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Biomedical subjects

G W Terman

Publications and source records attributed to G W Terman.

At least 37 records · Page 2Linked to original sources
PubMed1986

Effects of footshock stress and morphine on natural killer lymphocytes in rats: studies of tolerance and cross-tolerance.

Exposure to a form of footshock stress known to cause opioid-mediated analgesia suppresses the cytotoxic activity of natural killer (NK) cells in rats. This suppression is blocked by the opioid antagonist, naltrexone and is mimicked by morphine administration, suggesting mediation by opioid receptors. Supporting this hypothesis, we now report that the morphine-induced suppression of NK activity shows tolerance after 14 daily injections. The NK-suppressive effect of stress, however, shows neither tolerance with repetition nor cross-tolerance in morphine-tolerant rats.

Animals↗
PubMed1986

Opioid and non-opioid stress analgesia from cold water swim: importance of stress severity.

We have previously reported that stress severity plays an important role in determining the neurochemical basis of stress-induced analgesia from inescapable footshock. Increasing severity (duration or intensity of continuous footshock) causes a shift in mediation of the resultant analgesia from opioid to non-opioid. In this study, we find that stress severity plays a similar role in analgesia from cold water swim. More severe swims (longer duration or lower water temperature) produce stress analgesia insensitive to the opiate antagonist, naltrexone, whereas less severe swims produce analgesia significantly attenuated by this drug.

Analgesia↗
PubMed1986

Two opioid forms of stress analgesia: studies of tolerance and cross-tolerance.

We have previously reported that stress analgesia sensitive to and insensitive to opiate antagonists can be differentially produced in rats by varying the severity or temporal pattern of inescapable footshock. In these studies, we give further evidence for the opioid and non-opioid bases of these paradigms of stress analgesia. We find that naloxone-sensitive analgesia demonstrates tolerance with repeated stress and cross-tolerance with morphine, whereas naloxone-insensitive analgesia demonstrates neither of these characteristics. Moreover, different forms of opioid, but not non-opioid, stress analgesia manifest cross-tolerance with each other. These data are discussed in terms of the similarities and differences between two forms of opioid stress analgesia.

Analgesia↗
PubMed1986

Involvement of brain opiate receptors in the immune-suppressive effect of morphine.

We previously reported that a single systemic injection of a high dose of morphine (greater than or equal to 20 mg/kg) transiently suppresses splenic natural killer cell cytotoxicity in rats. The present study examined the possibility that the immune-suppressive effect of morphine is mediated by opiate receptors in the brain. Supporting this hypothesis, we found that morphine (20 or 40 micrograms) injected into the lateral ventricle suppressed natural killer cell activity to the same degree as a systemic dose higher by three orders of magnitude. This effect was blocked by an opiate antagonist, naltrexone. Natural killer cell activity was unaffected by systemic administration of N-methyl morphine, a morphine analogue that does not cross the blood-brain barrier. These data implicate opiate receptors in the brain in morphine-induced suppression of natural killer cell cytotoxicity.

Animals↗
PubMed1985

Analgesic, locomotor and lethal effects of morphine in the mouse: strain comparisons.

We have compared the analgesic, locomotor stimulatory and lethal effects of morphine in two strains of mice, C57BL/6BY and CXBK. The CXBK strain is known to be deficient in central opioid binding sites and to be less sensitive than the C57 strain to certain effects of morphine and endogenous opioids. We found that the CXBK strain was less sensitive than the C57s to the analgesic and locomotor effects of morphine, but did not significantly differ in regard to morphine's lethal effect. The strain differences in sensitivity to the analgesic and locomotor effects were not uniform. The CXBK strain was much less sensitive than the C57 strain to the analgesic effect but only moderately less sensitive to the locomotor stimulatory effect. These differences may relate to previously demonstrated strain differences in the amounts of mu 1 and mu 2 opioid binding in central nervous system areas thought to mediate these behaviors.

Analgesia↗
PubMed1985

Differential effects of scopolamine on 3 forms of stress analgesia.

We have previously reported that non-opioid stress analgesia and two forms of opioid stress analgesia can be differentially produced in rats by varying the severity or temporal pattern of inescapable footshock. In this study, we investigated the role of muscarinic cholinergic mechanisms in mediating these 3 forms of stress analgesia. Whereas the muscarinic anticholinergic drug, scopolamine, had no effect on either non-opioid stress analgesia or opioid stress analgesia from 1 min of continuous 2.5-mA footshock, it significantly attenuated opioid analgesia from 20 min of intermittent footshock at this same intensity. The data are discussed in reference to other similarities and differences between these two forms of opioid stress analgesia.

Analgesia↗
PubMed1985

Stimulation-produced and stress-induced analgesia: cross-tolerance between opioid forms.

Electrical stimulation of medial brainstem sites produces potent analgesia in rats that is either opioid- or non-opioid-mediated depending on the specific brain region stimulated. Footshock stress also causes opioid and non-opioid forms of analgesia in rats depending on the exact parameters of footshock administered. We now report that opioid, but not non-opioid, stress analgesia demonstrates cross-tolerance with opioid, but not non-opioid, stimulation-produced analgesia. This finding suggests that opioid forms of stimulation-produced and stress-induced analgesia share a common substrate.

Animals↗
PubMed1985

Stress, opioid peptides, the immune system, and cancer.

Our results indicate that a particular form of footshock stress can suppress immune function in rats and decrease their resistance to tumor challenge. These effects appear to be mediated by opioid peptides released by stress, and they can be mimicked by high doses of morphine given systemically or by a vastly smaller dose delivered intracerebroventricularly. Such findings fit well into the emerging field of behavioral neuroimmunology and reinforce continuing efforts to elucidate the neural and neurohumoral mechanisms by which the environment can affect the organism's immune system.

Animals↗
PubMed1984

Intrinsic mechanisms of pain inhibition: activation by stress.

Portions of the brain stem seem normally to inhibit pain. In man and laboratory animals these brain areas and pathways from them to spinal sensory circuits can be activated by focal stimulation. Endogenous opioids appear to be implicated although separate nonopioid mechanisms are also evident. Stress seems to be a natural stimulus triggering pain suppression. Properties of electric footshock have been shown to determine the opioid or nonopioid basis of stress-induced analgesia. Two different opioid systems can be activated by different footshock paradigms. This dissection of stress analgesia has begun to integrate divergent findings concerning pain inhibition and also to account for some of the variance that has obscured the reliable measurement of the effects of stress on tumor growth and immune function.

Adaptation, Physiological↗
PubMed1984

Body region shocked need not critically define the neurochemical basis of stress analgesia.

Both opioid and non-opioid forms of stress-induced analgesia have been demonstrated in rats, although the conditions leading to their selective activation are still being investigated. We have shown that variations in shock intensity, duration or temporal pattern can determine whether opioid or non-opioid stress analgesia occurs. Others have suggested that body region shocked is the critical determinant, analgesia from front paw shock being opioid and that from hind paw shock non-opioid. We now report that either opioid or non-opioid stress analgesia can be evoked from either front or hind paws depending only on footshock intensity when duration and temporal pattern are held constant.

Animals↗
PubMed1984

Opioid peptides mediate the suppressive effect of stress on natural killer cell cytotoxicity.

The cytotoxic activity of natural killer cells was investigated in rats subjected to one of two inescapable footshock stress paradigms, both of which induce analgesia, but only one via activation of opioid mechanisms. Splenic natural killer cell activity was suppressed by the opioid, but not the nonopioid, form of stress. This suppression was blocked by the opioid antagonist naltrexone. Similar suppression of natural killer activity was induced by high doses of morphine. These results suggest that endogenous opioid peptides mediate the suppressive effect of certain forms of stress on natural killer cell cytotoxicity.

Animals↗
PubMed1983

Opioid and non-opioid mechanisms of footshock-induced analgesia: role of the spinal dorsolateral funiculus.

Exposure to inescapable footshock causes either an opioid or non-opioid mediated analgesia in the rat depending on the temporal parameters of its administration. Lesions of the spinal dorsolateral funiculus significantly reduce both the opioid and non-opioid forms of this footshock-induced analgesia. Thus, these two neurochemically discrete pain-inhibitory systems appear to depend on the integrity of the same descending path, one known to be activated by morphine and by analgesic brain stimulation.

Analgesia↗
PubMed1983

Opioid and non-opioid mechanisms of stress analgesia: lack of cross-tolerance between stressors.

Qualitatively different analgesic responses can be evoked in rats by exposure to prolonged, intermittent or brief, continuous footshock stress. These two forms of stress analgesia appear to be mediated by opioid and nonopioid pain-inhibitory substrates, respectively. The present study confirms our previous observation that tolerance develops to only the opioid form of stress analgesia and shows that cross-tolerance does not occur between the opioid and nonopioid forms. These data provide further evidence that independent mechanisms underlie opioid and nonopioid stress analgesia.

Animals↗