PubMed Health⌕ Search

SEARCH · PubMed Health

Results for “fear”

Explore indexed PubMed citations for clinical trials, systematic reviews and public health research. Read source abstracts and follow each citation to its original PubMed record.

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

At least 163 records · Page 9Linked to original sources

Time of conditioning selectively influences contextual fear conditioning: further support for a multiple-memory systems view of fear conditioning.

Time of conditioning influences long-term retention of contextual but not auditory-cue fear conditioning. Long-Evans rats (Rattus norvegicus) conditioned at 12 noon displayed reduced contextual fear conditioning compared to rats conditioned at 8 a.m. or 4 p.m. This effect was eliminated by exposure to the context 24 hr prior to conditioning and by a posttrial injection of corticosterone (1.0 mg/kg). Time of conditioning did not influence short-term retention of contextual fear. These results suggest that time of conditioning influences the posttrial processes that construct a memory representation of the context. They also support the view that contextual and auditory-cue fear conditioning depend on different processes. These results are discussed in relation to the concept of memory storage modulators.

Animals↗

The benzodiazepine midazolam does not impair Pavlovian fear conditioning but regulates when and where fear is expressed.

Rats were injected with a benzodiazepine (midazolam) and shocked after presentation of an auditory conditioned stimulus (CS). They were then tested for fear reactions (freezing) to the CS in either the original context or a 2nd context after either a short (1-day) or long (21-day) retention interval. Rats tested in the original context froze less after 1 day than rats tested after that interval in the 2nd context or rats tested after 21 days. Moreover, rats tested after the long interval in the original context froze less than rats tested after that interval in the 2nd context. Therefore, midazolam does not impair the acquisition of conditioned fear but regulates when and where that fear is expressed. These effects of midazolam were interpreted as a contextually controlled deficit in the expression of conditioned fear that is similar to that associated with latent inhibition and extinction (M. E. Bouton, 1993).

Animals↗

The benzodiazepine inverse agonist DMCM as an unconditional stimulus for fear-induced analgesia: implications for the role of GABAA receptors in fear-related behavior.

When the benzodiazepine inverse agonist DMCM (6,7-dimethoxy-4-ethyl-beta-carboline-3-carboxylic acid methyl ester) occupies the benzodiazepine recognition site on the GABAA receptor complex, the inhibitory action of gamma-aminobutyric acid (GABA) is attenuated. DMCM acted as an unconditional stimulus for one response associated with fear or anxiety, analgesia, as indicated by a dose-dependent (0.25-1.0 mg/kg) suppression of rats' responses to a formalin injection. This was accompanied by other fearlike responses (defecation and urination). The opioid antagonist naltrexone (1.75-14 mg/kg) did not affect these behaviors. Environmental cues associated with DMCM provoked analgesia and defecation in the absence of the drug. The conditional analgesia was reversed by naltrexone (7 mg/kg). DMCM functions as an unconditional fear stimulus by eliciting fear-related behaviors and conditioning those responses to neutral stimuli. The neural circuitry underlying fear conditioning appears to involve tonically inhibitory GABAergic synapses.

Animals↗

Perceived self-efficacy domains as predictors of fear of the unknown and fear of dying among older adults.

Using a sample of 167 women and 121 men, aged 65-87, this study tested the hypothesis that self-efficacy beliefs of older persons are significantly stronger predictors of death fears than are demographics, social support, and physical health variables used in earlier predictor models. Standard self-report measures were used to assess all predictor variables, including perceived self-efficacy in 8 different domains. Findings from a series of hierarchical regression analyses that were conducted separately for men and women supported the hypothesis concerning the superiority of self-efficacy variables as predictors of fear of the unknown after death and fear of dying, with spiritual health efficacy and instrumental efficacy being the most potent predictors of death fears for women and men, respectively.

Aged↗

Why do we fear death? The construction and validation of the Reasons for Death Fear Scale.

Previous research has disclosed different meanings of death, varieties of death anxiety, and hundreds of factors extracted from the uni- and multi-dimensional death anxiety scales. However, there have been no empirical studies to elucidate the reasons for death fear. The Reasons for Death Fear Scale (RDFS) was constructed and validated. It consists of 18 brief items, with good reliabilities ( > .8). Four factors of the RDFS were labeled Fear of Pain and Punishment, Fear of Losing Worldly Involvements, Religious Transgressions and Failures, and Parting from Loved Ones. A high-loaded factor was extracted in which the RDFS's loading was .45, while the loadings of the scales of death anxiety, death depression, and death obsession ranged between .8 and .9. Of interest is that the correlation between the RDFS and death anxiety was higher than that with general anxiety. No gender-differences were detected with college students. It is important to note that the findings of this study were only researched through Arabic and mainly Muslim college students. The generalizability of the present results to other populations would seem to merit further investigation.

Adolescent↗

Contextual fear conditioning and baseline startle responses in the rat fear-potentiated startle test: a comparison of benzodiazepine/gamma-aminobutyric acid-A receptor agonists.

In the rat, fear-potentiated startle (FPS) test animals are first trained to associate brief light presentations with a mild electric footshock and then tested for startle responses to acoustic stimuli, delivered either in darkness (i.e. baseline startle) or after the conditioning stimulus. Following light presentation the magnitude of the startle response is markedly increased, and the test is commonly used to distinguish anxiolytic drug effects (i.e. a reduction in FPS) from non-specific effects such as sedation/muscle relaxation. However, recent studies suggest that the environment in which the animal is trained may also contribute towards the acquisition of a conditioned fear response (i.e. contextual fear conditioning) and that this may elevate startle responses recorded in the dark. In the present study, therefore, we have compared the benzodiazepine/gamma-aminobutyric acid-A receptor agonist chlordiazepoxide with the partial agonists FG 8205 and bretazenil, which are known to have a reduced propensity to produce sedation/myorelaxation, using two different FPS procedures: (i) conditioning and testing in stabilimeter chambers, and (ii) conditioning and testing in different environments. The results show that FPS can be demonstrated in both procedures and that treatment with chlordiazepoxide, FG 8205 or bretazenil dose-dependently attenuates the response. However, animals conditioned and tested in stabilimeter chambers also showed a significant increase in dark-startle amplitudes compared with non-shocked rats, suggesting that this response was elevated by contextual fear conditioning. Furthermore, despite clear differences in side-effect liabilities, FG 8205 and bretazenil significantly reduced dark-startle responses, suggesting that this measure is also sensitive to the anxiolytic effects of benzodiazepines. In contrast, when animals were conditioned and tested in different environments, dark-startle responses were not significantly different from those recorded in non-shocked rats and treatment with FG 8205 or bretazenil had no effect. Thus, conditioning and testing animals in different environments may provide a more effective means of distinguishing anxiolytic from non-specific drug effects in the rat FPS test.

Animals↗

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↗

4.5 to 7 years: fearful behaviour, fears and worries.

Fearful behaviour, fears and worries of young children are central not only to normal development, but also to the development of anxiety disorders. In a community sample, consistency from age 4.5 to 7 years was significant for all measures of behavioural approach/withdrawal, as well as for the degree of reported fears and worries. Observed approach/withdrawal behaviour was not correlated with fears and worries reported by either mothers or children. There were no sex differences in the levels of measures or their consistency, with one exception: maternal reports of worries were less consistent but possibly more valid for girls than for boys. When interviewed at 7 years, girls expressed worries about family members, while boys tended to worry about their own performance.

Anxiety↗

Comparison of the effects of diazepam on the fear-potentiated startle reflex and the fear-inhibited light reflex in man.

It has been shown previously that the amplitude of the acoustic startle reflex is enhanced, and the amplitude of the light reflex reduced, when subjects anticipate an aversive event, compared to periods when subjects are resting ('fear-potentiated startle reflex' and 'fear-inhibited light reflex'). We examined whether the anxiolytic diazepam would reverse the effects of threat on the startle and pupillary reflexes. Twelve male volunteers participated in three weekly sessions in which they received oral treatment with placebo, diazepam 5 mg and diazepam 10 mg, according to a balanced crossover double-blind design. One hour after ingestion of the treatments, miotic responses to light pulses and electromyographic responses of the orbicularis oculi muscle to sound pulses were elicited during alternating periods in which the threat of an electric shock (electrodes attached to the subject's wrist) was present (THREAT) and absent (SAFE). The THREAT condition was associated with a significant increase in the amplitude of the electromyographic (EMG) response, a significant reduction of the miotic response amplitude, and an increase in self-rated anxiety. Diazepam attenuated all these effects of THREAT. Diazepam did not affect the amplitude of the miotic response under the SAFE condition, but did suppress the EMG response under this condition. These results confirm the validity of the fear-potentiated startle reflex and fear-inhibited light reflex as laboratory models of human anxiety, and reveal some differences between the effects of diazepam on the two reflexes.

Acoustic Stimulation↗

Auditory fear conditioning and long-term potentiation in the lateral amygdala require ERK/MAP kinase signaling in the auditory thalamus: a role for presynaptic plasticity in the fear system.

In the present study, we examined the role of the auditory thalamus [medial division of the medial geniculate nucleus and the adjacent posterior intralaminar nucleus (MGm/PIN)] in auditory pavlovian fear conditioning using pharmacological manipulation of intracellular signaling pathways. In the first experiment, rats were given intrathalamic infusions of the MEK (mitogen-activated protein kinase-kinase) inhibitor 1,4-diamino-2,3-dicyano-1,4-bis(o-aminophenylmercapto) butadiene (U0126) before fear conditioning. Findings revealed that long-term memory (assessed at 24 h) was impaired, whereas short-term memory (assessed at 1-3 h) of fear conditioning was intact. In the second experiment, rats received immediate posttraining intrathalamic infusion of U0126, the mRNA synthesis inhibitor 5,6-dichloro-1-beta-D-ribofuranosylbenzimidazole (DRB), or infusion of the protein synthesis inhibitor anisomycin. Posttraining infusion of either U0126 or DRB significantly impaired long-term retention of fear conditioning, whereas infusion of anisomycin had no effect. In the final experiment, rats received intrathalamic infusion of U0126 before long-term potentiation (LTP)-inducing stimulation of thalamic inputs to the lateral nucleus of the amygdala (LA). Findings revealed that thalamic infusion of U0126 impaired LTP in the LA. Together, these results suggest the possibility that MGm/PIN cells that project to the LA contribute to memory formation via ERK (extracellular signal-regulated kinase)-mediated transcription, but that they do so by promoting protein synthesis-dependent plasticity locally in the LA.

Acoustic Stimulation↗

Girls' fearfulness as a product of mothers' fearfulness and fathers' authoritarianism.

Data from 27 girls of 10 to 12 years were obtained on the Fear Survey Schedule for Children--Revised and from their parents on the Fear Survey Schedule for Adults-III and the California F Scale. Analyses indicated fathers' authoritarianism scores and mothers' fear scores have independent associations with children's fears and suggested greater behavioural overcontrol by fathers and the greater propensity of mothers to communicate threatening information.

Adolescent↗

The amygdala modulates memory consolidation of fear-motivated inhibitory avoidance learning but not classical fear conditioning.

Although the lateral and basal nuclei of the amygdala are believed to be essential for the acquisition of Pavlovian fear conditioning, studies using post-training manipulations of the amygdala in the inhibitory avoidance learning paradigm have recently called this view into question. We used the GABA(A) agonist muscimol to functionally inactivate these nuclei immediately after single-trial Pavlovian fear conditioning or single-trial inhibitory avoidance learning. Immediate post-training infusions of muscimol had no effect on Pavlovian conditioning but produced a dose-dependent effect on inhibitory avoidance. However, pre-training infusions dose-dependently disrupted Pavlovian conditioning. These findings indicate that the amygdala plays an essential role in the acquisition of Pavlovian fear conditioning and contributes to the modulation of memory consolidation of inhibitory avoidance but not of Pavlovian fear conditioning.

Acoustic Stimulation↗

Utilizing parent report to investigate young children's fears: a modification of the Fear Survey Schedule for Children--II: A research note.

The Fear Survey Schedule for Children-II (FSSC-II) (Gullone & King, 1992) was modified for parent report and a younger age group. The modified instrument (FSSC-IIP) was completed by 753 parents of children within the age range 3.0 to 8.9 years. Results revealed a stable eight-factor solution that was sensitive to age and gender differences. Parents reported a higher overall level of fear for school children compared to preschool children, and a higher overall level of fearfulness for girls compared to boys. The most common fears reported were getting lost in a crowd and in a strange place.

Child↗

Factorial dimensions and correlates of blood, injury, injection and related medical fears: cross validation of the medical fear survey.

The Medical Fear Survey (MFS) and its companion scale, the Medical Avoidance Survey (MAS) were factor analyzed and the factor analysis was cross validated in sample of 934 participants. Seven reliable factors were derived from the MFS which cover the domain of blood, injury, and injection fears and phobias. These factors were entered into a discriminate analysis to predict blood injury-related fainting. The single factor, "fear of injections and blood draws" accounted for the majority of the MFS prediction of fainting, correctly classifying 72% of the fainters and 47% of non-fainters. The factors were examined in composite and individually in relation to gender and fainting. Overall, females and fainters scored significantly higher on the MFS although there was some variability. Implications for assessment and conceptualization of blood, injury, injection fears and phobias are discussed.

Adolescent↗

Fear-dependent variations in continuous avoidance behavior of pigs. II. Effects of diazepam on acquisition and performance of Pavlovian fear conditioning and plasma corticosteroid levels.

Previously acquired continuous avoidance performance of pigs in a shuttle-box was modified by a Pavlovian fear-conditioning procedure. Diazepam (1 mg/kg) given before the Pavlovian conditioning session prevented the increase in corticosteroids and the impairment of performance in the subsequent test session before the presentation of the fear signal. Diazepam given before the Pavlovian conditioning session and/or the test session did not prevent the increase of response to the CS presentation; however, the temporal pattern of increase differed according to the drug condition: the diazepam treatment on the day of the test significantly delayed the peak of responding to the CS; in pigs treated with diazepam on the day of Pavlovian conditioning and with saline on the day of test, the increase of response was diffuse instead of being localized to the CS presentation period. Pigs treated with diazepam both during learning and performance of fear conditioning showed some evidence of performance facilitation. Usual unitary interpretations cannot account for such results which would appear to be the net result of several intermingled effects among which state-dependent learning, acquisition deficit, and performance facilitation seem to be of importance.

Adrenal Cortex Hormones↗

Emotional processing and fear measurement synchrony as indicators of treatment outcome in fear of flying.

Minimal-therapist-involvement stress inoculation training was used to treat flying phobics. Relative to no-treatment controls, treatment subjects reported more fear reduction, were more likely to participate in an exposure session, and flew more during a two-month follow-up period. Subjects who exhibited synchronous changes in heart rate and report of anxiety during exposure had greater fear reduction than subjects showing less synchrony. Subjects who voluntarily took plane flights in the two months following treatment showed greater indications of emotional processing during in vivo exposure. Relative to flight avoiders, fliers had higher mean heart rate in the plane, a greater reduction in heart rate from the beginning to the end of the flight, and greater reported fear reduction from pre- to post-flight.

Adult↗

Fears of AIDS in Nigerian students: dimensions of the fear of AIDS Scale (FAIDSS) in west Africa.

A study based on a sample of 2500 individuals aged 18 years and over in six west African cities was undertaken for the purpose of determining the cross-cultural consistency and replicability of fears about AIDS. A factor analysis of the data obtained confirmed a similar factor structure to that reported in Australia. Implications for the prevention of HIV transmission in Nigeria and other west African countries is discussed. Our findings showed that the fear of AIDS Scale (FAIDSS) is a reliable index of fear of aids and is readily scaleable. Other implications for health education are considered.

Acquired Immunodeficiency Syndrome↗

Fear is fast in phobic individuals: amygdala activation in response to fear-relevant stimuli.

BACKGROUND: Two core characteristics of pathologic fear are its rapid onset and resistance to cognitive regulation. We hypothesized that activation of the amygdala early in the presentation of fear-relevant visual stimuli would distinguish phobics from nonphobics. METHODS: Chronometry of amygdala activation to phobia-relevant pictures was assessed in 13 spider phobics and 14 nonphobics using functional magnetic resonance imaging (fMRI). RESULTS: Blood oxygen level-dependent (BOLD) responses in the amygdala early in picture processing consistently differentiated between phobic and nonphobic subjects, as well as between phobogenic and nonphobogenic stimuli among phobics. Furthermore, amygdalar BOLD responses associated with timing but not magnitude of activation predicted affective responses to phobogenic stimuli. Computational modeling procedures were used to identify patterns of neural activation in the amygdala that could yield the observed BOLD data. These data suggest that phobic responses were characterized by strong but brief amygdala responses, whereas nonphobic responses were weaker and more sustained. CONCLUSIONS: Results are discussed in the context of the amygdala's role in rapid threat detection and the vigilance-avoidance hypothesis of anxiety. These data highlight the importance of examining the neural substrates of the immediate impact of phobogenic stimuli for understanding pathological fear.

Adolescent↗