Bradykinin as a mediator of human pain.
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Biomedical subjects
Publications and source records attributed to M E Jarvik.
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By means of a simple activity measure, mice with lesions of the septal forebrain were tested for passive avoidance (response inhibition) and fear conditioning. In two separate experiments animals with septal lesions showed little or no conditioning, as evidenced by lack of suppression of activity during and following activitycontingent foot shock. Results support and extend thehypothesis that these deficits in passive avoidance derive from the removal of normal inhibitory influences mediated by the septal area.
This experiment tested the general validity of recent findings that retrograde amnesia can be produced by electroconvulsive shock only if the shock is administered within 10 to 30 seconds after the learning trial. Precautions were taken to avoid confusion of other shock effects with retrograde amnesia. A temporal gradient of elec- troconvulsive shock-produced retrograde amnesia, extending up to at least 1 hour, for a well-discriminated stimulus, was demonstrated in mice in a one-trial learning passive avoidance situation.
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Seventeen methadone-maintained cigarette smokers received 4 weeks of contingency management (CM) as a stop-smoking intervention. Results indicated that CM patients significantly reduced breath CO levels from baseline to completion of treatment and that 23.4% of patients maintained 1 week or more of continued smoking abstinence. Results indicated a link between smoking abstinence and reduced cocaine use, although not reduced opiate use, which raised questions about possible shared biological and psychological mechanisms for tobacco and cocaine use.
Several recent studies have tried to link endogenous opioid peptides (endorphins) with smoking reinforcement. Karras and Kane (1980) showed a one-third decrease in smoking after administration of the opiate antagonist naloxone. However, Nemeth-Coslett and Griffiths (1986) failed to replicate this result with use of a wide range of doses. The current study was an attempt to replicate Karras and Kane's results using 10 male chronic smokers. Each subject received naloxone (10 mg sc) or placebo in a double-blind, cross-over design (cross-over interval 6-14 days) after overnight abstinence from tobacco use. Naloxone reduced the number of cigarettes smoked by 16% in the first 1/2 hour smoking period, with a 10% reduction in carbon monoxide level 1 hour later. Naloxone had no effect on subjective and physiological variables and did not cause any signs of a tobacco withdrawal syndrome. These results are consistent with those of Karras and Kane, and suggest a role for endorphins in smoking reinforcement. Inconsistent results across studies may be due to methodological factors, such as differences in smoking deprivation time and postnaloxone administration testing intervals because naloxone has a short half-life.