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Biomedical subjects

R F Westbrook

Publications and source records attributed to R F Westbrook.

At least 55 records · Page 3Linked to original sources
PubMed1991

Naloxone-induced hypoalgesia: effects of noradrenergic antagonists and agonist.

The present experiments confirmed that rats injected with naloxone and exposed to a heated floor acquired a hypoalgesic response, as indexed by the latencies to lick their paws. The expression of these latencies were unaffected by yohimbine, clonidine, propranolol, or by relatively moderate doses of prazosin, suggesting that the conditioned hypoalgesic response induced by pairings of naloxone and a heated floor is not mediated by the release and turnover of noradrenaline.

Animals↗
PubMed1991

Aversive conditioning in the rat: effects of a benzodiazepine and of an opioid agonist and antagonist on conditioned hypoalgesia and fear.

Hypoalgesia and fear co-occurred in rats trained on a heated floor and tested for their latencies to paw lick on that floor and to step down onto a nonheated floor. These responses were extinguished, suggesting a mediation by aversive conditioning processes. A benzodiazepine impaired the acquisition of aversive conditioning, but it did not attenuate the expression of conditioned hypoalgesia. The opioid agonist morphine also impaired acquisition across a range of drug doses and variations in hypoalgesic tolerance, whereas the opioid antagonist naloxone facilitated acquisition. The results are discussed in terms of the perceptual-defensive-recuperative (Fanselow, 1986) and working memory (Grau, 1987) models of the mechanisms for the co-occurrence of conditioned hypoalgesia and fear.

Animals↗
PubMed1991

Effects of morphine and naloxone upon the reactions of rats to a heat stressor.

Five experiments used rats to examine the conditioned hypoalgesia induced by exposure to a heated floor. Experiments 1 and 2 demonstrated that this hypoalgesia is mediated by non-opioid mechanisms of pain control, as evidenced by insensitivity to the opioid antagonist naloxone and by the absence of cross-tolerance with the opioid agonist morphine. Although non-opioid in nature, the acquisition of conditioned hypoalgesia was facilitated by naloxone and impaired by morphine (Experiments 3 and 4). These effects did not appear to be due to an opioid regulation of pain. (1) Pairing morphine with the heated floor attenuated acquisition in drug-tolerant rats. (2) This attenuation by morphine was removed when naloxone was given after exposure to the heated floor. (3) Conditioning was facilitated when naloxone was given after exposure to the heated floor (Experiment 5). The results were discussed in terms of an opioid regulation of (a) surprise, (b) arousal of an aversive motivational system, and (c) the affective component of pain.

Animals↗
PubMed1991

Naloxone-induced hypoalgesia: effects of heat, cold and novelty.

Experiment 1 confirmed that pairings of the opioid antagonist naloxone and a heated floor served to induce and then to maintain a conditioned hypoalgesia in rats. Experiments 2a and b demonstrated that this was not specific to some property of the heated floor: pairings of the drug and a cold floor (a) resulted in conditioned hypoalgesia and (b) maintained the hypoalgesia provoked by pairings of the drug with a heated floor. Experiments 3a and 4 showed that pairings of naloxone with the non-heated floor of the apparatus provoked hypoalgesia and provided evidence that this was due to the drug's disruption of a familiarization process. Experiment 3b revealed that pairings of naloxone with the non-heated floor maintained the hypoalgesia induced by pairings of the drug with a heated one. The results were interpreted to mean that naloxone interacts selectively with a stressor so as to maintain or enhance its aversive properties.

Animals↗
PubMed1990

Some effects of the opioid antagonist, naloxone, upon the rat's reactions to a heat stressor.

Eight experiments examined the apparently paradoxical analgesia that accrues when rats are repeatedly injected with an opiate antagonist, naloxone, and exposed to a heat stressor. Experiments 1 and 2 showed that such pairings came to enhance in a dose-dependent manner the latencies with which rats paw-licked in response to the stressor. Experiment 3 demonstrated that the latencies to paw-lick in saline-treated rats decreased with increases in the intensity of the heat, indicating that naloxone had not provoked long latencies to paw-lick by increasing the functional intensity of the stressor. Experiment 4 documented a role for conditioning processes in recruiting the naloxone-induced analgesia. Experiment 5 showed that the analgesic effect was due to the pairings of the drug and the heat stressor, as a history of exposure to naloxone in a distinctive environment did not render the animals analgesic when challenged with the drug and the stressor. Experiments 6 and 7 provided evidence that the conditioned analgesia that accrued from drug-stressor pairings was non-opioid in nature, as the analgesia was observed in morphine-tolerant rats and was not reversed by an administration of naloxone in advance of exposure to the conditioning context. Experiment 8 demonstrated that the administration of morphine in the context previously associated with naloxone-stressor pairings provoked a superanalgesia. Although analgesic on the paw-lick assay, naloxone-treated subjects did not appear to be insensitive to the heat or impaired motorically, as they persistently reared with short latencies. The results were discussed in terms of the collateral inhibition model of the endogenous pain control system, and some speculations were offered concerning the relation between paw-licking and rearing.

Animals↗
PubMed1990

Some effects of exposure to a heat stressor upon the rat's subsequent reactions to that stressor.

In six experiments, rats were placed on a heated plate on two occasions (test and retest), and the latencies with which they licked their paws were taken as an index of their sensitivity to nociceptive stimulation. Experiment 1 provided evidence that rats were selectively analgesic on retest depending upon the intensity of the heat experienced on the initial test. Experiment 2 showed that this analgesia was recruited rapidly and was long-lasting, as it was observed when retest was scheduled as early as 0.2 and as late as 48 h after the initial exposure to the hot-plate. Experiment 3 documented a role for conditioning processes, as this analgesia was removed by an extinction-like procedure conducted between test and retest. Experiments 4 and 5 provided evidence for a non-opioid mechanism of pain control, because the analgesia was not diminished by the opioid antagonist, naloxone, nor by a history of morphine injections. These experiments also revealed that the analgesia observed on retest was enhanced and reduced when rats were given naloxone and morphine, respectively, on the initial test. Finally, Experiment 6 showed that the analgesia on retest summated with that produced by morphine. The results were taken to mean that the hot-plate assay for analgesia can itself activate endogenous mechanisms of pain control, and some speculations were offered as to how this occurred.

Animals↗
PubMed1983

Odor-aversion learning in neonate rat pups: the role of duration of exposure to an odor.

Five experiments employed 2- and 10-day-old rat pups to examine the ontogeny of odor-aversion learning. When duration of exposure to the to-be-conditioned odor stimulus (CS) was long, Experiments 1 and 2 demonstrated substantial and similar aversions across the two ages regardless of whether the toxin unconditioned stimulus (US) occurred simultaneously with, immediately before, immediately after, or some time after the CS. These experiments, therefore, did not support the claim of Rudy and Cheatle (Ontogeny of Learning and Memory. Hillsdale, N.J.: Erlbaum (1979) ) that the 2-day old pup suffers a deficit in its learning about the relation between successively presented events. The remaining experiments showed, however, that the 2-day-old pups did not acquire an aversion to a briefly presented CS, that the failure to condition this CS was not due to its overshadowing by contextual cues, and that the 10-day-old pup did acquire an aversion to that CS. The experiments have revealed, therefore, that there are age-related differences in the rat pup's ability to learn about the relation between a briefly-presented CS and the effects of a US.

Animals↗
PubMed1981

Short- and long-term decrements in toxicosis-induced odor-aversion learning: the role of duration of exposure to an odor.

Six experiments employed an odor-aversion paradigm to investigate the role of the duration of exposure to an odor in determining that odor's subsequent associability with illness. Rats were exposed to an odor at times T1 and T2, and the second of these exposures was followed by toxicosis. When the initial odor exposure was brief, the odor aversion was attenuated with a moderate T1-T2 interval of 3 hr (Experiment 1) but not with long intervals of 28 hr and 76 hr (Experiment 2). In contrast, when the initial odor exposure was long, the odor aversion was attenuated at a long T1-T2 interval (Experiment 3). With a T1-T2 interval of 24 hr, a brief initial exposure did not attenuate odor aversions when the context either remained the same or was changed from T1 to T2, whereas a long initial exposure attenuated such aversions when the context remained the same but not when the context was changed (Experiment 4). With a T1-T2 interval of 3 hr, a brief initial exposure attenuated odor aversions when the context remained the same or was changed from T1 to T2, whereas a long initial exposure attenuated such aversions when the context remained the same but not when the context was changed (Experiment 5). A brief exposure at T1, either with or without a subsequent context "extinction," attenuated odor aversions when the T1-T2 interval was 3 hr but not when this interval was 24 hr; a long initial exposure at T1, without a subsequent context "extinction," attenuated odor aversions when the T1-T2 interval was 4 hr and 24 hr but with a subsequent context "extinction" did not attenuate such aversions at either 4-hr or 24-hr T1-T2 intervals (Experiment 6). The results demonstrate that the duration of exposure to an odor determined whether that odor presentation caused short- or long-term decrements in odor conditionability and are discussed in terms of the relation between self- and retrieval-generated processes.

Animals↗
PubMed1980

Second-order autoshaped key pecking based on an auditory stimulus.

In Experiment 1, pigeons were exposed either to paired or to unpaired presentations of a tone and grain, and then to paired presentations of a keylight with the tone. Substantial second-order conditioned pecking to the keylight was produced in the birds that had received paired presentations of tone and grain. In Experiment 2, second-order pecking to the keylight increased in probability across four groups that had received, respectively, 20, 80, 140, or 200 paired presentations of tone and grain. In Experiment 3, the amount of pecking directed towards a keylight which predicted the first-order, tone CS was as substantial in birds without a prior history of key pecking as in birds with such a history. A further experiment failed to discover any significant differences in the levels of second-order pecking to a keylight paired with a first-order tone CS or with a first-order keylight CS. Thus, an auditory signal that does not itself support pecking may enable a localized visual stimulus to evoke key pecking.

Animals↗