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Journal articles on the topic 'Fear conditioning'

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Author: Grafiati

Published: 4 June 2021

Last updated: 20 February 2023

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1

Dygdon, Judith A., Anthony J. Conger, and Esther Y. Strahan. "Multimodal Classical Conditioning of Fear: Contributions of Direct, Observational, and Verbal Experiences to Current Fears." Psychological Reports 95, no. 1 (August 2004): 133–53. http://dx.doi.org/10.2466/pr0.95.1.133-153.

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The authors propose that a multimodal classical conditioning model be considered when clinicians or clinical researchers study the etiology of fears and anxieties learned by human beings. They argue that fears can be built through the combined effects of direct, observed, and verbally presented classical conditioning trials. Multimodal classical conditioning is offered as an alternative to the three pathways to fear argument prominent in the human fear literature. In contrast to the three pathways position, the authors present theoretical arguments for why “learning by observation” and “learning through the receipt of verbal information” should be considered classical conditioning through observational and verbal modes. The paper includes a demonstration of how data, commonly collected in research on the three pathways to fear, would be studied differently using a multimodal classical conditioning perspective. Finally, the authors discuss implications for assessment, treatment, and prevention of learned fears in humans.

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2

Iwasaki, Satoshi, Tetsuya Sakaguchi, and Yuji Ikegaya. "Brief fear preexposure facilitates subsequent fear conditioning." Neuroscience Research 95 (June 2015): 66–73. http://dx.doi.org/10.1016/j.neures.2015.02.001.

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3

Serim-Yıldız, Begüm, Özgür Erdur-Baker, and Aslı Bugay. "The Common Fears and Their Origins Among Turkish Children and Adolescents." Behaviour Change 30, no. 3 (August 12, 2013): 199–209. http://dx.doi.org/10.1017/bec.2013.18.

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The present study aimed to investigate the common fears and their origins among children and adolescents from different age, gender, and socioeconomic levels (SES). The sample was comprised of 642 females (48.8%) and 673 males (51.2%) with a total of 1,315 participants aged between 8 and 18 (M = 13.15; SD = 3.18). The Fear interview was utilised to examine the common fears and the role of conditioning, modelling and negative information in the development of children's fears. The result showed that the most common fear in Turkey was ‘God’, followed by ‘losing my friends’ and ‘going to Hell’. In addition, the findings revealed that Turkish students are more likely to learn fears by modelling rather than negative information transmission and conditioning. The results also indicated that negative information transmission had a more intensifying effect on the children and adolescents’ existing fear rather than modelling and conditioning. Furthermore, multinomial logistic regression was conducted to examine the effects of age, gender and SES on the origins of fear. Results showed that age and gender were significant predictors of origins of fear.

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4

Izquierdo, Ivan, Cristiane R. G. Furini, and Jociane C. Myskiw. "Fear Memory." Physiological Reviews 96, no. 2 (April 2016): 695–750. http://dx.doi.org/10.1152/physrev.00018.2015.

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Fear memory is the best-studied form of memory. It was thoroughly investigated in the past 60 years mostly using two classical conditioning procedures (contextual fear conditioning and fear conditioning to a tone) and one instrumental procedure (one-trial inhibitory avoidance). Fear memory is formed in the hippocampus (contextual conditioning and inhibitory avoidance), in the basolateral amygdala (inhibitory avoidance), and in the lateral amygdala (conditioning to a tone). The circuitry involves, in addition, the pre- and infralimbic ventromedial prefrontal cortex, the central amygdala subnuclei, and the dentate gyrus. Fear learning models, notably inhibitory avoidance, have also been very useful for the analysis of the biochemical mechanisms of memory consolidation as a whole. These studies have capitalized on in vitro observations on long-term potentiation and other kinds of plasticity. The effect of a very large number of drugs on fear learning has been intensively studied, often as a prelude to the investigation of effects on anxiety. The extinction of fear learning involves to an extent a reversal of the flow of information in the mentioned structures and is used in the therapy of posttraumatic stress disorder and fear memories in general.

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5

Åsli, Ole, and Magne Arve Flaten. "How Fast is Fear?" Journal of Psychophysiology 26, no. 1 (January 2012): 20–28. http://dx.doi.org/10.1027/0269-8803/a000063.

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The minimum latency of potentiated startle after delay and trace fear conditioning was investigated. Delay conditioning is hypothesized to be mediated by automatic processes, whereas trace conditioning is hypothesized to involve controlled cognitive processes. In a group receiving delay conditioning, a tone conditioned stimulus (CS) signaled an electric shock unconditioned stimulus (US) presented 1,000 ms after CS onset. In a group receiving trace conditioning, a 200 ms tone CS was followed by an 800 ms gap prior to US presentation. Two control groups received unpaired CS/US presentations. It was hypothesized that fear-potentiated startle should be observed at shorter time intervals after CS onset in the group receiving delay conditioning compared to the group receiving trace conditioning. The results showed increased startle at 100 and 150 ms after CS onset in the group receiving delay conditioning compared to the unpaired group. In the group receiving trace conditioning, increased startle was observed at 1,500 ms after CS onset compared to the unpaired group. This supports the idea that conditioned fear after delay conditioning may be due to automatic processes, whereas trace conditioning is dependent on controlled processes.

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6

Carmel, D., C. Raio, E. A. Phelps, and M. Carrasco. "Fast unconscious fear conditioning." Journal of Vision 11, no. 11 (September 23, 2011): 314. http://dx.doi.org/10.1167/11.11.314.

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7

Critchley, Hugo D., Christopher J. Mathias, and Raymond J. Dolan. "Fear Conditioning in Humans." Neuron 33, no. 4 (February 2002): 653–63. http://dx.doi.org/10.1016/s0896-6273(02)00588-3.

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8

Lai, Cora Sau Wan, Avital Adler, and Wen-Biao Gan. "Fear extinction reverses dendritic spine formation induced by fear conditioning in the mouse auditory cortex." Proceedings of the National Academy of Sciences 115, no. 37 (August 27, 2018): 9306–11. http://dx.doi.org/10.1073/pnas.1801504115.

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Fear conditioning-induced behavioral responses can be extinguished after fear extinction. While fear extinction is generally thought to be a form of new learning, several lines of evidence suggest that neuronal changes associated with fear conditioning could be reversed after fear extinction. To better understand how fear conditioning and extinction modify synaptic circuits, we examined changes of postsynaptic dendritic spines of layer V pyramidal neurons in the mouse auditory cortex over time using transcranial two-photon microscopy. We found that auditory-cued fear conditioning induced the formation of new dendritic spines within 2 days. The survived new spines induced by fear conditioning with one auditory cue were clustered within dendritic branch segments and spatially segregated from new spines induced by fear conditioning with a different auditory cue. Importantly, fear extinction preferentially caused the elimination of newly formed spines induced by fear conditioning in an auditory cue-specific manner. Furthermore, after fear extinction, fear reconditioning induced reformation of new dendritic spines in close proximity to the sites of new spine formation induced by previous fear conditioning. These results show that fear conditioning, extinction, and reconditioning induce cue- and location-specific dendritic spine remodeling in the auditory cortex. They also suggest that changes of synaptic connections induced by fear conditioning are reversed after fear extinction.

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9

Nesse, Randolph M., and James L. Abelson. "Natural selection and fear regulation mechanisms." Behavioral and Brain Sciences 18, no. 2 (June 1995): 309–10. http://dx.doi.org/10.1017/s0140525x00038620.

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AbstractExpectations can facilitate rapid fear conditioning and this may explain some phenomena that have been attributed to preparedness. However, preparedness remains the best explanation for some aspects of clinical phobias and the difficulty of creating fears of modern dangers. Rapid fear conditioning based on expectancy is not an alternative to an evolutionary explanation, but has, like preparedness, been shaped by natural selection.

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10

Sarowar, Tasnuva, and Andreas M. Grabrucker. "Rho GTPases in the Amygdala—A Switch for Fears?" Cells 9, no. 9 (August 26, 2020): 1972. http://dx.doi.org/10.3390/cells9091972.

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Fear is a fundamental evolutionary process for survival. However, excess or irrational fear hampers normal activity and leads to phobia. The amygdala is the primary brain region associated with fear learning and conditioning. There, Rho GTPases are molecular switches that act as signaling molecules for further downstream processes that modulate, among others, dendritic spine morphogenesis and thereby play a role in fear conditioning. The three main Rho GTPases—RhoA, Rac1, and Cdc42, together with their modulators, are known to be involved in many psychiatric disorders that affect the amygdala′s fear conditioning mechanism. Rich2, a RhoGAP mainly for Rac1 and Cdc42, has been studied extensively in such regard. Here, we will discuss these effectors, along with Rich2, as a molecular switch for fears, especially in the amygdala. Understanding the role of Rho GTPases in fear controlling could be beneficial for the development of therapeutic strategies targeting conditions with abnormal fear/anxiety-like behaviors.

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11

Ferreira, Tatiana L., Karin M. Moreira, Daniela C. Ikeda, Orlando F. A. Bueno, and Maria Gabriela M. Oliveira. "Effects of dorsal striatum lesions in tone fear conditioning and contextual fear conditioning." Brain Research 987, no. 1 (October 2003): 17–24. http://dx.doi.org/10.1016/s0006-8993(03)03217-7.

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12

McEchron, Matthew D., Hans Bouwmeester, Wilbur Tseng, Craig Weiss, and John F. Disterhoft. "Hippocampectomy disrupts auditory trace fear conditioning and contextual fear conditioning in the rat." Hippocampus 8, no. 6 (January 6, 1999): 638–46. http://dx.doi.org/10.1002/(sici)1098-1063(1998)8:6<638::aid-hipo6>3.0.co;2-q.

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13

Lipp, Ottmar V., Clare Kempnich, Sang Hoon Jee, and Derek H. Arnold. "Fear Conditioning to Subliminal Fear Relevant and Non Fear Relevant Stimuli." PLoS ONE 9, no. 9 (September 8, 2014): e99332. http://dx.doi.org/10.1371/journal.pone.0099332.

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14

Maren, Stephen. "Neurobiology of Pavlovian Fear Conditioning." Annual Review of Neuroscience 24, no. 1 (March 2001): 897–931. http://dx.doi.org/10.1146/annurev.neuro.24.1.897.

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15

Kenney, Justin W., Ian C. Scott, Sheena A. Josselyn, and Paul W. Frankland. "Contextual fear conditioning in zebrafish." Learning & Memory 24, no. 10 (September 15, 2017): 516–23. http://dx.doi.org/10.1101/lm.045690.117.

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16

Bradfield, Laura, and Gavan P. McNally. "Unblocking in Pavlovian fear conditioning." Journal of Experimental Psychology: Animal Behavior Processes 34, no. 2 (2008): 256–65. http://dx.doi.org/10.1037/0097-7403.34.2.256.

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17

Carter, R. M., C. Hofstotter, N. Tsuchiya, and C. Koch. "Working memory and fear conditioning." Proceedings of the National Academy of Sciences 100, no. 3 (January 27, 2003): 1399–404. http://dx.doi.org/10.1073/pnas.0334049100.

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18

Carpenter, Russ E., and Cliff H. Summers. "Learning strategies during fear conditioning." Neurobiology of Learning and Memory 91, no. 4 (May 2009): 415–23. http://dx.doi.org/10.1016/j.nlm.2009.01.009.

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19

Bauer, Elizabeth P. "Serotonin in fear conditioning processes." Behavioural Brain Research 277 (January 2015): 68–77. http://dx.doi.org/10.1016/j.bbr.2014.07.028.

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20

Beckers, Tom, Angelos-Miltiadis Krypotos, Yannick Boddez, Marieke Effting, and Merel Kindt. "What's wrong with fear conditioning?" Biological Psychology 92, no. 1 (January 2013): 90–96. http://dx.doi.org/10.1016/j.biopsycho.2011.12.015.

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21

Hellman, Kevin, and Ted Abel. "Fear conditioning increases NREM sleep." Behavioral Neuroscience 121, no. 2 (2007): 310–23. http://dx.doi.org/10.1037/0735-7044.121.2.310.

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22

Qu, Chen, Aiyi Zhang, and Qishan Chen. "Monetary Effects on Fear Conditioning." Psychological Reports 112, no. 2 (April 2013): 353–64. http://dx.doi.org/10.2466/16.17.pr0.112.2.353-364.

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Previous research has found that the loss of money as a negative secondary reinforcer was as effective as a primary reinforcer during fear conditioning. The purpose of the present study was to explore the effect of monetary gain as a positive secondary reinforcer in fear conditioning. Participants were assigned to a high-reward group or low-reward group. Three kinds of squares prompting non-compensation shock, compensation shock, and no shock were presented. Skin conductance responses (SCRs) and self-ratings were recorded. The results revealed that (a) both SCRs and self-ratings in the compensation shock condition were lower than in the non-compensation shock condition, suggesting that money might block the learning stage of fear conditioning; and (b) a higher ratio of fear reduction was present in self-rating when compared to SCRs, suggesting that people might overstate the utility of money, subjectively. Monetary effects, the effects of different amounts of money, and the differences between subjective and physiological levels are discussed.

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23

Bast, Tobias, Wei-Ning Zhang, and Joram Feldon. "Hippocampus and classical fear conditioning." Hippocampus 11, no. 6 (2001): 828–31. http://dx.doi.org/10.1002/hipo.1098.

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24

Hermans, Dirk, Michelle G. Craske, Susan Mineka, and Peter F. Lovibond. "Extinction in Human Fear Conditioning." Biological Psychiatry 60, no. 4 (August 2006): 361–68. http://dx.doi.org/10.1016/j.biopsych.2005.10.006.

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25

Birbaumer, Niels, Ralf Veit, Martin Lotze, Michael Erb, Christiane Hermann, Wolfgang Grodd, and Herta Flor. "Deficient Fear Conditioning in Psychopathy." Archives of General Psychiatry 62, no. 7 (July 1, 2005): 799. http://dx.doi.org/10.1001/archpsyc.62.7.799.

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26

Gould, Thomas J., and Joel A. Lommock. "Nicotine Enhances Contextual Fear Conditioning and Ameliorates Ethanol-Induced Deficits in Contextual Fear Conditioning." Behavioral Neuroscience 117, no. 6 (2003): 1276–82. http://dx.doi.org/10.1037/0735-7044.117.6.1276.

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27

Ivanova-Serokhvostova, Anastasiya, Beatriz Molinuevo, David Torrents-Rodas, Albert Bonillo, Iris Pérez-Bonaventura, Montserrat Corrales, Montserrat Pamias, Josep Antoni Ramos-Quiroga, and Rafael Torrubia. "Fear Conditioning Deficits in Children and Adolescents with Psychopathic Traits: a Study in a Clinical Population." Journal of Psychopathology and Behavioral Assessment 44, no. 1 (January 10, 2022): 11–25. http://dx.doi.org/10.1007/s10862-021-09947-3.

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AbstractDeficits in fear conditioning related to psychopathy have been widely studied in adults. However, evidence in children and adolescents is scarce and inconsistent. This research aimed to expand knowledge about fear conditioning in psychopathy and its dimensions in child and early adolescent clinical populations. Participants were 45 boys (outpatients) aged 6–14 years (M = 10.59, SD = 2.04). They were assessed with the parents’ and teachers’ versions of the Child Problematic Traits Inventory (CPTI). A fear conditioning paradigm (Neumann et al., in Biological Psychology, 79(3), 337–342, 2008) for children and adolescents was used. Conditioned stimuli (CS+ and CS-) were geometric shapes and the unconditioned stimulus (US) was an unpleasant sound of metal scraping on slate (83 dB). Difference scores (CS+ minus CS-) in skin conductance responses (SCR) and self-reported cognitive and affective measures were considered as indices of fear conditioning. Results showed that: a) deficits in fear conditioning were related to some psychopathy dimensions but not to psychopathy as a unitary construct; b) the Impulsivity-Need for Stimulation dimension was a predictor of impaired fear conditioning at a cognitive level; c) the interaction of Callous-Unemotional and Impulsivity-Need for Stimulation dimensions was a significant predictor of impaired electrodermal fear conditioning; d) by contrast, the Grandiose-Deceitful dimension, was marginally associated with a greater electrodermal fear conditioning. In conclusion, psychopathy dimensions and their interactions, but not psychopathy as a whole, predicted deficits in fear conditioning as measured by SCR and cognitive indices. These findings confirm the notion that psychopathic traits are associated with deficits in fear conditioning in child and adolescent clinical populations and provide support for a multidimensional approach to youth psychopathy.

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28

Shultz, Brianna, Abigail Farkash, Bailey Collins, Negin Mohammadmirzaei, and Dayan Knox. "Fear learning-induced changes in AMPAR and NMDAR expression in the fear circuit." Learning & Memory 29, no. 3 (February 15, 2022): 83–92. http://dx.doi.org/10.1101/lm.053525.121.

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NMDA receptors (NMDARs) and AMPA receptors (AMPARs) in amygdala nuclei and the dorsal hippocampus (dHipp) are critical for fear conditioning. Enhancements in synaptic AMPAR expression in amygdala nuclei and the dHipp are critical for fear conditioning, with some studies observing changes in AMPAR expression across many neurons in these brain regions. Whether similar changes occur in other nodes of the fear circuit (e.g., ventral hippocampus [vHipp]) or changes in NMDAR expression in the fear circuit occur with fear conditioning have not been sufficiently examined. To address this we used near-infrared immunohistochemistry (IHC) to measure AMPAR and NMDAR subunit expression in several nodes of the fear circuit. Long-term changes in GluR1 and GluR2 expression in the ventral hippocampus (vHipp) and anterior cingulate cortex (ACC), enhanced NR2A expression in amygdala nuclei, and changes in the ratio of GluR1/NR2A and GluR2/NR2A in the dHipp was observed with fear conditioning. Most of these changes were dependent on protein synthesis during fear conditioning and were not observed immediately after fear conditioning. The results of the study suggest that global changes in AMPARs and NMDARs occur in multiple nodes within the fear circuit and raise the possibility that these changes contribute to fear memory. Further research examining how global changes in AMPAR, NMDAR, and AMPAR/NMDAR ratios within nodes of the fear circuit contribute to fear memory is needed.

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29

Bartholomew, Morgan E., Vincent Rozalski, Anne Richards, Joyce Gurdock, Mary Thornton, Connie Fee, Sa'ar L. Lipshitz, Thomas J. Metzler, Thomas C. Neylan, and Sabra S. Inslicht. "Impact of hormonal contraceptives on sex differences in fear conditioning and fear extinction in PTSD." Learning & Memory 29, no. 9 (September 2022): 332–39. http://dx.doi.org/10.1101/lm.053597.122.

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Sex differences in the neurobiological mechanisms involved in fear conditioning and extinction have been suggested to contribute to differential vulnerability for the development of posttraumatic stress disorder (PTSD) in women compared with men. Reproductive hormones, such as estradiol, have been shown to facilitate fear conditioning and extinction learning and may explain some of these differences. However, the effect of commonly used hormonal contraceptives on the neurobiological mechanisms of fear conditioning and extinction is poorly understood. A laboratory study was conducted in trauma-exposed men and women with and without full or partial PTSD to examine effects of sex and use of hormonal birth control on fear conditioning, fear extinction learning, and extinction retention. Participants underwent fear conditioning with stimuli that were paired (CS+) or unpaired (CS−) with shock. Extinction learning occurred 72 h later, and extinction retention was tested 1 wk after extinction. Women on hormonal contraceptives (HCs) demonstrated enhanced acquisition of fear conditioning and enhanced extinction of fear as compared with women off hormonal birth control and men. While clinical implications have yet to be determined, these results suggest that hormonal contraceptives may facilitate learning during both fear acquisition and extinction. Understanding the impact of sex and hormones on fear conditioning and extinction processes may lead to new insights into the pathophysiology of PTSD and result in advancements in treatment that may vary by sex.

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30

Schafe, Glenn E., Nicole V. Nadel, Gregory M. Sullivan, Alexander Harris, and Joseph E. LeDoux. "Memory Consolidation for Contextual and Auditory Fear Conditioning Is Dependent on Protein Synthesis, PKA, and MAP Kinase." Learning & Memory 6, no. 2 (March 1, 1999): 97–110. http://dx.doi.org/10.1101/lm.6.2.97.

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Fear conditioning has received extensive experimental attention. However, little is known about the molecular mechanisms that underlie fear memory consolidation. Previous studies have shown that long-term potentiation (LTP) exists in pathways known to be relevant to fear conditioning and that fear conditioning modifies neural processing in these pathways in a manner similar to LTP induction. The present experiments examined whether inhibition of protein synthesis, PKA, and MAP kinase activity, treatments that block LTP, also interfere with the consolidation of fear conditioning. Rats were injected intraventricularly with Anisomycin (100 or 300 μg), Rp-cAMPS (90 or 180 μg), or PD098059 (1 or 3 μg) prior to conditioning and assessed for retention of contextual and auditory fear memory both within an hour and 24 hr later. Results indicated that injection of these compounds selectively interfered with long-term memory for contextual and auditory fear, while leaving short-term memory intact. Additional control groups indicated that this effect was likely due to impaired memory consolidation rather than to nonspecific effects of the drugs on fear expression. Results suggest that fear conditioning and LTP may share common molecular mechanisms.

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31

Rudy, Jerry W., and C. Rachal Pugh. "Time of conditioning selectively influences contextual fear conditioning: Further support for a multiple-memory systems view of fear conditioning." Journal of Experimental Psychology: Animal Behavior Processes 24, no. 3 (1998): 316–24. http://dx.doi.org/10.1037/0097-7403.24.3.316.

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32

Baumann, Christian, Miriam A. Schiele, Martin J. Herrmann, Tina B. Lonsdorf, Peter Zwanzger, Katharina Domschke, Andreas Reif, Jürgen Deckert, and Paul Pauli. "Effects of an Anxiety-Specific Psychometric Factor on Fear Conditioning and Fear Generalization." Zeitschrift für Psychologie 225, no. 3 (July 2017): 200–213. http://dx.doi.org/10.1027/2151-2604/a000304.

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Abstract. Conditioning and generalization of fear are assumed to play central roles in the pathogenesis of anxiety disorders. Here we investigate the influence of a psychometric anxiety-specific factor on these two processes, thus try to identify a potential risk factor for the development of anxiety disorders. To this end, 126 healthy participants were examined with questionnaires assessing symptoms of anxiety and depression and with a fear conditioning and generalization paradigm. A principal component analysis of the questionnaire data identified two factors representing the constructs anxiety and depression. Variations in fear conditioning and fear generalization were solely associated with the anxiety factor characterized by anxiety sensitivity and agoraphobic cognitions; high-anxious individuals exhibited stronger fear responses (arousal) during conditioning and stronger generalization effects for valence and UCS-expectancy ratings. Thus, the revealed psychometric factor “anxiety” was associated with enhanced fear generalization, an assumed risk factor for anxiety disorders. These results ask for replication with a longitudinal design allowing to examine their predictive validity.

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33

Sun, Yajie, Helen Gooch, and Pankaj Sah. "Fear conditioning and the basolateral amygdala." F1000Research 9 (January 28, 2020): 53. http://dx.doi.org/10.12688/f1000research.21201.1.

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Fear is a response to impending threat that prepares a subject to make appropriate defensive responses, whether to freeze, fight, or flee to safety. The neural circuits that underpin how subjects learn about cues that signal threat, and make defensive responses, have been studied using Pavlovian fear conditioning in laboratory rodents as well as humans. These studies have established the amygdala as a key player in the circuits that process fear and led to a model where fear learning results from long-term potentiation of inputs that convey information about the conditioned stimulus to the amygdala. In this review, we describe the circuits in the basolateral amygdala that mediate fear learning and its expression as the conditioned response. We argue that while the evidence linking synaptic plasticity in the basolateral amygdala to fear learning is strong, there is still no mechanism that fully explains the changes that underpin fear conditioning.

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34

Hettema, John M., Peter Annas, Michael C. Neale, Mats Fredrikson, and Kenneth S. Kendler. "The Genetic Covariation Between Fear Conditioning and Self-Report Fears." Biological Psychiatry 63, no. 6 (March 2008): 587–93. http://dx.doi.org/10.1016/j.biopsych.2007.06.009.

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35

Vurbic, Drina, and Mark E. Bouton. "Secondary extinction in Pavlovian fear conditioning." Learning & Behavior 39, no. 3 (February 1, 2011): 202–11. http://dx.doi.org/10.3758/s13420-011-0017-7.

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36

Yau, Joanna O. Y., and Gavan P. McNally. "Brain mechanisms controlling Pavlovian fear conditioning." Journal of Experimental Psychology: Animal Learning and Cognition 44, no. 4 (October 2018): 341–57. http://dx.doi.org/10.1037/xan0000181.

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37

Cai, D. J., T. Shuman, E. M. Harrison, J. R. Sage, and S. G. Anagnostaras. "Sleep deprivation and Pavlovian fear conditioning." Learning & Memory 16, no. 10 (September 30, 2009): 595–99. http://dx.doi.org/10.1101/lm.1515609.

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38

Mongeluzi, Donna L., Robert A. Rosellini, Ronald Ley, Barbara J. Caldarone, and Howard S. Stock. "The Conditioning of Dyspneic Suffocation Fear." Behavior Modification 27, no. 5 (October 2003): 620–36. http://dx.doi.org/10.1177/0145445503256316.

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39

Duvarci, S., D. Popa, and D. Pare. "Central Amygdala Activity during Fear Conditioning." Journal of Neuroscience 31, no. 1 (January 5, 2011): 289–94. http://dx.doi.org/10.1523/jneurosci.4985-10.2011.

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40

PEZZE, M., and J. FELDON. "Mesolimbic dopaminergic pathways in fear conditioning." Progress in Neurobiology 74, no. 5 (December 2004): 301–20. http://dx.doi.org/10.1016/j.pneurobio.2004.09.004.

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41

Fanselow, Michael S. "NEURAL MECHANISMS OF CONTEXTUAL FEAR CONDITIONING." Behavioural Pharmacology 10, SUPPLEMENT 1 (August 1999): s32. http://dx.doi.org/10.1097/00008877-199908001-00080.

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42

Büchel, C. "Classical fear conditioning in functional neuroimaging." Current Opinion in Neurobiology 10, no. 2 (April 1, 2000): 219–23. http://dx.doi.org/10.1016/s0959-4388(00)00078-7.

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43

Soler-Cedeño, Omar, Emmanuel Cruz, Marangelie Criado-Marrero, and James T. Porter. "Contextual fear conditioning depresses infralimbic excitability." Neurobiology of Learning and Memory 130 (April 2016): 77–82. http://dx.doi.org/10.1016/j.nlm.2016.01.015.

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44

Merz, Christian, and Oliver Wolf. "Fear conditioning, social groups and stress." Psychoneuroendocrinology 61 (November 2015): 44. http://dx.doi.org/10.1016/j.psyneuen.2015.07.509.

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45

Elias, G. A., D. Gulick, D. S. Wilkinson, and T. J. Gould. "Nicotine and extinction of fear conditioning." Neuroscience 165, no. 4 (February 2010): 1063–73. http://dx.doi.org/10.1016/j.neuroscience.2009.11.022.

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46

Rosenkranz, J. Amiel, and Anthony A. Grace. "Response: Mechanisms of Pavlovian fear conditioning." Trends in Neurosciences 25, no. 9 (September 2002): 437–38. http://dx.doi.org/10.1016/s0166-2236(02)02239-7.

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Brunzell, Darlene H., Abigail E. Coy, John J. B. Ayres, and Jerrold S. Meyer. "Prenatal cocaine effects on fear conditioning:." Neurotoxicology and Teratology 24, no. 2 (March 2002): 161–72. http://dx.doi.org/10.1016/s0892-0362(01)00212-4.

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Palomares, Nerea, Armando Cuesta-Diaz, Judy R. Burke, Amanda Fisher, Sukhbir Kaur, and M. Mercedes Perez-Rodriguez. "Fear Conditioning in Borderline Personality Disorder." Current Behavioral Neuroscience Reports 3, no. 1 (January 19, 2016): 10–18. http://dx.doi.org/10.1007/s40473-016-0062-9.

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Hong, Ingie, Taewook Kang, Ki Na Yun, YongCheol Yoo, Sungmo Park, Jihye Kim, Bobae An, et al. "Quantitative proteomics of auditory fear conditioning." Biochemical and Biophysical Research Communications 434, no. 1 (April 2013): 87–94. http://dx.doi.org/10.1016/j.bbrc.2013.03.060.

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Hamann, Stephan, Elena S. Monarch, and Felicia C. Goldstein. "Impaired fear conditioning in Alzheimer’s disease." Neuropsychologia 40, no. 8 (January 2002): 1187–95. http://dx.doi.org/10.1016/s0028-3932(01)00223-8.

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