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Biomedical subjects

S F Maier

Publications and source records attributed to S F Maier.

162 records · Page 9Linked to original sources
PubMed1982

Extent and control of shock affects naltrexone sensitivity of stress-induced analgesia and reactivity to morphine.

Opioid and nonopioid mediated changes in pain sensitivity have been observed after exposure to various stressful conditions. A series of inescapable shocks sequentially produces an early form of analgesia which is not affected by the opiate antagonist, naltrexone, and a late antinociceptive response which is sensitive to reversal by naltrexone. Here, this is shown to be true over a wide range of doses. In a further experiment subjects given either escapable or inescapable shock were analgesic immediately after the stress session. However, the analgesia of inescapably shocked subjects was more sensitive to reversal by naltrexone. A final experiment revealed that inescapably shocked subjects, but not escapably shocked subjects, were hyperreactive to the analgesic effects of morphine 24 hr after shock. These results suggest that activation of an opiate system occurs only after extended exposure to stress and that this activation is greater when the stress is inescapable. Implications for opioid versus nonopioid mechanisms of stress-induced analgesia are discussed.

Animals↗
PubMed1982

Dissociation of long-term analgesia and the shuttle box escape deficit caused by inescapable shock.

Inescapably shocked rats perform poorly on a two-way shuttle box escape task 24 hr after the shock. Because inescapably shocked rats become analgesic upon reexposure to a small amount of shock 24 hr after inescapable shock, they are likely to be analgesic during the shuttle box escape task. Subjects receiving an equivalent amount of escapable shock display neither the escape dificit nor the analgesia. Both the analgesia and the escape deficit respond in a similar fashion to the manipulation of a variety of other variables. These findings have led to the suggestion that the analgesia ("long-term analgesia") may cause the inescapable-shock-produced escape deficit. However, the present experiments demonstrated that two pituitary manipulations that completely eliminate the analgesia have no effect on the escape deficit. Both hypophysectomy and dexamethasone administration blocked the analgesic consequences of inescapable shock but did not reduce the magnitude of the escape deficit. Therefore, the long-term analgesia produced by inescapable shock does not cause the deficit in shuttle box escape performance displayed by inescapably shocked rats. Furthermore, these results indicate that the pituitary is not essential in the production of this escape deficit.

Analgesia↗
PubMed1981

Cross tolerance between morphine and the long-term analgesic reaction to inescapable shock.

Animals exposed to a variety of stressors display a temporary analgesic reaction. This short-term analgesia has been shown to be reversible by opiate antagonists and cross-tolerant with morphine following some stress conditions, but not following others. It has recently been shown that inescapable shock parameters which produce behavioral '"learned helplessness" effects also produce a short-term analgesic reaction, and that this reaction can be re-aroused by a brief exposure to shock 24 hours later. Further, both the immediate and long-term antinociceptive reaction which follow shocks of this type have been shown to be reversible by opiate antagonists. Here it is shown that the long-term analgesic reaction is completely cross tolerant with morphine. Implications of these results for opioid mediation of learned helplessness and opioid versus nonopioid mediation of stress-induced analgesia are discussed.

Animals↗
PubMed1980

Opiate antagonists and long-term analgesic reaction induced by inescapable shock in rats.

Five experiments examined the influence of opiate antagonists on both the short-term analgesic reaction resulting 30 min after exposure to inescapable shock and the long-term analgesic reaction resulting after reexposure to shock 24 hr after inescapable shock exposure. Experiment 1 showed that the long-term analgesic reaction could be reduced by administration of naltrexone prior to exposure to inescapable tail shock. Experiment 2 showed that the reduction in the long-term analgesic reaction produced by naltrexone was dose-dependent. Experiment 3 showed that the long-term analgesic reaction could also be reduced by administration of naltrexone prior to reexposure to shock. Experiment 4 showed that the long-term analgesic reaction could be reduced by administration of large dose of naloxone prior to reexposure to shock. Experiment 5 showed that the short-term analgesic reaction was reduced by naltrexone administered prior to inescapable shock. Some implications of these results for the biochemical substrates of both learned helplessness and stress-induced analgesia are discussed.

Animals↗
PubMed1980

Learned helplessness, inactivity, and associative deficits: effects of inescapable shock on response choice escape learning.

These experiments explored whether exposure to inescapable shock produces a subsequent deficit in the organism's propensity to associate its behavior with shock termination. Previous experiments are incapable of resolving this question because they confound reduced associability and decreased activity. Four experiments examined the effects of inescapable shock on the acquisition of Y-maze escape. Here, escape is accomplished by choosing the correct response from two available alternatives rather than by simple locomotion as in a shuttle box. By itself, reduced activity should not produce inaccurate choices, only slow choices. Experiment 1 found that inescapable shock produced slow learning of the correct choice for escape, even though active choices occurred on every trial. Further, the speed and accuracy of choice were not correlated. The second experiment showed that the choice escape learning deficit was produced by the inescapability of the shocks. Experiment 3 demonstrated that the choice accuracy of inescapably shocked rats was not improved by increases in Y-maze shock intensity, even though speed of responding was increased. The final experiment revealed that the effects of inescapable shock on Y-maze acquisition did not dissipate across a 1-wk period.

Animals↗
PubMed1979

Long-term analgesic effects of inescapable shock and learned helplessness.

Although exposure to inescapable shocks induced analgesia in rats, the analgesia was not manifest 24 hours later. A brief reexposure to shock, however, restored the analgesia. This reexposure to shock had an analgesic effect only if the rats had been shocked 24 hours previously. Further, long-term analgesic effects depended on the controllability of the original shocks and not on shock exposure per se. Implications of these results for learned helplessness and stress-induced analgesia are discussed.

Analgesia↗
PubMedDate not supplied

Exercise does not modify spatial memory, brain autoimmunity, or antibody response in aged F-344 rats.

Old F-344 rats were given endurance training over a 10-week period on a motorized treadmill. This treatment resulted in substantial heart-to-body weight ratio increases, indicative of effective training. To determine whether endurance training might alter some of the known immune system and cognitive changes observed during aging, exercised old rats were compared to nonexercised old and young controls on three variables: in vivo antigen-specific immune activity, brain-reactive antibody formation, and spatial memory. The exercise training did not influence any of these measures in the old rats. Both groups of old rats showed poorer antibody response to a specific antigen, more brain-reactive antibody formation, and poorer spatial memory than the young controls. There was, however, a significant relationship between brain-reactive antibody formation and spatial memory performance, regardless of training condition.

Aging↗
PubMedDate not supplied

Bacterial endotoxin induces fos immunoreactivity in primary afferent neurons of the vagus nerve.

Subdiaphragmatic vagotomy inhibits brain-mediated illness responses to peripherally administered bacterial endotoxin, including fever, hyperalgesia, sickness behavior, and activation of the hypothalamic-pituitary-adrenal axis. However, direct evidence implicating vagal afferents specifically in conveying information about peripheral immune activation to the brain is still lacking. This study assessed whether (1) endotoxin induces the expression of the functional activation marker Fos in the vagal sensory ganglia, and (2) vagotomy abrogates endotoxin-induced Fos expression in these ganglia. Male rats, which had previously received vagotomy or sham surgery, were injected intraperitoneally or intravenously with either endotoxin or saline. Fos immunolabeling was absent in saline-treated rats. In contrast, scattered cells within the vagal sensory ganglia showed Fos immunoreactivity after both intraperitoneal and intravenous endotoxin administration in sham-operated rats. Vagotomy abolished Fos expression after intraperitoneal endotoxin administration, whereas after intravenous administration Fos expression was strongly attenuated, but not eliminated. These findings implicate vagal afferents as a potential signaling pathway to brain regions that generate illness responses to pro-inflammatory mediators.

Animals↗
PubMedDate not supplied

Acute stress may facilitate recovery from a subcutaneous bacterial challenge.

The effects of stress on the immune system vary with both the duration and type of stressor. Many studies suggest that stress may compromise an organism's ability to recover from immune challenge. However, recent findings suggest that stress may actually enhance some aspects of immune function. For example, exposure to a single session ( approximately 2 h) of intermittent inescapable tailshocks (IS) has been shown to activate the acute phase response and increase some aspects of macrophage function. Thus, the following experiments assessed whether IS exposure would alter local inflammation produced by peripheral injection of streptomycin-killed bacteria. Rats (Harlan Sprague Dawley) were exposed to IS (100 1. 6-mA, 60 s variable intertrial interval) and injected with Escherichia coli ( approximately 2.5 x 10(8) CFU s.c. posterior to the shoulder blades). The area of inflammation was measured until the inflammation had completely resolved (typically 7-8 days). When bacteria were administered immediately after IS, rats resolved inflammation significantly faster than did nonstressed rats. Since adrenalectomy did not reduce the effect of IS, it is unlikely that this effect is a result of elevated corticosterone levels. Furthermore, IS does not appear to alter the rat's ability to sequester bacteria in the subcutaneous space since no swelling of lymph nodes or chronic activation of the hypothalamic-pituitary-adrenal axis was observed.

Animals↗