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Artykuły w czasopismach na temat „Conditioned fear”

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Autor: Grafiati

Data publikacji: 4 czerwca 2021

Data aktualizacji: 4 lutego 2022

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1

Inoue, Takeshi, Yuji Kitaichi i Tsukasa Koyama. "SSRIs and conditioned fear". Progress in Neuro-Psychopharmacology and Biological Psychiatry 35, nr 8 (grudzień 2011): 1810–19. http://dx.doi.org/10.1016/j.pnpbp.2011.09.002.

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Homberg, Judith R. "Serotonergic Modulation of Conditioned Fear". Scientifica 2012 (2012): 1–16. http://dx.doi.org/10.6064/2012/821549.

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Conditioned fear plays a key role in anxiety disorders as well as depression and other neuropsychiatric conditions. Understanding how neuromodulators drive the associated learning and memory processes, including memory consolidation, retrieval/expression, and extinction (recall), is essential in the understanding of (individual differences in vulnerability to) these disorders and their treatment. The human and rodent studies I review here together reveal, amongst others, that acute selective serotonin reuptake inhibitor (SSRI) treatment facilitates fear conditioning, reduces contextual fear, and increases cued fear, chronic SSRI treatment reduces both contextual and cued fear, 5-HT1Areceptors inhibit the acquisition and expression of contextual fear, 5-HT2Areceptors facilitates the consolidation of cued and contextual fear, inactivation of 5-HT2Creceptors facilitate the retrieval of cued fear memory, the 5-HT3receptor mediates contextual fear, genetically induced increases in serotonin levels are associated with increased fear conditioning, impaired cued fear extinction, or impaired extinction recall, and that genetically induced 5-HT depletion increases fear conditioning and contextual fear. Several explanations are presented to reconcile seemingly paradoxical relationships between serotonin levels and conditioned fear.

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3

Shalev, Arieh Y., Yael Rogel-Fuchs i Roger K. Pitman. "Conditioned fear and psychological trauma". Biological Psychiatry 31, nr 9 (maj 1992): 863–65. http://dx.doi.org/10.1016/0006-3223(92)90113-e.

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Mulckhuyse, Manon, Geert Crombez i Stefan Van der Stigchel. "Conditioned fear modulates visual selection." Emotion 13, nr 3 (2013): 529–36. http://dx.doi.org/10.1037/a0031076.

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Wixted, John T. "Sleep aromatherapy curbs conditioned fear". Nature Neuroscience 16, nr 11 (28.10.2013): 1510–12. http://dx.doi.org/10.1038/nn.3556.

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6

Ho, Yiling, i Ottmar V. Lipp. "Faster acquisition of conditioned fear to fear-relevant than to nonfear-relevant conditional stimuli". Psychophysiology 51, nr 8 (14.04.2014): 810–13. http://dx.doi.org/10.1111/psyp.12223.

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Sanchez, Christopher J., i Barbara A. Sorg. "Conditioned fear stimuli reinstate cocaine-induced conditioned place preference". Brain Research 908, nr 1 (lipiec 2001): 86–92. http://dx.doi.org/10.1016/s0006-8993(01)02638-5.

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Yoshida, Masahide, Yuki Takayanagi i Tatsushi Onaka. "The Medial Amygdala-Medullary PrRP-Synthesizing Neuron Pathway Mediates Neuroendocrine Responses to Contextual Conditioned Fear in Male Rodents". Endocrinology 155, nr 8 (1.08.2014): 2996–3004. http://dx.doi.org/10.1210/en.2013-1411.

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Fear responses play evolutionarily beneficial roles, although excessive fear memory can induce inappropriate fear expression observed in posttraumatic stress disorder, panic disorder, and phobia. To understand the neural machineries that underlie these disorders, it is important to clarify the neural pathways of fear responses. Contextual conditioned fear induces freezing behavior and neuroendocrine responses. Considerable evidence indicates that the central amygdala plays an essential role in expression of freezing behavior after contextual conditioned fear. On the other hand, mechanisms of neuroendocrine responses remain to be clarified. The medial amygdala (MeA), which is activated after contextual conditioned fear, was lesioned bilaterally by infusion of N-methyl-d-aspartate after training of fear conditioning. Plasma oxytocin, ACTH, and prolactin concentrations were significantly increased after contextual conditioned fear in sham-lesioned rats. In MeA-lesioned rats, these neuroendocrine responses but not freezing behavior were significantly impaired compared with those in sham-lesioned rats. In contrast, the magnitudes of neuroendocrine responses after exposure to novel environmental stimuli were not significantly different in MeA-lesioned rats and sham-lesioned rats. Contextual conditioned fear activated prolactin-releasing peptide (PrRP)-synthesizing neurons in the medulla oblongata. In MeA-lesioned rats, the percentage of PrRP-synthesizing neurons activated after contextual conditioned fear was significantly decreased. Furthermore, neuroendocrine responses after contextual conditioned fear disappeared in PrRP-deficient mice. Our findings suggest that the MeA-medullary PrRP-synthesizing neuron pathway plays an important role in neuroendocrine responses to contextual conditioned fear.

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9

Davis, Michael, David L. Walker i Younglim Lee. "Amygdala and bed nucleus of the stria terminalis: differential roles in fear and anxiety measured with the acoustic startle reflex". Philosophical Transactions of the Royal Society of London. Series B: Biological Sciences 352, nr 1362 (29.11.1997): 1675–87. http://dx.doi.org/10.1098/rstb.1997.0149.

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Neural stimuli associated with traumatic events can readily become conditioned so as to reinstate the memory of the original trauma. These conditioned fear responses can last a lifetime and may be especially resistant to extinction. A large amount of data from many different laboratories indicate that the amygdala plays a crucial role in conditioned fear. The amygdala receives information from all sensory modalities and projects to a variety of hypothalamic and brainstem target areas known to be critically involved in specific signs that are used to define fear and anxiety. Electrical stimulation of the amygdala elicits a pattern of behaviours that mimic natural or conditioned states of fear. Lesions of the amygdala block innate or conditioned fear and local infusion of drugs into the amygdala have anxiolytic effects in several behavioural tests. Excitatory amino acid receptors in the amygdala are critical for the acquisition, expression and extinction of conditioned fear.

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10

Hodes, Robert L., Edwin W. Cook i Peter J. Lang. "Individual Differences in Autonomic Response: Conditioned Association or Conditioned Fear?" Psychophysiology 22, nr 5 (wrzesień 1985): 545–60. http://dx.doi.org/10.1111/j.1469-8986.1985.tb01649.x.

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11

Pezze, M. A. "S.15.03 Dopamine and conditioned fear". European Neuropsychopharmacology 16 (styczeń 2006): S186. http://dx.doi.org/10.1016/s0924-977x(06)70076-1.

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Castegnetti, Giuseppe, Athina Tzovara, Matthias Staib, Philipp C. Paulus, Nicolas Hofer i Dominik R. Bach. "Modeling fear-conditioned bradycardia in humans". Psychophysiology 53, nr 6 (7.03.2016): 930–39. http://dx.doi.org/10.1111/psyp.12637.

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13

Abrahamsen, Glenn C., Barbara J. Caldarone, Howard S. Stock, Amy D. Schutz i Robert A. Rosellini. "Conditioned fear exacerbates acute morphine dependence". Pharmacology Biochemistry and Behavior 51, nr 2-3 (czerwiec 1995): 407–13. http://dx.doi.org/10.1016/0091-3057(94)00415-f.

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14

Gaspar, Jessica C., Bright N. Okine, Alvaro Llorente-Berzal, Michelle Roche i David P. Finn. "Pharmacological Blockade of PPAR Isoforms Increases Conditioned Fear Responding in the Presence of Nociceptive Tone". Molecules 25, nr 4 (24.02.2020): 1007. http://dx.doi.org/10.3390/molecules25041007.

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Peroxisome proliferator-activated receptors (PPARs) are nuclear receptors with three isoforms (PPARα, PPARβ/δ, PPARγ) and can regulate pain, anxiety, and cognition. However, their role in conditioned fear and pain-fear interactions has not yet been investigated. Here, we investigated the effects of systemically administered PPAR antagonists on formalin-evoked nociceptive behaviour, fear-conditioned analgesia (FCA), and conditioned fear in the presence of nociceptive tone in rats. Twenty-three and a half hours following fear conditioning to context, male Sprague-Dawley rats received an intraplantar injection of formalin and intraperitoneal administration of vehicle, PPARα (GW6471), PPARβ/δ (GSK0660) or PPARγ (GW9662) antagonists, and 30 min later were re-exposed to the conditioning arena for 15 min. The PPAR antagonists did not alter nociceptive behaviour or fear-conditioned analgesia. The PPARα and PPARβ/δ antagonists prolonged context-induced freezing in the presence of nociceptive tone without affecting its initial expression. The PPARγ antagonist potentiated freezing over the entire trial. In conclusion, pharmacological blockade of PPARα and PPARβ/δ in the presence of formalin-evoked nociceptive tone, impaired short-term, within-trial fear-extinction in rats without affecting pain response, while blockade of PPARγ potentiated conditioned fear responding. These results suggest that endogenous signalling through these three PPAR isoforms may reduce the expression of conditioned fear in the presence of nociceptive tone.

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15

Paré, Denis, Gregory J. Quirk i Joseph E. Ledoux. "New Vistas on Amygdala Networks in Conditioned Fear". Journal of Neurophysiology 92, nr 1 (lipiec 2004): 1–9. http://dx.doi.org/10.1152/jn.00153.2004.

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It is currently believed that the acquisition of classically conditioned fear involves potentiation of conditioned thalamic inputs in the lateral amygdala (LA). In turn, LA cells would excite more neurons in the central nucleus (CE) that, via their projections to the brain stem and hypothalamus, evoke fear responses. However, LA neurons do not directly contact brain stem-projecting CE neurons. This is problematic because CE projections to the periaqueductal gray and pontine reticular formation are believed to generate conditioned freezing and fear-potentiated startle, respectively. Moreover, like LA, CE may receive direct thalamic inputs communicating information about the conditioned and unconditioned stimuli. Finally, recent evidence suggests that the CE itself may be a critical site of plasticity. This review attempts to reconcile the current model with these observations. We suggest that potentiated LA outputs disinhibit CE projection neurons via GABAergic intercalated neurons, thereby permitting associative plasticity in CE. Thus plasticity in both LA and CE would be necessary for acquisition of conditioned fear. This revised model also accounts for inhibition of conditioned fear after extinction.

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16

DeVito, Paul L., i Harry Fowler. "Effects of contingency violations on the extinction of a conditioned fear inhibitor and a conditioned fear excitor." Journal of Experimental Psychology: Animal Behavior Processes 12, nr 2 (1986): 99–115. http://dx.doi.org/10.1037/0097-7403.12.2.99.

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17

McNish, Kenneth A., Stephanie L. Betts, Susan E. Brandon i Allan R. Wagner. "Divergence of conditioned eyeblink and conditioned fear in backward Pavlovian training". Animal Learning & Behavior 25, nr 1 (marzec 1997): 43–52. http://dx.doi.org/10.3758/bf03199023.

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18

Kim, Stephen D., Steven Rivers, Rick A. Bevins i John J. B. Ayres. "Conditioned stimulus determinants of conditioned response form in Pavlovian fear conditioning." Journal of Experimental Psychology: Animal Behavior Processes 22, nr 1 (1996): 87–104. http://dx.doi.org/10.1037/0097-7403.22.1.87.

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19

Nonaka, Ayako, Norio Matsuki i Hiroshi Nomura. "Fear conditioning changes responsiveness of fear-related neurons to conditioned stimulus". Neuroscience Research 71 (wrzesień 2011): e376. http://dx.doi.org/10.1016/j.neures.2011.07.1650.

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20

Leung, Hiu T., Nathan M. Holmes i R. Frederick Westbrook. "An appetitive conditioned stimulus enhances fear acquisition and impairs fear extinction". Learning & Memory 23, nr 3 (16.02.2016): 113–20. http://dx.doi.org/10.1101/lm.040337.115.

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21

Pace-Schott, Edward F., Anne Germain i Mohammed R. Milad. "Effects of sleep on memory for conditioned fear and fear extinction." Psychological Bulletin 141, nr 4 (2015): 835–57. http://dx.doi.org/10.1037/bul0000014.

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22

Prado-Lima, Pedro. "Topiramate diminishes fear memory consolidation and extinguishes conditioned fear in rats". Journal of Psychiatry & Neuroscience 36, nr 4 (1.07.2011): 250–55. http://dx.doi.org/10.1503/jpn.100115.

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23

Dunsmoor, J. E., S. R. Mitroff i K. S. LaBar. "Generalization of conditioned fear along a dimension of increasing fear intensity". Learning & Memory 16, nr 7 (24.06.2009): 460–69. http://dx.doi.org/10.1101/lm.1431609.

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24

Minor, Thomas R. "Conditioned fear and neophobia following inescapable shock". Animal Learning & Behavior 18, nr 2 (czerwiec 1990): 212–26. http://dx.doi.org/10.3758/bf03205261.

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25

Hudgins, Caleb, i Tim Otto. "Hippocampal Arc protein expression and conditioned fear". Neurobiology of Learning and Memory 161 (maj 2019): 175–91. http://dx.doi.org/10.1016/j.nlm.2019.04.004.

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26

McGaugh, James L., Claudio Castellano i Jorge Brioni. "Picrotoxin enhances latent extinction of conditioned fear." Behavioral Neuroscience 104, nr 2 (1990): 264–67. http://dx.doi.org/10.1037/0735-7044.104.2.264.

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CORODIMAS, KEITH P., JOSEPH E. LeDOUX, PHILIP W. GOLD i JAY SCHULKIN. "Corticosterone Potentiation of Conditioned Fear in Ratsa". Annals of the New York Academy of Sciences 746, nr 1 (17.12.2006): 392–93. http://dx.doi.org/10.1111/j.1749-6632.1994.tb39264.x.

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Sekiguchi, Masayuki. "Biological Systems that Control Conditioned Fear Memory". Anxiety Disorder Research 5, nr 2 (2014): 85–92. http://dx.doi.org/10.14389/adr.5.85.

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Siemiątkowski, Marek, Dariusz Rokicki, Agnieszka I. Członkowska, Helena Sienkiewicz-Jarosz, Andrzej Bidziński i Adam Płaźnik. "Locomotor activity and a conditioned fear response". NeuroReport 11, nr 18 (grudzień 2000): 3953–56. http://dx.doi.org/10.1097/00001756-200012180-00010.

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Rosenbaum, Blake L., Eric Bui, Marie-France Marin, Daphne J. Holt, Natasha B. Lasko, Roger K. Pitman, Scott P. Orr i Mohammed R. Milad. "Demographic factors predict magnitude of conditioned fear". International Journal of Psychophysiology 98, nr 1 (październik 2015): 59–64. http://dx.doi.org/10.1016/j.ijpsycho.2015.06.010.

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Quirk, Gregory J., René Garcia i Francisco González-Lima. "Prefrontal Mechanisms in Extinction of Conditioned Fear". Biological Psychiatry 60, nr 4 (sierpień 2006): 337–43. http://dx.doi.org/10.1016/j.biopsych.2006.03.010.

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Schell, Anne M., i Michael E. Dawson. "Responses conditioned to fear-relevant stimuli survive extinction of the expectancy of the UCS". Behavioral and Brain Sciences 18, nr 2 (czerwiec 1995): 312–13. http://dx.doi.org/10.1017/s0140525x00038656.

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AbstractDavey suggests that increased resistance to extinction of CRs conditioned to fear-relevant stimuli may be due to more persistent expectancies of the UCS following these stimuli. However, this viewpoint is contradicted by existing empirical evidence that fear-relevant CRs survive an extinction trials series producing extinction of expectancies whereas CRs conditioned to non-fear-relevant CSs do not.

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33

Hagsäter, S. Melker, Johan Thorén, Robert Pettersson i Elias Eriksson. "Selective serotonin reuptake inhibition increases noise burst-induced unconditioned and context-conditioned freezing". Acta Neuropsychiatrica 31, nr 1 (8.11.2018): 46–51. http://dx.doi.org/10.1017/neu.2018.26.

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AbstractObjectiveWhereas long-term administration of selective serotonin reuptake inhibitors (SSRIs) is effective for the treatment of anxiety disorders, acute administration of these drugs may exert a paradoxical anxiogenic effect. The aim of the present study was to explore the possible effect of an SSRI in situations of unconditioned or limited conditioned fear.MethodsMale Sprague Dawley rats were administered a single dose of an SSRI, escitalopram, before acquisition or expression of context conditioned fear, where noise bursts were used as the unconditioned stimulus. Freezing was assessed as a measure of unconditioned fear (=the acute response to noise bursts) or conditioned fear (=the response to the context), respectively.ResultsNoise bursts elicited an acute increase in freezing but no robust conditioned response 7 days after exposure. Administration of escitalopram before testing exacerbated the freezing response during presentation of the unconditioned stimulus and also unmasked a conditioned response; in contrast, administration of escitalopram prior to acquisition did not influence the conditioned response.ConclusionThe data suggest that freezing in rats exposed to a stimulus inducing relatively mild fear may be enhanced by acute pretreatment with an SSRI regardless of whether the freezing displayed by the animals is an acute unconditioned response to the stimulus in question or a conditioned response to the same stimulus.

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34

Thompson, Alina, i Ottmar V. Lipp. "Extinction during reconsolidation eliminates recovery of fear conditioned to fear-irrelevant and fear-relevant stimuli". Behaviour Research and Therapy 92 (maj 2017): 1–10. http://dx.doi.org/10.1016/j.brat.2017.01.017.

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Kita, Serina, Ryuji Hashiba, Saya Ueki, Yukari Kimoto, Yoshito Abe, Yuta Gotoda, Ryoko Suzuki i in. "Does Conditioned Taste Aversion Learning in the Pond SnailLymnaea stagnalisProduce Conditioned Fear?" Biological Bulletin 220, nr 1 (luty 2011): 71–81. http://dx.doi.org/10.1086/bblv220n1p71.

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Norrholm, S. D., T. Jovanovic, B. Vervliet, K. M. Myers, M. Davis, B. O. Rothbaum i E. J. Duncan. "Conditioned fear extinction and reinstatement in a human fear-potentiated startle paradigm". Learning & Memory 13, nr 6 (1.11.2006): 681–85. http://dx.doi.org/10.1101/lm.393906.

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Davis, Michael, Karyn M. Myers, Kerry J. Ressler i Barbara O. Rothbaum. "Facilitation of Extinction of Conditioned Fear by D-Cycloserine". Current Directions in Psychological Science 14, nr 4 (sierpień 2005): 214–19. http://dx.doi.org/10.1111/j.0963-7214.2005.00367.x.

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Excessive fear and anxiety are characteristic of disorders such as post-traumatic stress disorder (PTSD) and phobias and are believed to reflect abnormalities in neural systems governing the development and reduction of conditioned fear. Conditioned fear can be suppressed through a process known as extinction, in which repeated exposure to a feared stimulus in the absence of an aversive event leads to a gradual reduction in the fear response to that stimulus. Like conditioned fear learning, extinction is dependent on a particular protein (the N-methyl-D-aspartate or NMDA receptor) in a part of the brain called the amygdala. Blockade of this receptor blocks extinction and improving the activity of this receptor with a drug called D-cycloserine speeds up extinction in rats. Because exposure-based psychotherapy for fear disorders in humans resembles extinction in several respects, we investigated whether D-cycloserine might facilitate the loss of fear in human patients. Consistent with findings from the animal laboratory, patients receiving D-cycloserine benefited more from exposure-based psychotherapy than did placebo-treated controls. Although very preliminary, these data provide initial support for the use of cognitive enhancers in psychotherapy and demonstrate that preclinical studies in rodents can have direct benefits to humans.

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38

BREMNER, J. DOUGLAS, ERIC VERMETTEN, CHRISTIAN SCHMAHL, VIOLA VACCARINO, MEENA VYTHILINGAM, NADEEM AFZAL, CHRISTIAN GRILLON i DENNIS S. CHARNEY. "Positron emission tomographic imaging of neural correlates of a fear acquisition and extinction paradigm in women with childhood sexual-abuse-related post-traumatic stress disorder". Psychological Medicine 35, nr 6 (29.09.2004): 791–806. http://dx.doi.org/10.1017/s0033291704003290.

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Background. In the conditioned fear paradigm, repeated pairing of an aversive unconditioned stimulus (US) (e.g. electric shock) with a neutral conditioned stimulus (CS) (e.g. bright light) results in a conditioned fear response to the light alone. Animal studies have shown that the amygdala plays a critical role in acquisition of conditioned fear responses, while the medial prefrontal cortex (including anterior cingulate), through inhibition of amygdala responsiveness, has been hypothesized to play a role in extinction of fear responses. No studies have examined neural correlates of fear conditioning and extinction in patients with post-traumatic stress disorder (PTSD).Method. Women with early childhood sexual-abuse-related PTSD (n=8) and women without abuse or PTSD (n=11) underwent measurement of psychophysiological (skin conductance) responding as well as positron emission tomographic (PET) measurement of cerebral blood flow during habituation, acquisition and extinction conditions. During habituation subjects were repeatedly exposed to a blue square on a screen. During acquisition, exposure to the blue square (CS) was paired with an electric shock to the forearm (US). With extinction, subjects were again exposed to the blue squares without shock. On a different day subjects went through the same procedure with electric shocks administered randomly in the absence of the blue square.Results. Skin conductance responding to the CS was consistent with the development of conditioned responses with this paradigm. PTSD patients had increased left amygdala activation with fear acquisition, and decreased anterior cingulate function during extinction, relative to controls.Conclusions. These findings implicate amygdala and anterior cingulate in the acquisition and extinction of fear responses, respectively, in PTSD.

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39

Chorot, Paloma, i Bonifacio Sandín. "Effects of UCS Intensity and Duration of Exposure of Nonreinforced CS on Conditioned Electrodermal Responses: An Experimental Analysis of the Incubation Theory of Anxiety". Psychological Reports 73, nr 3_part_1 (grudzień 1993): 931–41. http://dx.doi.org/10.1177/00332941930733pt132.

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Eysenck's incubation theory of fear or anxiety was examined in a human Pavlovian conditioning experiment with skin-conductance responses as the dependent variable. The conditioned stimuli (CSs) were fear-relevant slides (snakes and spiders) and the unconditioned stimuli (UCSs) were aversive tones. Different groups of subjects were presented two tone intensities during the acquisition phase and three durations of nonreinforced CS (extinction phase) in a delay differential conditioning paradigm. Resistance to extinction of conditioned skin-conductance responses (conditioned fear responses) exhibited was largest for high intensity of tone and short presentations of the nonreinforced CS (CS + presented alone). The result tends to support Eysenck's incubation theory of anxiety.

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40

Faul, Leonard, Daniel Stjepanović, Joshua M. Stivers, Gregory W. Stewart, John L. Graner, Rajendra A. Morey i Kevin S. LaBar. "Proximal threats promote enhanced acquisition and persistence of reactive fear-learning circuits". Proceedings of the National Academy of Sciences 117, nr 28 (29.06.2020): 16678–89. http://dx.doi.org/10.1073/pnas.2004258117.

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Physical proximity to a traumatic event increases the severity of accompanying stress symptoms, an effect that is reminiscent of evolutionarily configured fear responses based on threat imminence. Despite being widely adopted as a model system for stress and anxiety disorders, fear-conditioning research has not yet characterized how threat proximity impacts the mechanisms of fear acquisition and extinction in the human brain. We used three-dimensional (3D) virtual reality technology to manipulate the egocentric distance of conspecific threats while healthy adult participants navigated virtual worlds during functional magnetic resonance imaging (fMRI). Consistent with theoretical predictions, proximal threats enhanced fear acquisition by shifting conditioned learning from cognitive to reactive fear circuits in the brain and reducing amygdala–cortical connectivity during both fear acquisition and extinction. With an analysis of representational pattern similarity between the acquisition and extinction phases, we further demonstrate that proximal threats impaired extinction efficacy via persistent multivariate representations of conditioned learning in the cerebellum, which predicted susceptibility to later fear reinstatement. These results show that conditioned threats encountered in close proximity are more resistant to extinction learning and suggest that the canonical neural circuitry typically associated with fear learning requires additional consideration of a more reactive neural fear system to fully account for this effect.

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41

Holahan, Matthew R., i Norman M. White. "Conditioned Memory Modulation, Freezing, and Avoidance as Measures of Amygdala-Mediated Conditioned Fear". Neurobiology of Learning and Memory 77, nr 2 (marzec 2002): 250–75. http://dx.doi.org/10.1006/nlme.2001.4012.

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42

Richardson, Rick, Tania Q. Duffield, Glynis K. Bailey i R. Frederick Westbrook. "Reinstatement of fear to an extinguished conditioned context". Animal Learning & Behavior 27, nr 4 (grudzień 1999): 399–415. http://dx.doi.org/10.3758/bf03209977.

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Hicks, Robert A., Gregory J. Hicks i Joe R. Reyes. "REM sleep deprivation and conditioned fear in rats". Bulletin of the Psychonomic Society 26, nr 1 (lipiec 1988): 59–60. http://dx.doi.org/10.3758/bf03334861.

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Thompson, Robert S., Paul V. Strong i Monika Fleshner. "Physiological Consequences of Repeated Exposures to Conditioned Fear". Behavioral Sciences 2, nr 2 (18.05.2012): 57–78. http://dx.doi.org/10.3390/bs2020057.

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45

Falls, William A., i Michael Davis. "Fear-potentiated startle using three conditioned stimulus modalities". Animal Learning & Behavior 22, nr 4 (grudzień 1994): 379–83. http://dx.doi.org/10.3758/bf03209157.

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Klucken, T., J. Schweckendiek, G. Koppe, C. J. Merz, S. Kagerer, B. Walter, G. Sammer, D. Vaitl i R. Stark. "Neural correlates of disgust- and fear-conditioned responses". Neuroscience 201 (styczeń 2012): 209–18. http://dx.doi.org/10.1016/j.neuroscience.2011.11.007.

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