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Some earlier work, not rigorously controlled, suggested that conditional increases in sympathoadrenal stress hormones could occur. The purpose of this experiment was to test this idea further using an appropriately controlled design. To do this, we subjected rats living in a tether-type apparatus to differential fear conditioning. Chronic catheterization allowed us to sample blood before and after conditional stimulus probes without having to touch the rats. No evidence for conditional changes in norepinephrine and corticosterone was found. In contrast, differential conditioning of epinephrine responses was found. The conditional response, however, was not a simple one in that conditional increases in epinephrine following CS+ probes were not always seen. These data support the idea that learned changes in hormonal stress respondents can occur. But they leave open the question of why clear cut conditional changes in these visceral systems are so difficult to obtain.  相似文献   

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Some earlier work, not rigorously controlled, suggested that conditional increases in sympathoadrenal stress hormones could occur. The purpose of this experiment was to test this idea further using an appropriately controlled design. To do this, we subjected rats living in a tether-type apparatus to differential fear conditioning. Chronic catheterization allowed us to sample blood before and after conditional stimulus probes without having to touch the rats. No evidence for conditional changes in norepinephrine and corticosterone was found. In contrast, differential conditioning of epinephrine responses was found. The conditional response, however, was not a simple one in that conditional increases in epinephrine following CS+ probes were not always seen. These data support the idea that learned changes in hormonal stress respondents can occur. But they leave open the question of why clear cut conditional changes in these visceral systems are so difficult to obtain.  相似文献   

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The interaction of heart rate and blood pressure responses was studied in four male rhesus monkeys (M. mulatta) during classical delay conditioning and extinction. During initial conditioning sessions, heart rate was held constant by means of an external cardiac pacemaker; in follow-up conditioning sessions, the heart was free of constraint. Observations were made after these conditioning sessions, (a) during several sessions given over to continued training while different pacing rates were in effect; (b) during a series of extinction sessions in which the heart was paced and unpaced; and, (c) when a heart rate CR was simulated by manipulation of the pacer with no conditioned or unconditioned stimuli present. Throughout all sessions, systolic and diastolic pressures were measured at each heart beat. It was found that blood pressure conditioning was largely unaffected when heart rate changes were prevented during acquisition. Extinction of blood pressure responses was also seen to proceed relatively unimpeded when the heart was paced at a fixed frequency. During the postacquisition conditioning sessions, the several different pacing rates that were tested did not produce any significant differential effects in the blood pressure CRs. Simulated heart rate CRs were accompanied by small changes in pressures, sometimes opposite in direction from the pressure CRs observed during unpaced conditioning trials.  相似文献   

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Sucrose was used to reinforce heart rate (HR) increases in one group of unrestrained rats and to reinforce decreases in another. A third group received noncontingent sucrose presentations, and a fourth was presented with an empty dipper. After 10 conditioning sessions HR, as measured by changes in tonic levels, was significantly greater in the Fast group than in the Noncontingent group, which in turn maintained significantly higher levels than the Slow group. There was no difference between the Noncontingent and No-sucrose groups. Behavioral observations indicated that the Fast animals increased the percentage of time spent in such high-HR categories as rearing and walking; however, there were no corresponding systematic decreases in the Slow animals. Moreover, the Fast and Slow groups differed significantly with regard to the HRs associated with five behavioral categories. The overall pattern of results suggests that some degree of cardiospecific effect may have been exerted by the operant contingencies.  相似文献   

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Fifty-five male and female undergraduates underwent 3 sessions of conditioning and one of extinction. Shock (UCS) occurred intermittently during light-on (CS+) and never in light-off (CS-). Results showed that (1) pressure in CS+ was significantly higher than CS-throughout all sessions; (2) within session adaptation was significantly retarded while incoming pressure levels did not adapt across sessions; (3) conditioned effects persisted 6 months after the last shock session; (4) verbal information as to non-appearance of shock significantly dropped pressure levels and reduced the discriminative light effect; (5) the post-shock unconditioned pressure response was a peak rise at 52 seconds, then a decrease which stabilized to the pre-shock level at 2 minutes. Pavlovian control of blood pressure was demonstrated and the present methodology offers an explicit procedure for further laboratory exploration.  相似文献   

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The physiological mechanism involved in human operant heart rate conditioning is not known. If skeletal muscle tension is a mediator, it should be possible to generate significant heart rate increases by inconspicuous voluntary muscle tension. Eleven subjects were instructed to generate inconspicuous muscle tension for 90-second periods. No gross muscle movements were observed, but average heart rate during the trials was over 13 beats-per-minute greater than pre-trial base lines. Respiratory pattern changes and surface electromyogram changes did not reliably correlate with heart rate increases. Inconspicuous muscle tension could be a mediator in human operant heart rate conditioning, and cannot be ruled out by absence of change in respiratory pattern or electromyogram.  相似文献   

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The treatment of choice for a number of anxiety disorders is exposure therapy. However, successful reduction of fear through exposure is sometimes followed by a (partial) return of symptoms of fear (return of fear, ROF; Clin. Psychol. Rev. 9 (1989) 147). Several possible learning mechanisms have been suggested to explain ROF (e.g. mechanisms related to spontaneous recovery, renewal, reacquisition and reinstatement). The present study focuses on reinstatement, which refers to the observation that mere US-only presentations can 'reinstate' previously extinguished fear responses. Although animal research has repeatedly demonstrated this phenomenon, little is known about fear reinstatement in humans. The present study employed a differential aversive conditioning procedure: after acquisition and a subsequent extinction procedure, a series of four unpredicted US-only trials was scheduled in the reinstatement group. The control group did not receive additional US presentations. A significant reinstatement effect was observed for US-expectancy ratings and fear ratings in the reinstatement group, but not in the control group. No differences were observed in a reaction time measure of resource allocation to the conditioned stimuli. These findings constitute a first demonstration of reinstatement of conditioned fear responses in humans. Implications for exposure treatment and suggestions for future research are discussed.  相似文献   

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We show that the attentional-associative SLG model of classical conditioning, based on the 1996 research of Schmajuk, Lam, and Gray, correctly describes experimental results regarded as evidence of causal learning in rats: (a) interventions attenuate responding following common-cause training but do not interfere on subsequent responding during observation, and (b) interventions do not affect responding after direct-cause training or (c) causal-chain training. According to the model, responding to the weakly attended test stimulus is strongly inhibited by the intervention in the common-cause case. Instead, in the direct-cause and causal-chain cases, the strongly attended test stimulus becomes inhibitory, thereby overshadowing the inhibitory effect of interventions. Most importantly, the model predicted that with relatively few test trials (a) the 2008 results of Experiment 3 by Leising, Wong, Waldmann, and Blaisdell should be similar to those of Dwyer, Starns, and Honey's 2009 Experiment 1, showing that interventions equally affect responding after common-cause and direct-cause training; and (b) the 2006 results of Experiment 2a by Blaisdell, Sawa, Leising, and Waldmann should be similar to those of Dwyer, Starns, and Honey's 2009 Experiment 2, showing that interventions equally affect responding after common-cause and causal-chain training. When those data were made available to us, we confirmed those predictions. In agreement with the SLG associative model, but not with causal model theory, this evidence supports the notion that the attenuation of responding by interventions only following common-cause training is the consequence of well-known learning processes-latent inhibition, sensory preconditioning, conditioned inhibition, protection from extinction, and overshadowing.  相似文献   

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