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Biomedical subjects

M W Meagher

Publications and source records attributed to M W Meagher.

6 recordsLinked to original sources
PubMed1991

Role of cholinergic systems in pain modulation: I. Impact of scopolamine on environmentally induced hypoalgesia and pain reactivity.

Scopolamine was found to block both brief shock-induced (3 0.75-s, 1.0-mA shocks) and conditioned hypoalgesia on the tail-flick test in rats. The drug also produced a general increase in pain reactivity as measured by both the tail-flick test and shock-induced vocalization. It was shown that this hyperalgesia cannot account for the effect of the drug on brief-shock or conditioned hypoalgesia. Scopolamine did not block the nonopioid analgesia observed after long shock (3 25-s, 1.0-mA shocks). When the effect of the drug on baseline levels of pain reactivity was controlled, it potentiated long shock-induced hypoalgesia. Scopolamine also increased reactivity to tactile stimulation, which suggests the hyperalgesia reflects a general increase in arousal. None of these effects were observed with methylscopolamine, which suggests they are not peripherally mediated.

Animals↗
PubMed1990

Role of supraspinal systems in environmentally induced antinociception: effect of spinalization and decerebration on brief shock-induced and long shock-induced antinociception.

Prior research suggests that afferent nociceptive information can directly activate the opioid and nonopioid brainstem antinociceptive systems. Grau (1987a) has hypothesized that direct activation occurs when an organism is exposed to severe aversive stimuli and that forebrain systems mediate the activation of the antinociception systems when mild aversive stimuli are used. The present experiments tested this hypothesis by examining the impact of spinalization and decerebration on the antinociception observed after mild (3 0.75-s 1.0-mA shocks) and vs. severe (3 25-s 1.0-mA shocks) tailshocks. It was found that spinal transection eliminated the antinociception observed after both shock schedules, whereas decerebration blocked mild shock-induced, but not severe shock-induced, antinociception. Surprisingly, decerebration potentiated severe shock-induced antinociception. The opioid antagonist naltrexone had no effect on the antinociception observed after severe shock in sham or decerebrate rats.

Afferent Pathways↗
PubMed1990

Associative learning and memory for an antinociceptive response in the spinalized rat.

Prior research suggests that associative and memorial processes can modulate the activation of the endogenous antinociceptive systems. It has been generally assumed that forebrain systems play an essential role in mediating the impact of these processes. The present experiments explored whether the behavioral effects indicative of associative and memorial processes can be obtained in spinalized rats. Experiment 1 demonstrated that a conditioned nonopioid antinociception can be established after rats have experienced a spinal transection at the level of the 2nd thoracic vertebrae. Experiment 2 showed that a postshock distractor can speed the decay of shock-induced antinociception in the spinalized rat. These findings suggest that the circuitry needed to obtain associative and memorylike effects is present within the spinal cord.

Animals↗
PubMed1989

Frontal cortex lesions block the opioid and nonopioid hypoalgesia elicited by brief shocks but not the nonopioid hypoalgesia elicited by long shocks.

Previous research (Grau, 1987a, 1987b) suggests that forebrain systems play an essential role in the hypoalgesia observed after brief shock but not long shock. Additional research has shown that pentobarbital anesthesia and decerebration block the hypoalgesia observed after 3 brief (0.75-s) shocks but not the hypoalgesia observed after 3 long (25-s) shocks. This is a study of whether a specific forebrain lesion, a frontal cortex lesion, would have a similar impact on hypoalgesia induced by brief (0.75 s) and long (25-s) shocks. Frontal cortex lesions, like decerebration and pentobarbital anesthesia, eliminated the hypoalgesia observed after brief but not long shocks. Because other research suggests that the stress of surgery may influence whether the hypoalgesia elicited by shock is opioid or nonopioid, the 2nd experiment was to examine whether the sham operation per se alters the form of the hypoalgesia observed after brief shock. It does not; in the sham-treated subjects, brief shock induced the usual transient nonopioid hypoalgesia followed by prolonged opioid hypoalgesia. These data suggest that frontal cortex lesions block nonopioid and opioid hypoalgesia observed after brief shock.

Animals↗
PubMed1987

Effects of opiate manipulations on latent inhibition in rabbits: sensitivity of the medial septal region to intracranial treatments.

The effects of opiate manipulations were examined on latent inhibition of classically conditioned heart rate in rabbits. Animals were exposed to an auditory stimulus that was later used as a conditioned stimulus (CS). Administration of the agonist levorphanol into the medial septal region either preceding or immediately following CS preexposure sessions attenuated latent inhibition of the conditioned response. This effect was observed in animals that showed no change in long-term retention of habituation. Administration of levorphanol into the central nucleus of the amygdala, a sensitive site for opiate manipulations on aversive conditioning tasks, was ineffective. Further analysis of the effect obtained within the septal region revealed pharmacological specificity. The effect of posttraining levorphanol was also time dependent and exhibited neuroanatomical specificity. Posttraining opiate antagonist administration into the medial septum produced a modest augmentation of latent inhibition. The medial septal region appears to provide a site where opiate manipulations alter some aspect of retention for events that occur in the absence of reinforcement.

Acoustic Stimulation↗