Conditioned fear and startle magnitude: Effects of different footshock or backshock intensities used in training.

Davis, Michael J.; Astrachan, David I.

doi:10.1037/0097-7403.4.2.95

Cited by 219 publications

(192 citation statements)

References 11 publications

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“…When tested following such intensive training, those animals do not exhibit potentiated startle in the presence of the odor, possibly because active escape behaviors are incompatible with startle (Walker and Davis 1997). When these animals are later retested, they do exhibit significant potentiated startle, which is reminiscent of the non-monotonic relationship between shock intensity in training and level of fear-potentiated startle in testing (Davis and Astrachan 1978). Further, following weaker training, rats do a lot of sniffing when the odor is presented at testing, perhaps also incompatible with startle.…”

Section: Discussionmentioning

confidence: 91%

Second-Order Olfactory-Mediated Fear-Potentiated Startle

Paschall¹,

Davis²

2002

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Recently, we reported that discrete (4-sec) olfactory cues paired with footshock serve as effective conditioned stimuli (CSs) for potentiating the acoustic startle response in rats using the fear-potentiated startle paradigm. Because odors are such salient cues for the rat, and because of the robust olfactory conditioning observed previously, the current studies investigated second-order fear conditioning using olfactory and visual cues. In Experiments 1 and 2, we used a small number of first-order and second-order training trials on separate days to investigate second-order fear-potentiated startle. Significant potentiated startle was observed in animals receiving Paired/Paired training in both studies, but surprisingly, control animals in the Unpaired/Paired group (Exp. 1) also showed significant potentiated startle to a light S2 at testing. These findings are addressed in the Discussion. Overall, the results of both experiments suggest that olfactory cues serve as efficient S1 and S2 stimuli in second-order fear-potentiated startle paradigms when only a small number of first and second-order training trials are presented.Recently, we reported that discrete (4-sec) olfactory cues paired with footshock serve as effective conditioned stimuli (CSs) for potentiating the acoustic startle response in rats using the fear-potentiated startle paradigm (Paschall and Davis 2002). In those studies, amyl acetate (5%) had no significant effect on startle in untrained rats, but potentiated startle in animals receiving 1, 2, 5, or 10 odor-shock pairings. Olfactory-mediated fear-potentiated startle decreased, but was still significant up to 40 d after conditioning, and could be measured using test trials separated by as little as 30 sec. Those studies confirmed a previous report by Richardson et al. (1999), showing that ambient odors are also effective CSs for potentiating the startle response. Because odors are such salient cues for the rat, and because of the robust olfactory conditioning observed previously, the current studies investigated second-order olfactory fear conditioning.Pavlov (1927) proposed that once a stimulus has been conditioned, it can serve the role of an unconditioned stimulus (US). In first-order Pavlovian conditioning, a previously neutral stimulus (i.e., a light), is paired with a biologically significant US that can be either aversive (i.e., footshock) or rewarding (i.e., food). The animal learns an association between the CS and the US, and later exhibits a conditioned response (CR) to that stimulus in the absence of the US. Conditioning of a second neutral stimulus (S2) with the previously conditioned (and now excitatory) firstorder stimulus (S1) is known as higher-order (or secondorder) conditioning. When later tested with S2, the animal exhibits a CR, although S2 was never paired directly with the US.The existence of second-order conditioning is important, as it increases the range of situations in which classical conditioning occurs, even without a primary unconditioned stimulus (cf. Domjan 1998...

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Section: Discussionmentioning

confidence: 91%

Second-Order Olfactory-Mediated Fear-Potentiated Startle

Paschall¹,

Davis²

2002

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“…In addition to the above, existing human paradigms applying psychophysiological techniques measure generalization with skin conductance responses (SCR), and it is yet to be demonstrated whether such generalization can be captured by fear-potentiated startle (FPS: the reliable enhancement of the startle reflex when an organism is in a state of fear [Davis & Astrachan, 1978]). Measuring conditioned fear and its generalization with FPS may be advantageous over SCR for a few important reasons.…”

Section: Introductionmentioning

confidence: 99%

Generalization of conditioned fear-potentiated startle in humans: Experimental validation and clinical relevance

Lissek

Biggs

Rabin

et al. 2008

Behaviour Research and Therapy

338

382

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Though generalization of conditioned fear has been implicated as a central feature of pathological anxiety, surprisingly little is known about the psychobiology of this learning phenomenon in humans. Whereas animal work has frequently applied methods to examine generalization gradients to study the gradual weakening of the conditioned-fear response as the test stimulus increasingly differs from the conditioned stimulus (CS), to our knowledge no psychobiological studies of such gradients have been conducted in humans over the last 40 years. The current effort validates an updated generalization paradigm incorporating more recent methods for the objective measurement of anxiety (fear-potentiated startle). The paradigm employs 10, quasi-randomly presented, rings of graduallyincreasing size with extremes serving as CS+ and CS-. The eight rings of intermediary size serve as generalization stimuli (GS's) and create a continuum-of-similarity from CS+ to CS-. Both startle data and online self-report ratings demonstrate continuous decreases in generalization as the presented stimulus becomes less similar to the CS+. The current paradigm represents an updated and efficacious tool with which to study fear generalization-a central, yet understudied conditioningcorrelate of pathologic anxiety.

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“…The unconditioned stimulus, a 0.6 mA foot shock, was generated by five Lehigh Valley SGS-004 constant current shockers located outside of the chamber. Shock intensity was measured using a method described previously (Davis and Astrachan, 1978). The shock was delivered during the last 500 msec of the 3700 msec light at an average I TI of 4 min (range, 3-5 min).…”

Section: Test Procedures and Drug Administrationmentioning

confidence: 99%

Role of the Hippocampus, the Bed Nucleus of the Stria Terminalis, and the Amygdala in the Excitatory Effect of Corticotropin-Releasing Hormone on the Acoustic Startle Reflex

1997

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Previously, we demonstrated that transection of the fimbria/ fornix blocked the excitatory effect of corticotropin-releasing hormone (CRH) on startle (CRH-enhanced startle), suggesting that the hippocampus and its efferent target areas that communicate via the fimbria may be critically involved in CRHenhanced startle. The bed nucleus of the stria terminalis (BNST) receives direct projections from the ventral hippocampus via the fimbria/fornix. Therefore, the role of the ventral hippocampus, the BNST, and the amygdala in CRH-enhanced startle was investigated. NMDA lesions of the BNST completely blocked CRH-enhanced startle, whereas chemical lesions of the ventral hippocampus and the amygdala failed to block CRH-enhanced startle. However, the same amygdala-lesioned animals showed a complete blockade of fear-potentiated startle, a conditioned fear response sensitive to manipulations of the amygdala. In contrast, BNST-lesioned rats had normal fear-potentiated startle. This indicates a double dissociation between the BNST and the amygdala in two different paradigms that enhance startle amplitude. Microinfusions of CRH into the BNST, but not into the ventral hippocampus, mimicked intracerebroventricular CRH effects. Furthermore, infusion of a CRH antagonist into the BNST blocked CRH-enhanced startle in a dose-dependent manner. Control studies showed that this blockade did not result from either leakage of the antagonist into the ventricular system or a local anesthetic effect caused by infusion of the antagonist into the BNST. The present studies strongly suggest that CRH in the CSF can activate the BNST, which could lead to activation of brainstem and hypothalamic BNST target areas involved in anxiety and stress responses. Key words: bed nucleus of the stria terminalis (BNST ); amygdala; hippocampus; corticotropin-releasing hormone (CRH); startle; anxiety; fearIntracerebroventricular inf usion of corticotropin-releasing hormone (CRH) elicits a constellation of behavioral, physiological, and endocrinological changes similar to those produced by natural stressors (cf. Dunn and Berridge, 1990). Thus far, however, the exact anatomical sites responsible for these behavioral and physiological actions of CRH after intracerebroventricular administration have not been identified. As part of an effort to delineate the neural circuitry underlying intracerebroventricular CRH effects, recently we investigated a possible involvement of the septum, using increased acoustic startle amplitude after CRH (CRH-enhanced startle) as a behavioral measure (Lee and Davis, 1997). Electrolytic lesions of the whole septum and the medial septum, but not the lateral septum, blocked CRH-enhanced startle. However, fiber-sparing chemical lesions of the medial septum failed to block CRH-enhanced startle, suggesting that the blockade seen with electrolytic lesions was probably caused by damage to fibers of passage, presumably the fornix. Supporting this conclusion, f unctional lesions of the fornix induced by knife cuts of the fimbria /fornix complete...

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Conditioned fear and startle magnitude: Effects of different footshock or backshock intensities used in training.

Cited by 219 publications

References 11 publications

Second-Order Olfactory-Mediated Fear-Potentiated Startle

Second-Order Olfactory-Mediated Fear-Potentiated Startle

Generalization of conditioned fear-potentiated startle in humans: Experimental validation and clinical relevance

Role of the Hippocampus, the Bed Nucleus of the Stria Terminalis, and the Amygdala in the Excitatory Effect of Corticotropin-Releasing Hormone on the Acoustic Startle Reflex

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