1976
DOI: 10.1016/0301-0511(76)90010-7
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Heart-rate decelerative Pavlovian conditioning with tilt as UCS: Towards behavioural control of cardiac dysfunction

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Cited by 70 publications
(11 citation statements)
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“…Heart rate is yet another measure of autonomic activity commonly used in Pavlovian fear conditioning [17], and several studies have examined the heart rate response in these experiments (e.g. [28][29][30][31]). Differences in these autonomic responses have also been noted between healthy subjects and neuropsychiatric patients (e.g.…”
Section: Introductionmentioning
confidence: 99%
“…Heart rate is yet another measure of autonomic activity commonly used in Pavlovian fear conditioning [17], and several studies have examined the heart rate response in these experiments (e.g. [28][29][30][31]). Differences in these autonomic responses have also been noted between healthy subjects and neuropsychiatric patients (e.g.…”
Section: Introductionmentioning
confidence: 99%
“…In contrast to a long-lasting, sympathetically mediated tachycardia observed during aversive contextual conditioning in rats (Nijsen et al, 1998;Roozendaal, Koolhaas, & Bohus, 1991), cue conditioning typically elicits short-latency, parasympathetically mediated bradycardia in humans (Furedy & Poulos, 1976;Headrick & Graham, 1969;Klorman & Ryan, 1980) as well as rabbits (Gallagher, Kapp, McNall, & Pascoe, 1981;Gentile, Jarrell, Teich, McCabe, & Schneiderman, 1986) and rats (Supple & Leaton, 1990), thus providing comparability across species.…”
mentioning
confidence: 99%
“…Albeit speculative, based on the fact that in our experiments with haloperidol we used only 4 pairings of the context-CS and the drug-US, compared to the 8 pairings in the experiments of Schmidt & Beninger (2006), or the 10 employed by Banasikowsky & Beninger (2012) or Dias et al (2012), and taking into account that the CR is usually of a lower intensity than the UR (56,57), we suggest that in our experiments the presentation of the context associated with the 0.5 mg / kg dose of haloperidol may have led to a low intensity CR that would have been functionally equivalent to the response induced by a low dose of haloperidol. This CR could have blocked the presynaptic dopamine autoreceptors, preventing the feedback mechanism that would limit the release of the neurotransmitter, while the postsynaptic receptors would not have been affected, leading to an excessive dopamine reuptake that could have caused the conditioned increase in locomotor activity.…”
Section: Discussionmentioning
confidence: 99%