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Biomedical subjects

S A Baron

Publications and source records attributed to S A Baron.

5 recordsLinked to original sources
PubMed1987

Effects of hypophysectomy and dexamethasone treatment on plasma beta-endorphin and pain threshold during pregnancy.

During pregnancy, rats and humans show an increase in pain threshold that is mediated by an endorphin system. In order to determine whether plasma beta-endorphin and/or other factors of pituitary origin are involved in pregnancy-induced analgesia in the rat, the effects of hypophysectomy (day 12 of pregnancy) or pharmacological suppression of pituitary function via dexamethasone administration (day 14-21 of pregnancy) were investigated. Hypophysectomy did not affect either the magnitude of the increase or the pattern of change in pain threshold despite the resulting decrease in stress-induced plasma beta-endorphin concentrations. However, the observed effect of the surgical and/or postsurgical procedure on pain threshold confounded unequivocal interpretation of these results. Pharmacological suppression of pituitary function with dexamethasone (2 micrograms/ml), a non-invasive procedure, also produced a significant decrease in resting plasma beta-endorphin levels. As was observed for surgical removal of the pituitary gland, this treatment did not produce a significant alteration in the magnitude of the increase in jump threshold. Furthermore, no correlation was found between plasma beta-endorphin concentrations and jump threshold values on day 21 of pregnancy. These results indicate that the pituitary gland does not play an essential role in the maintenance of opioid analgesia during pregnancy. It is suggested that pregnancy-induced analgesia depends on central rather than peripheral opioid systems.

Animals↗
PubMed1985

Simultaneous quantitation of norepinephrine, dopamine and serotonin in brain during and following chronic naltrexone administration.

The effects of chronic administration of the narcotic antagonist naltrexone on regional brain levels of norepinephrine, dopamine and serotonin were studied in order to determine whether central monoaminergic neurons are tonically modulated by central opioid systems. Chronic exposure to naltrexone (8 days) is associated with a significant increase in the content of norepinephrine in the mesolimbic forebrain and the content of dopamine in the frontal cortex and striatum. Ten days following naltrexone pellet removal the above levels returned to control values but thalamic dopamine content was reduced 10-fold. These data suggest that the affected brain regions receive an opioidergic input that is tonically active.

Animals↗
PubMed1984

Pregnancy-induced analgesia: effects of adrenalectomy and glucocorticoid replacement.

During pregnancy, rats show a progressive increase in jump threshold which is followed by a precipitous decrease after delivery. Overall, this pattern of change in pain threshold was not affected by adrenalectomy, with or without corticosterone replacement. It appears, therefore, that the adrenal glands are not necessary for the manifestation of opioid analgesia during pregnancy.

Adrenalectomy↗
PubMed1983

Release of substance P from the enteric nervous system: direct quantitation and characterization.

A dynamic system has been developed in which in vitro release of substance P (SP) from two longitudinal muscle-myenteric plexus strips from the guinea-pig ileum is obtained during continuous superfusion and measured directly by using a highly sensitive radioimmunoassay specific for SP. Electrical stimulation (0.5-40 Hz) produced a marked increase in the rate of release of SP. The magnitude of the increase in the rate of electrically evoked release was dependent on the frequency of stimulation but this dependence did not appear to be linear over the entire range tested. Electrically evoked release elicited by 20 Hz stimulation was reduced by 95% by omitting Ca++ from the superfusion buffer or by cooling the preparation to 3 degrees C. Pretreatment with tetrodotoxin (1 micrograms/ml for 15 min) substantially reduced the magnitude of the increase in the rate of release of SP but did not abolish it. Despite tetrodotoxin pretreatment, a significant portion (53%) of the electrically induced increase in SP release remained. The ability of electrical stimulation to release SP from the myenteric plexus in amounts sufficient to produce a physiological response in a Ca++- and temperature-dependent fashion in combination with data provided by indirect pharmacological experiments strongly suggests that SP functions as a neurotransmitter in the enteric nervous system.

Animals↗