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Biomedical subjects

A Randich

Publications and source records attributed to A Randich.

47 records · Page 3Linked to original sources
PubMed1985

Genetic differences in avoidance behavior: cardiovascular activity, pain sensitivity and stress-induced analgesia.

Four experiments are reported which examine cardiovascular activity, pain sensitivity and stress-induced analgesia in rats selectively bred for differences in shuttlebox avoidance behavior. The results of Experiments 1 and 2 indicate that the two genetic lines differ in basal pain sensitivity, as measured by the hot-plate test. This difference in pain sensitivity appears not to be mediated by endogenous opioids, because it was not altered by pretreatment with a large dose of naloxone. In Experiments 1, 3 and 4 tail-flick tests of basal pain sensitivity failed to reveal line differences. Basal and stress levels of cardiovascular activity also showed no differences between the lines. In Experiment 3, LA but not HA animals showed profound stress-induced analgesia which was not blocked by a large dose of naltrexone. In Experiment 4, both LA and HA animals showed stress-induced analgesia, perhaps because the procedure of this experiment permitted conditioning mechanisms to contribute to the analgesia. Differential genetic selection for avoidance behavior also selected for differential pain sensitivity and some forms of non-opioid stress-induced analgesia but without concomitant selection for differential cardiovascular activity.

Analgesia↗
PubMed1984

Role of the right vagal nerve trunk in antinociception.

Activation of the cardiopulmonary reflex arc by volume expansion results in antinociception of the tail-flick response to radiant heat, and this antinociception can be attenuated by resection of the right vagal nerve trunk. Resection of the right vagal nerve trunk also attenuates foot-shock induced analgesia ( FSIA ), but this vagal influence appears to be qualitatively different from that produced by volume expansion. These findings indicate that pain perception is modulated by cardiovascular input.

Afferent Pathways↗
PubMed1984

Interactions between cardiovascular and pain regulatory systems.

A review of pharmacological, neuroanatomical, electrophysiological, and behavioral data indicates that systems controlling cardiovascular function are closely coupled to systems modulating the perception of pain. This view is directly supported by experiments from our laboratory showing that activation of either the cardiopulmonary baroreceptor reflex arc or the sinoaortic baroreceptor reflex arc induces antinociception. The outcomes of studies using pharmacological treatments, peripheral nerve stimulation, peripheral nerve resection, and CNS lesions are also presented as a preliminary means of characterizing cardiovascular input to pain regulatory systems. The network formed by these systems is proposed to participate in the elaboration of adaptive responses to physical and psychological stressors at various levels of the neuroaxis, and possibly to participate in "diseases of adaptation." In particular, the present analysis suggests that the inhibition of pain brought about by elevations in either arterial or venous blood pressure may provide a form of psychophysiological relief under situations of stress and contribute to the development of essential hypertension in humans.

Afferent Pathways↗
PubMed1984

[D-Ala2]-methionine enkephalinamide reflexively induces antinociception by activating vagal afferents.

Experiment 1 showed that intravenous administration of [D-Ala2]-methionine enkephalinamide resulted in dose-dependent inhibition of the tail-flick reflex, mild hypotension, and bradycardia. The enkephalinamide-induced inhibition of the tail-flick reflex and cardiovascular effects were eliminated in the bilateral cervical vagotomized anesthetized rat preparation, but were unaffected by either a unilateral right vagotomy or bilateral sinoaortic deafferentation in the conscious rat preparation. Experiment 2 demonstrated that the antinociceptive and cardiovascular actions of enkephalinamide were eliminated by pretreatment with intravenous administration of the opioid-receptor antagonist naloxone. These experiments strongly suggest that peripherally circulating enkephalins could reflexively induce analgesia by activating cardiopulmonary receptors whose afferents travel in the vagi.

Afferent Pathways↗
PubMed1984

Unconditioned stress-induced analgesia following exposure to brief footshock.

Four experiments examined the properties of unconditioned analgesia elicited by electric footshock stimuli using unconditioned stimulus (US) parameters typical of aversive conditioning paradigms. In all experiments, analgesia was inferred from the latency to paw lick in response to painful thermal stimulation in the hot-plate assay. In Experiment 1, rats exposed to a 1-s, 2-mA electric shock US showed significantly longer latencies to respond to painful thermal stimulation than nonshocked controls, whereas nonsignificant increases in response latencies were observed with 1-s shock USs of either 0.5 or 1.25 mA. In Experiment 2, rats exposed to a 2-mA electric shock US showed systematic increases in latencies to respond to painful thermal stimulation as the duration of the shock was varied between 0.5 and 2 s. Experiment 3 showed that this form of shock-induced analgesia was of short temporal duration. Specifically, significant increases in latencies to respond to painful thermal stimulation occurred 30 s but not 90 or 300 s following exposure to a 1-s, 2-mA shock US. Experiment 4 demonstrated that this form of analgesia was unaffected by pretreatment with the opiate receptor antagonist naloxone in dosages of 1, 5, 10, or 20 mg/kg. Finally, there was no evidence showing that environmental stimuli paired with shock presentations acquired the capacity to evoke analgesia as a conditioned response. The implications of shock-induced analgesia for the study of aversive conditioning and behavior are discussed.

Animals↗
PubMed1983

Exposure to the unconditioned stimulus alone: effects on retention and acquisition of conditioned suppression.

Three experiments demonstrated that repeated exposure to an electric-shock unconditioned stimulus (US) resulted in a decrement in retention of conditioned suppression evoked by a previously established excitatory conditioned stimulus (CS) and retarded subsequent acquisition of conditioned suppression to a novel CS paired with shock. Experiment 1 showed that 10 sessions of exposure to shock alone were required to produce a decrement in retention of conditioned suppression, whereas retardation in the acquisition of conditioned suppression was obtained following either 5 or 10 sessions of exposure to shock alone. Experiment 2 demonstrated that the magnitude of both the decrement in retention of conditioned suppression and the retardation in the acquisition of conditioned suppression produced by exposure to shock alone was directly related to the intensity of those shocks. Experiment 3 demonstrated that the decrement in retention of conditioned suppression produced by 10 sessions of exposure to shock alone was inversely related to the interval between the last exposure to shock and the test of the target CS. These findings are discussed in terms of associative and nonassociative accounts of the effects of US-alone procedures.

Animals↗
PubMed1978

Visual dominance in the pigeon.

In Experiment 1, three pigeons were trained to obtain grain by depressing one foot treadle in the presence of a 746-Hertz tone stimulus and by depressing a second foot treadle in the presence of a red light stimulus. Intertrial stimuli included white light and the absence of tone. The latencies to respond on auditory element trials were as fast, or faster, than on visual element trials, but pigeons always responded on the visual treadle when presented with a compound stimulus composed of the auditory and visual elements. In Experiment 2, pigeons were trained on the auditory-visual discrimination task using as trial stimuli increases in the intensity of auditory or visual intertrial stimuli. Again, pigeons showed visual dominance on subsequent compound stimulus test trials. In Experiment 3, on compound test trials, the onset of the visual stimulus was delayed relative to the onset of the auditory stimulus. Visual treadle responses generally occurred with delay intervals of less than 500 milliseconds, and auditory treadle responses generally occurred with delay intervals of greater than 500 milliseconds. The results are discussed in terms of Posner, Nissen, and Klein's (1976) theory of visual dominance in humans.

Journal Article↗
PubMedDate not supplied

Vagal afferent modulation of nociception.

Chemical, electrical or physiological activation of cardiopulmonary vagal (cervical, thoracic or cardiac), diaphragmatic vagal (DVAG) or subdiaphragmatic vagal (SDVAG) afferents can result in either facilitation or inhibition of nociception in some species. In the rat, these effects depend upon vagal afferent input to the NTS and subsequent CNS relays, primarily in the NRM and ventral LC/SC, although specific relay nuclei vary as a function of the vagal challenge stimulus. Spinal pathways and neurotransmitters have been identified for vagally mediated effects on nociception and consistently implicate the involvement of descending 5-HT and noradrenergic systems, as well as intrinsic spinal opioid receptors. Species differences may exist with respect to both the effects of DVAG and SDVAG afferents on nociception and the efficacy of vagal afferents to modulate nociception. However, it is also possible that such differences reflect the modality of noxious input (e.g., visceral versus cutaneous), the type of neuronal activity investigated (e.g., resting versus noxious-evoked), spinal location of recording (e.g., thoracic versus lumbosacral) and/or parameters of stimulation. It is also possible that activation of some vagal afferents is aversive, but whether this contributes to changes in nociception produced by vagal activation has not clearly been established. Finally, the vagal-nociceptive networks described in this review provide a fertile area for future study. These networks can provide an understanding of physiological and pathophysiological peripheral events that affect nociception.

Afferent Pathways↗