rats received a 2-s, 0.8-mA footshock or no shock once daily over 4 days of conditioning. During 3 days of extinction, access to an adjacent chamber enabled the observation of four additional measures of fear: side crossing, latency, nose crossing, and side-differential. There were gender-dependent effects of conditioning on freezing and the four added measures of fear. Males showed higher levels of context conditioning and extinguished more slowly than females. The measures of nose crossing and side-differential revealed that prenatal cocaine exposure exaggerated gender-specific effects of context conditioning. The effects of prenatal cocaine exposure on context extinction are sexually dimorphic.

Animals↗
PubMed2001

Patterns of Fos expression in the amygdala and ventral perirhinal cortex induced by training in an olfactory fear conditioning paradigm.

The activation of amygdaloid nuclei, the ventral perirhinal cortex (vPRh), and several other brain areas in the rat during the acquisition and expression of olfactory fear conditioning was assessed through Fos immunocytochemistry in 3 separate experiments. The results of Experiment 1 suggest that olfactory and somatosensory inputs may functionally converge in the anterior region ot the medial nucleus (aMe). The results of Experiment 2 indicate that the aMe exhibited significantly greater Fos-like immunoreactivity (FLI) in subjects acquiring conditioned stimulus-unconditioned stimulus associations than in those presented with the same olfactory and somatosensory stimuli in a manner that precluded acquisition. The results of Experiment 3 indicate that the vPRh appeared to exhibit learning-related increases in FLI during the expression of previously acquired associations. Collectively, these data suggest that the aMe and vPRh may be critically involved in different aspects of olfactory fear conditioning.

Amygdala↗
PubMed2000

Conditioned fear to environmental context: cardiovascular and behavioral components in the rat.

This study compares the time course of the cardiovascular changes (mean arterial blood pressure, heart rate) and behavioral changes (freezing, rearing, grooming and activity) evoked by 30 min long exposures to a footshock chamber before and after conditioning with footshocks. The main finding is that the conditioned fear evoked by re-exposure to the footshock chamber after conditioning is associated with a prolonged freezing response, a marked rise in mean arterial pressure (+35 mm Hg above a resting baseline of 105 mm Hg) and a delayed rise in heart rate. The pattern of behavioral and cardiovascular changes is the same as with conditioned fear to a discrete stimulus but the effect is a lot longer.

Animals↗
PubMedDate not supplied

Overexpression of hAPPswe impairs rewarded alternation and contextual fear conditioning in a transgenic mouse model of Alzheimer's disease.

One of the hallmarks of the pathology in Alzheimer's disease is the deposition of amyloid plaques throughout the brain, especially within the hippocampus and amygdala. Transgenic mice that overexpress the Swedish mutation of human amyloid precursor protein (hAPPswe; Tg2576) show age-dependent memory deficits in hippocampus-dependent learning tasks. However, the performance of aged Tg2576 mice in amygdala-dependent learning tasks has not been thoroughly assessed. We trained young (2-4 mo) and old (16-18 mo) Tg2576 and wild-type mice in a T-maze alternation task (hippocampus-dependent) and a Pavlovian fear-conditioning task (amygdala- and hippocampus-dependent). As previously reported, old Tg2576 mice showed impaired acquisition of rewarded alternation; none of these mice reached the criterion of at least five out of six correct responses over three consecutive days. In contrast, old Tg2576 mice showed normal levels of conditional freezing to an auditory conditional stimulus (CS) and acquired a contextual discrimination normally. However, when the salience of the fear-conditioning context was decreased, old (12-14 mo) Tg2576 mice were impaired at acquiring fear to the conditioning context, but not to the tone CS. Histological examination of a subset of the mice verified the existence of amyloid plaques in the cortex, hippocampus, and amygdala of old, but not young, Tg2576 mice. Hence, learning and memory deficits in old Tg2576 mice are limited to hippocampus-dependent tasks, despite widespread amyloid deposition in cortex, hippocampus, and amygdala.

Age Factors↗
PubMed1998

Anterograde effects of a single electroconvulsive shock on inhibitory avoidance and on cued fear conditioning.

A single electroconvulsive shock (ECS) or a sham ECS was administered to male 3-4-month-old Wistar rats 1, 2, and 4 h before training in an inhibitory avoidance test and in cued classical fear conditioning (measured by means of freezing time in a new environment). ECS impaired inhibitory avoidance at all times and, at 1 or 2 h before training, reduced freezing time before and after re-presentation of the ECS. These results are interpreted as a transient conditioned stimulus (CS)-induced anxiolytic or analgesic effect lasting about 2 h after a single treatment, in addition to the known amnesic effect of the stimulus. This suggests that the effect of anterograde learning impairment is demonstrated unequivocally only when the analgesic/anxiolytic effect is over (about 4 h after ECS administration) and that this impairment of learning is selective, affecting inhibitory avoidance but not classical fear conditioning to a discrete stimulus.

Amnesia↗
PubMed2005

Olfactory-mediated fear conditioning in mice: simultaneous measurements of fear-potentiated startle and freezing.

This study demonstrates that mice display olfactory-cued fear as measured with both freezing and fear-potentiated startle. Following a preconditioning test to measure any unconditioned responses to odor, mice received 5 pairings of a 10-s odor with a 0.25-s, 0.4-mA footshock. The next day, startle and freezing were measured in the presence and absence of the odor. Both fear measures increased after training with amyl acetate (Experiment 1) and acetophenone (Experiment 2). The enhancement of startle did not occur when the same number of odors and shocks were presented in an unpaired fashion (Experiment 3). Furthermore, mice were able to discriminate between an odor paired with shock and a nonreinforced odor (Experiment 4).

Acetophenones↗
PubMed2006

Long-term memory deficits in Pavlovian fear conditioning in Ca2+/calmodulin kinase kinase alpha-deficient mice.

Signaling by the Ca(2+)/calmodulin kinase (CaMK) cascade has been implicated in neuronal gene transcription, synaptic plasticity, and long-term memory consolidation. The CaM kinase kinase alpha (CaMKKalpha) isoform is an upstream component of the CaMK cascade whose function in different behavioral and learning and memory paradigms was analyzed by targeted gene disruption in mice. CaMKKalpha mutants exhibited normal long-term spatial memory formation and cued fear conditioning but showed deficits in context fear during both conditioning and long-term follow-up testing. They also exhibited impaired activation of the downstream kinase CaMKIV/Gr and its substrate, the transcription factor cyclic AMP-responsive element binding protein (CREB) upon fear conditioning. Unlike CaMKIV/Gr-deficient mice, the CaMKKalpha mutants exhibited normal long-term potentiation and normal levels of anxiety-like behavior. These results demonstrate a selective role for CaMKKalpha in contextual fear memory and suggest that different combinations of upstream and downstream components of the CaMK cascade may serve distinct physiological functions.

Animals↗
PubMed2003

Affective blindsight: intact fear conditioning to a visual cue in a cortically blind patient.

Blindsight refers to remarkable residual visual abilities of patients with damage to the primary visual cortex (V1). Recent studies revealed that such residual abilities do not apply only to relatively simple object discriminations, but that these patients can also differentially categorize and respond to emotionally salient stimuli. The current study reports on a case of intact fear conditioning to a visual cue in a male patient with complete bilateral cortical blindness. The patient was admitted to the stroke unit of the neurological department because of complete loss of vision. Both CT and structural MRI scans confirmed lesions in both territories of the posterior cerebral artery. No visual evoked potentials could be detected confirming complete cortical blindness. During fear conditioning, a visual cue predicted the occurrence of an aversive electric shock. Acoustic startle probes were presented during and between the conditioned stimuli. Relative to the control condition, startle reflexes were substantially potentiated when elicited in the presence of the conditioned stimuli. No such potentiation was observed prior to conditioning. These data suggest that fear learning to visual cues does not require a cortical representation of the conditioned stimulus in the primary sensory cortex and that subcortical pathways are sufficient to activate the fear module in humans.

Aged↗
PubMed2000

Mutant mice lacking ryanodine receptor type 3 exhibit deficits of contextual fear conditioning and activation of calcium/calmodulin-dependent protein kinase II in the hippocampus.

As it is known that ryanodine receptor type 3 is expressed in the hippocampus, we examined the contribution of this receptor to contextual fear conditioning behavior and to the activation of Ca(2+)/calmodulin-dependent protein kinase II using mice lacking the receptor. Ryanodine receptor type 3-deficient mice exhibited impairments of performance in the contextual fear conditioning test, passive avoidance test, and Y-maze learning test. Both the activities of Ca(2+)/calmodulin-dependent protein kinase IIbeta and Ca(2+)/calmodulin-dependent protein kinase IIalpha were significantly increased in the experimental group compared to the control group in the hippocampus, but not in the cingulate cortex on the testing day 24 h after contextual fear training. However, the activities of Ca(2+)/calmodulin-dependent protein kinase IIbeta and alpha were almost the same in the experimental and control groups in the hippocampus on the training day. Ryanodine receptor type 3-deficient mice did not show the increment of Ca(2+)/calmodulin-dependent protein kinase IIbeta and alpha activities in the hippocampus on the testing day. In addition, these mutant mice showed the reduction of fear response in the elevated plus-maze test. The present results suggest that calcium-induced calcium release through the activation of ryanodine receptor type 3 in the hippocampus is important to the expression of the performance of contextual learning through the elevation of Ca(2+)/calmodulin-dependent protein kinase IIbeta and alpha activities.

Animals↗