Biomedical subjects

J D Greeley

Publications and source records attributed to J D Greeley.

10 recordsLinked to original sources

PubMed2001

Factorial invariance for combined Wechsler Adult Intelligence Scale-Revised and Wechsler Memory Scale-Revised scores in a sample of clients with alcohol dependency.

This study examined the joint factor structure of the WAIS-R and WMS-R in a sample of 289 participants (mostly males) with alcohol dependency. In a confirmatory phase we contrasted a range of factor models derived from previous analyses of the Wechsler scales. The best fitting model incorporated five factors representing Verbal Comprehension, Perceptual Organization, Attention-Concentration, Verbal Memory, and Visual Memory, with reassignment of factor loadings for two subtests. The invariance of the measurement model was then examined comparing data from a large sample of healthy participants (J. R. Carstairs & E. A. Shores, 1999). The results indicated that the number of factors was invariant across samples, and four of the factors satisfied the criterion of partial measurement invariance.

Adolescent↗

PubMed1999

Alcohol exposure therapy: generalisation and changes in responsivity.

Fifty male alcohol-dependent individuals presenting for treatment were randomly assigned to either a cue exposure (CE) or control group. The experimental group were presented with 10 exposure trials to the sight and smell of alcohol, whilst the control group were presented with a neutral beverage. Following this, subjects received exposure to alcohol in a different room to examine whether extinguished responses generalised to a different environment. Results showed that only those subjects presented with the alcohol cue showed a significant reduction in cue-elicited swallowing, subjective withdrawal symptoms, arousal and urge to drink alcohol and that these extinguished responses remained diminished in magnitude in a different environment. These results provide additional support for the effectiveness of CE in reducing responsivity to alcohol cues.

Adult↗

PubMed1993

To drink or not to drink? Assessing conflicting desires in dependent drinkers in treatment.

Reactivity to Alcohol and Neutral Cues was compared in male, inpatient problem drinkers (N = 30). Subjects reported an overall desire not to drink alcohol which decreased in the presence of the Alcohol Cue. There were no cue-specific changes in heart rate, blood pressure and arousal level and a non-significant trend for increased stress in the Alcohol Cue condition. Subgroups of subjects reporting positive and negative desire for alcohol were identified. Subjects who reported negative desire for alcohol in the Alcohol Cue condition also reported greater self-efficacy to resist drinking in the future. These findings have implications for understanding the nature of self-reported desire for alcohol and its potential role in the treatment of alcohol dependence.

Adult↗

PubMed1993

Reactivity to alcohol-related cues in heavy and light drinkers.

Physiological responses and self-reported desire for alcohol were compared in heavy (n = 21) and light (n = 29) drinkers under each of two cue conditions. The cues were presented in a counterbalanced order and consisted of the sight, smell and taste of the subject's preferred alcoholic beverage (alcohol cue) and of a nonalcoholic lemon-flavored drink (neutral cue). Heavy drinkers showed a significant linear increase in reported desire for alcohol over time in the presence of the alcohol cue. This persistent increase in desire for alcohol seen in heavy drinkers contrasted with the initial increase shown by light drinkers which dissipated over time. Neither group showed any significant change in desire for alcohol when presented with the neutral cue. Heavy drinkers showed lower levels of skin conductance than light drinkers and all subjects showed changes in heart rate during exposure to both cues. Heart rate was affected differentially in the two groups of drinkers but only when the alcohol cue was presented first. Neither blood pressure nor stress and arousal levels changed significantly from pre- to post-cue presentations. The findings of this study have implications for understanding the nature and time course of cue-elicited desire for alcohol and its potential role in the development and treatment of alcohol dependence.

Adolescent↗

PubMed1992

Conditioned tolerance to morphine hypoalgesia: compensatory hyperalgesia in the experimental group or conditioned hypoalgesia in the control group?

Five experiments used rats to examine the role of noxious stimulation in the development of contextually controlled morphine hypoalgesic tolerance and in the mediation of this tolerance by an associated hyperalgesic response. There was evidence for contextually controlled tolerance to morphine's hypoalgesic effects and an associated hyperalgesic response in rats injected with morphine and trained with noxious stimulation, but not in rats repeatedly exposed to morphine in the absence of that stimulation (Experiments 1 and 5). Latent inhibition (Experiment 2) and extinction (Experiment 3) of tolerance also depended upon pairing drug-related cues with noxious stimulation. The level of sensitivity-reactivity to noxious stimulation in morphine-tolerant rats tested with the drug was related to the intensity of the noxious stimulation that had been paired with the test context (Experiment 4). The results were interpreted to mean that some of the evidence for a Pavlovian involvement in tolerance development can be explained in terms of morphine's interference with the acquisition, but not with the expression of the hypoalgesic response otherwise acquired by cues paired with noxious stimulation.

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↗

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↗

PubMed1988

"Paradoxical" analgesia induced by naloxone and naltrexone.

Analgesic effects of pellet implantation of the opiate antagonists naloxone and naltrexone and of chronic administration of naloxone by subcutaneous injection were examined. Rats were implanted with a slow-release pellet containing 10 mg naloxone or 10 mg naltrexone and tested for paw-lick latency on a hotplate apparatus. Controls were implanted with placebo pellets or given saline injections as appropriate. There were five test trials at intervals up to 72 h after implantation of naloxone and up to 120 h after the implantation of naltrexone. In a separate experiment, 5 mg/kg naloxone was injected; there were single trials on 5 consecutive days. All drug-treated animals displayed clear and substantial analgesia by their second test trial. This "paradoxical" analgesia was gradually reversed in the pellet-implant groups as tissue levels of the antagonists declined, but increased progressively with each trial involving injections. It was hypothesized that blockade of endogenous opiates by antagonists resulted in a form of "super-pain" on the hotplate, which in turn activated a normally redundant "backup" analgesic system. The results with naloxone injections show that unlike opiate-mediated analgesia, this hypothetical system is resistant to tolerance.

Analgesics↗