Fear Response (fear + response)

Distribution by Scientific Domains


Selected Abstracts


Arousal, but not nursing, is necessary to elicit a decreased fear reaction toward humans in rabbit (Oryctolagus cuniculus) pups

DEVELOPMENTAL PSYCHOBIOLOGY, Issue 3 2003
Péter Pongrácz
Abstract Rabbits that are handled at the time of feeding during the first week postpartum show reduced fear of humans later in their lives as compared to unhandled controls. Effective handling has been shown to be confined to a sensitive period. Our study aimed to investigate if feeding itself (provided by a second doe, 6 hr after the standard nursing time) affects the levels of fear of humans later in life. Our results showed that (a) the prenursing state of excitement is only characteristic of the standard nursing and is not elicited by a second feeding 6 hr past the usual nursing time, repeated daily across the first week postpartum; and (b) handling linked to a second feeding 6 hr after the standard nursing does not reduce fear responses toward humans at weaning. We conclude that the aroused state, per se, is essential for the reduction of a rabbit's fear response toward humans provoked by early handling. © 2003 Wiley Periodicals, Inc. Dev Psychobiol 43: 192,199, 2003. [source]


Premotor sympathetic neurons of conditioned fear in the rat

EUROPEAN JOURNAL OF NEUROSCIENCE, Issue 3 2008
Pascal Carrive
Abstract Conditioned fear to context, a pure form of psychological stress, is associated with sympathetically mediated changes including a marked hypertension. To identify the possible premotor sympathetic neurons mediating these changes, we conducted double-immunolabelling experiments combining fear-induced Fos with retrograde tracing from the thoracic cord (T2-L1). Presympathetic groups showing the greatest increase in the proportion of spinally projecting cells double-labelled with Fos compared with resting controls were the perifornical area (PeF; 22.7% vs. 0.4%) and paraventricular nucleus (Pa; 10.5% vs. 0.2%) in the hypothalamus, and the A5 noradrenergic group (33.6% vs. 0.2%) in the pons. In contrast, there was only a small increase in the presympathetic groups of the rostral ventral medulla, including the lateral paragigantocellular group (LPGi; 4.3% vs. 0.5%), raphe magnus and pallidus (1.1% vs. 0.6% and 1.8% vs. 0.5%), and the vasopressor group of the rostral ventrolateral medulla (RVLM; 1.9% vs. 0.8%). PeF, Pa, A5 and LPGi accounted for 21, 15, 16 and 6% of all the double-labelled cells, respectively, and RVLM for only 1%. Double-immunolabelling of Fos and tyrosine hydroxylase confirmed that many A5 neurons were activated (19%) and that practically no C1 neurons in RVLM were (1.3%). The results suggest that the main premotor sympathetic drive of the fear response comes from hypothalamic (PeF and Pa) and A5 neurons that project directly to the thoracic cord and bypass medullary presympathetic groups, and that the vasopressor premotor sympathetic neurons of the RVLM are unlikely to mediate the hypertensive pressure response of contextual fear. [source]


Impaired Pavlovian fear extinction is a common phenotype across genetic lineages of the 129 inbred mouse strain

GENES, BRAIN AND BEHAVIOR, Issue 8 2009
M. Camp
Fear extinction is impaired in psychiatric disorders such as post-traumatic stress disorder and schizophrenia, which have a major genetic component. However, the genetic factors underlying individual variability in fear extinction remain to be determined. By comparing a panel of inbred mouse strains, we recently identified a strain, 129S1/SvImJ (129S1), that exhibits a profound and selective deficit in Pavlovian fear extinction, and associated abnormalities in functional activation of a key prefrontal-amygdala circuit, as compared with C57BL/6J. The first aim of the present study was to assess fear extinction across multiple 129 substrains representing the strain's four different genetic lineages (parental, steel, teratoma and contaminated). Results showed that 129P1/ReJ, 129P3/J, 129T2/SvEmsJ and 129X1/SvJ exhibited poor fear extinction, relative to C57BL/6J, while 129S1 showed evidence of fear incubation. On the basis of these results, the second aim was to further characterize the nature and specificity of the extinction phenotype in 129S1, as an exemplar of the 129 substrains. Results showed that the extinction deficit in 129S1 was neither the result of a failure to habituate to a sensitized fear response nor an artifact of a fear response to (unconditioned) tone per se. A stronger conditioning protocol (i.e. five × higher intensity shocks) produced an increase in fear expression in 129S1, relative to C57BL/6J, due to rapid rise in freezing during tone presentation. Taken together, these data show that impaired fear extinction is a phenotypic feature common across 129 substrains, and provide preliminary evidence that impaired fear extinction in 129S1 may reflect a pro-fear incubation-like process. [source]


Altered conditioned fear behavior in glutamate decarboxylase 65 null mutant mice

GENES, BRAIN AND BEHAVIOR, Issue 2 2003
O. Stork
We investigated the involvement of the 65 kDa isoform of glutamic acid decarboxylase (GAD65) and GAD65-mediated ,-aminobutyric acid (GABA) synthesis in the formation and expression of Pavlovian fear memory. To this end, behavioral, endocrine and autonomic parameters were examined during conditioned fear retrieval of mice with targeted ablation of the GAD65 gene (GAD65,/, mice). These mutant mice were found to display specific fear behavior (freezing, escape), as well as autonomic (increased defecation) and endocrine activation (increased plasma corticosterone) during fear memory retrieval. However, freezing was reduced and flight and escape behavior were increased in GAD65,/, mice compared to their wild type and heterozygous littermates, while corticosterone levels and defecation rates did not differ between genotypes. Active defensive behavior of GAD65,/, mice was observed during both auditory cued and contextual retrieval of fear memory, as well as immediately after conditioning. These data indicate a selectively altered behavioral fear response in GAD65,/, mice, most likely due to deficits in threat estimation or the elicitation of appropriate conditioned fear behavior, and suggest that GAD65 is a genetic determinant of conditioned fear behavior. GAD65,/, mice provide a valuable tool to further dissect the GABAergic mechanisms involved in fear and anxiety and to model GABA-related neurological and psychiatric disorders. [source]


Personality traits and fear response to print advertisements: Theory and an empirical study

PSYCHOLOGY & MARKETING, Issue 11 2004
John C. Mowen
This study investigates the hypothesis that different personality traits influence fear responses to advertising appeals for two types of driver safety behavior. An experiment was conducted in which personality traits taken from the 3M model of motivation and personality (Mowen, 2000) were employed to predict fear responses to advertisements that targeted either aggressive driving or inattentive driving. For the aggressive-driving ad, introversion and need to protect and enhance body resources positively predicted fear response. For the inattentive-driving ad, introversion and need to protect and enhance body resources were again positive predictors of fear, but so also were emotional instability and agreeableness, whereas competitiveness, need for arousal, and the need for material resources were negative predictors. It is not clear why more traits predicted fear for inattentive driving than for aggressive driving. © 2004 Wiley Periodicals, Inc. [source]


Panic comorbidity with bipolar disorder: what is the manic,panic connection?

BIPOLAR DISORDERS, Issue 6 2006
Dean F MacKinnon
Context:, Bipolar/panic comorbidity has been observed in clinical, community and familial samples. As both are episodic disorders of affect regulation, the common pathophysiological mechanism is likely to involve deficits in amygdala-mediated, plasticity-dependent emotional conditioning. Evidence:, Neuronal genesis and synaptic remodeling occur in the amygdala; bipolar and panic disorders have both been associated with abnormality in the amygdala and related structures, as well as in molecules that modulate plasticity, such as serotonin, norepinephrine, brain-derived neurotrophic factor (BDNF) and corticotrophin releasing factor (CRF). These biological elements are involved in behavioral conditioning to threat and reward. Model:, Panic attacks resemble the normal acute fear response, but are abnormally dissociated from any relevant threat. Abnormal reward-seeking behavior is central to both manic and depressive syndromes. Appetites can be elevated or depressed; satisfaction of a drive may fail to condition future behavior. These dissociations may be the result of deficits in plasticity-dependent processes of conditioning within different amygdala subregions. Conclusions:, This speculative model may be a useful framework with which to connect molecular, cellular, anatomic and behavioral processes in panic and bipolar disorders. The primary clinical implication is that behavioral treatment may be critical to restore function in some bipolar patients who respond only partially to medications. [source]


DUAL ACTIVATION OF CARDIAC SYMPATHETIC AND PARASYMPATHETIC COMPONENTS DURING CONDITIONED FEAR TO CONTEXT IN THE RAT

CLINICAL AND EXPERIMENTAL PHARMACOLOGY AND PHYSIOLOGY, Issue 12 2006
Pascal Carrive
SUMMARY 1The present study investigates the contribution of the sympathetic and vagal parasympathetic systems to the tachycardic response of long-lasting (40 min) conditioned fear responses to context. 2The conditioned fear response evoked by re-exposure to a footshock chamber was tested 10 min after intravenous injection of the ,-adrenoceptor antagonist propranolol (2 mg/kg) or the muscarinic antagonist atropine methyl nitrate (2 mg/kg) in rats implanted with radiotelemetric probes. 3Compared with saline controls, the drugs did not change the behavioural component of the response (freezing, 22 kHz ultrasonic vocalizations) or its pressor component (+28 mmHg). 4Propranolol abolished the tachycardic response of fear, whereas atropine more than doubled it (from +75 to +175 b.p.m. above resting baseline). 5The results demonstrate that both sympathetic and vagal parasympathetic outflows to the heart are strongly activated during conditioned fear. The vagal activation may act to hold back cardiac acceleration while the animal waits for the aversive stimulus to come. [source]


Initial symptoms and reactions to trauma-related stimuli and the development of posttraumatic stress disorder

DEPRESSION AND ANXIETY, Issue 2 2005
Karin Elsesser Ph.D.
Abstract We investigated laboratory and experimental variables as predictors of the development of posttraumatic stress disorder (PTSD). Evoked heart rate response to trauma-related pictures, attentional bias in the dot-probe task, and viewing time were assessed in 35 victims of a traumatic event and again after 3 months. Data was compared to 26 control participants. At first assessment trauma victims showed heart rate (HR) acceleration and controls showed HR deceleration to trauma-related material. The group of trauma victims improved clinically over time. Predictors of the number of PTSD symptoms after 3 months were re-experiencing (33% of the variance) and amplitude of the evoked HR reaction to trauma-related pictures (15%). The two variables were highly correlated. Trauma victims were also more anxious, viewed trauma-related pictures for a longer time, and had a longer reaction time in the dot-probe task (but no distinct attentional bias) than control participants. Results indicate that specific fear responses and re-experiencing contribute to the development of posttraumatic stress disorder. Depression and Anxiety 21:61,70, 2005. © 2005 Wiley-Liss, Inc. [source]


Arousal, but not nursing, is necessary to elicit a decreased fear reaction toward humans in rabbit (Oryctolagus cuniculus) pups

DEVELOPMENTAL PSYCHOBIOLOGY, Issue 3 2003
Péter Pongrácz
Abstract Rabbits that are handled at the time of feeding during the first week postpartum show reduced fear of humans later in their lives as compared to unhandled controls. Effective handling has been shown to be confined to a sensitive period. Our study aimed to investigate if feeding itself (provided by a second doe, 6 hr after the standard nursing time) affects the levels of fear of humans later in life. Our results showed that (a) the prenursing state of excitement is only characteristic of the standard nursing and is not elicited by a second feeding 6 hr past the usual nursing time, repeated daily across the first week postpartum; and (b) handling linked to a second feeding 6 hr after the standard nursing does not reduce fear responses toward humans at weaning. We conclude that the aroused state, per se, is essential for the reduction of a rabbit's fear response toward humans provoked by early handling. © 2003 Wiley Periodicals, Inc. Dev Psychobiol 43: 192,199, 2003. [source]


Impairment of conditioned freezing to tone, but not to context, in Fyn-transgenic mice: relationship to NMDA receptor subunit 2B function

EUROPEAN JOURNAL OF NEUROSCIENCE, Issue 5 2005
N. Kojima
Abstract We previously demonstrated that transgenic mice overexpressing Fyn tyrosine kinase exhibit higher seizure susceptibility and enhanced tyrosine phosphorylation of several proteins, including the N -methyl-D-aspartate (NMDA) receptor subunit 2B (NR2B). In the present study, we analysed behavioural phenotypes, especially conditioned fear responses, of Fyn-transgenic (TG) mice to better understand the role of Fyn in learned emotional behaviour. Tone-dependent conditioned freezing was significantly attenuated in Fyn-TG mice, whereas context-dependent freezing was unaffected. Neither massed nor spaced conditioning ameliorated the attenuation of tone-dependent freezing. However, the selective NR2B antagonist ifenprodil, when administered before conditioning, restored tone-dependent freezing in Fyn-TG mice at a dose that did not affect freezing in wild-type (WT) mice. These results suggest that impairment of tone-dependent conditioned freezing in Fyn-TG mice is caused by disruption of the NR2B-containing NMDA receptor function. Tyrosine phosphorylation of brain proteins, including NR2B, was enhanced in Fyn-TG mice compared with that in WT mice. We also found that ifenprodil significantly suppressed the enhanced tyrosine phosphorylation. Thus, our data support the notion that NMDA receptor activity is tightly correlated with protein tyrosine phosphorylation, and Fyn might be one key molecule that controls tone-dependent conditioned freezing through the regulation of NMDA receptor function. [source]


Neurogenesis may relate to some but not all types of hippocampal-dependent learning

HIPPOCAMPUS, Issue 5 2002
Tracey J. Shors
Abstract The hippocampal formation generates new neurons throughout adulthood. Recent studies indicate that these cells possess the morphology and physiological properties of more established neurons. However, the function of adult generated neurons is still a matter of debate. We previously demonstrated that certain forms of associative learning can enhance the survival of new neurons and a reduction in neurogenesis coincides with impaired learning of the hippocampal-dependent task of trace eyeblink conditioning. Using the toxin methylazoxymethanol acetate (MAM) for proliferating cells, we tested whether reduction of neurogenesis affected learning and performance associated with different hippocampal dependent tasks: spatial navigation learning in a Morris water maze, fear responses to context and an explicit cue after training with a trace fear paradigm. We also examined exploratory behavior in an elevated plus maze. Rats were injected with MAM (7 mg/kg) or saline for 14 days, concurrent with BrdU, to label new neurons on days 10, 12, and 14. After treatment, groups of rats were tested in the various tasks. A significant reduction in new neurons in the adult hippocampus was associated with impaired performance in some tasks, but not with others. Specifically, treatment with the antimitotic agent reduced the amount of fear acquired after exposure to a trace fear conditioning paradigm but did not affect contextual fear conditioning or spatial navigation learning in the Morris water maze. Nor did MAM treatment affect exploration in the elevated plus maze. These results combined with previous ones suggest that neurogenesis may be associated with the formation of some but not all types of hippocampal-dependent memories. Hippocampus 2002;12:578,584. © 2002 Wiley-Liss, Inc. [source]


Force transducer-based movement detection in fear conditioning in mice: A comparative analysis

HIPPOCAMPUS, Issue 1 2002
Thomas Fitch
Abstract Fear conditioning (FC) allows the dissociation of hippocampal and nonhippocampal behavioral function in rodents, and has become a diagnostic tool in transgenic mouse research employed to investigate mutation-induced changes in brain function. Although the procedural details of the paradigm have been established, quantification of the behavioral output, freezing, remains problematic in mice. Observation-based techniques are time-consuming and may be subject to bias, while movement detection with photocells is imprecise. Here we describe an alternative method for movement detection, based on an electronic force transducer system that allows the quantification of acceleration forces generated by a moving subject. We compare the behavior of two inbred strains of mice (C57BL/6 and DBA/2) whose performance is known to differ in hippocampal tasks, including FC. The comparison is made using multiple techniques: the force transducer approach, and three observation-based methods, a computer-aided event-recording approach, a traditional time-sampling paper/pencil method, and a subjective impression-based scoring system. In addition, we investigate the correlation structures of behavioral elements quantified by event recording, using principal component analyses; we conclude that fear may manifest in multiple forms and in a stimulus- and genotype-dependent manner. We suggest that the force transducer system provides precise quantification of movements in an automated manner and will allow high-throughput screening for mutation and drug effects in mice. However, we also argue that fear responses can be complex, and freezing behavior may not be the only measure of fear or fear-associated memory. Hippocampus 2002;12:4,17. © 2002 Wiley-Liss, Inc. [source]


Blockade of NMDA receptors and nitric oxide synthesis in the dorsolateral periaqueductal gray attenuates behavioral and cellular responses of rats exposed to a live predator

JOURNAL OF NEUROSCIENCE RESEARCH, Issue 11 2009
Daniele Cristina Aguiar
Abstract Innate fear stimulus induces activation of neurons containing the neuronal nitric oxide synthase enzyme (nNOS) in defensive-related brain regions such as the dorsolateral periaqueductal gray (dlPAG). Intra-dlPAG administration of nitric oxide synthase (NOS) inhibitors and glutamate antagonists induce anxiolytic-like responses. We investigated the involvement of nitric oxide (NO) and glutamate neurotransmission in defensive reactions modulated by dlPAG. We tested if intra-dlPAG injections of the selective nNOS inhibitor, N-propyl- L -arginine (NP), or the glutamate antagonist, AP7 (2-amino-7-phosphonoheptanoic acid), would attenuate behavioral responses and cellular activation induced by predator exposure (cat). Fos-like immunoreactivity (FLI) was used as a marker of neuronal functional activation, whereas nNOS immunohistochemistry was used to identify NOS neurons. Cat exposure induced fear responses and an increase of FLI in the dlPAG and dorsal premammillary nucleus (PMd). NP and AP7 attenuated the cat-induced behavioral responses. Whereas NP tended to attenuate FLI in the dlPAG, AP7 induced a significant reduction in cellular activation of this region. The latter drug, however, increased FLI and double-labeled cells in the PMd. Cellular activation of this region was significantly correlated with time spent near the cat (r = 0.7597 and 0.6057 for FLI and double-labeled cells). These results suggest that glutamate/NO-mediated neurotransmission in the dlPAG plays an important role in responses elicit by predator exposure. Blocking these neurotransmitter systems in this brain area impairs defensive responses. The longer time spent near the predator that follows AP7 effect could lead to an increased cellular activation of the PMd, a more rostral brain area that has also been related to defensive responses. © 2009 Wiley-Liss, Inc. [source]


Personality traits and fear response to print advertisements: Theory and an empirical study

PSYCHOLOGY & MARKETING, Issue 11 2004
John C. Mowen
This study investigates the hypothesis that different personality traits influence fear responses to advertising appeals for two types of driver safety behavior. An experiment was conducted in which personality traits taken from the 3M model of motivation and personality (Mowen, 2000) were employed to predict fear responses to advertisements that targeted either aggressive driving or inattentive driving. For the aggressive-driving ad, introversion and need to protect and enhance body resources positively predicted fear response. For the inattentive-driving ad, introversion and need to protect and enhance body resources were again positive predictors of fear, but so also were emotional instability and agreeableness, whereas competitiveness, need for arousal, and the need for material resources were negative predictors. It is not clear why more traits predicted fear for inattentive driving than for aggressive driving. © 2004 Wiley Periodicals, Inc. [source]


Peptides of love and fear: vasopressin and oxytocin modulate the integration of information in the amygdala

BIOESSAYS, Issue 9 2005
Jacek D
Neuropeptides vasopressin and oxytocin regulate a variety of behaviors ranging from maternal and pair bonding to aggression and fear. Their role in modulating fear responses has been widely recognized, but not yet well understood. Animal and human studies indicate the major role of the amygdala in controlling fear and anxiety. The amygdala is involved in detecting threat stimuli and linking them to defensive behaviors. This is accomplished by projections connecting the central nucleus of the amygdala (CeA) to the brain stem and to hypothalamic structures, which organize fear responses. A recent study by Huber et al1 demonstrates that vasopressin and oxytocin modulate the excitatory inputs into the CeA in opposite manners. Therefore this finding elucidates the mechanisms through which these neuropeptides may control the expression of fear. BioEssays 27:869,873, 2005. © 2005 Wiley Periodicals, Inc. [source]


DUAL ACTIVATION OF CARDIAC SYMPATHETIC AND PARASYMPATHETIC COMPONENTS DURING CONDITIONED FEAR TO CONTEXT IN THE RAT

CLINICAL AND EXPERIMENTAL PHARMACOLOGY AND PHYSIOLOGY, Issue 12 2006
Pascal Carrive
SUMMARY 1The present study investigates the contribution of the sympathetic and vagal parasympathetic systems to the tachycardic response of long-lasting (40 min) conditioned fear responses to context. 2The conditioned fear response evoked by re-exposure to a footshock chamber was tested 10 min after intravenous injection of the ,-adrenoceptor antagonist propranolol (2 mg/kg) or the muscarinic antagonist atropine methyl nitrate (2 mg/kg) in rats implanted with radiotelemetric probes. 3Compared with saline controls, the drugs did not change the behavioural component of the response (freezing, 22 kHz ultrasonic vocalizations) or its pressor component (+28 mmHg). 4Propranolol abolished the tachycardic response of fear, whereas atropine more than doubled it (from +75 to +175 b.p.m. above resting baseline). 5The results demonstrate that both sympathetic and vagal parasympathetic outflows to the heart are strongly activated during conditioned fear. The vagal activation may act to hold back cardiac acceleration while the animal waits for the aversive stimulus to come. [source]