[Blockade of morphine analgesia by intracerebroventricular or subarachnoid injections of cholecystokinin in rats].
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Biomedical subjects
Publications and source records attributed to S G Fan.
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Using a rapid, simple and sensitive radioreceptor assay, a Ca2+-dependent K+-evoked release of endogenous GABA was demonstrated from rat cortical and hippocampal slices in vitro. This evoked-release of endogenous GABA was similar to that of [3H]GABA release (in its Ca2+ dependency) but differed from the latter in having a higher signal to noise level. Neither 5-HT nor a stable enkephalin analogue had any effect on endogenous GABA release from hippocampus slices.
3-Mercaptopropionic acid (3MP) (1 mM) inhibited the potassium-evoked release of endogenous GABA from slices of rat hippocampus and cerebral cortex in vitro. This did not appear to be due to an inhibition of GABA biosynthesis, since 3MP failed to affect the basal rate of GABA release or to accelerate the decline in the GABA content of tissue slices during prolonged exposure to 3MP (up to 120 min). 3MP, furthermore, inhibited the potassium-evoked release of [3H]GABA from preloaded brain slices, suggesting a direct inhibitory effect on GABA release. The threshold concentration was approximately 0.1 mM. 3MP at 1 mM failed to inhibit the potassium-evoked release of [3H]5-hydroxytryptamine, [3H]noradrenaline or somatostatin under similar conditions. The ability of 3MP to inhibit GABA release may contribute to the convulsant properties of this substance in vivo.
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The role played by central neurotransmitters in acupuncture analgesia was evaluated by correlating neurochemical changes in central nervous system with the acupuncture effect, as well as modification of the acupuncture effects by pharmacological manipulations of central neurotransmitters. The results of experimental studies which were performed mainly on rats and rabbits indicated that central serotonin and endogenous opiate-like substances (OLS) seem to be the most important substrates for mediation of acupuncture analgesia while central catecholamines, especially norepinephrine through alpha receptors, may exert an antagonistic effect. It was also found that prolonged and repeated acupuncture resulted in a gradual decrease of the acupuncture effects. The development of some endogenous anti-opiate substrates (AOS) in central nervous system was tentatively implicated.
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Our previous work showed that a factor (a protein with a high molecular weight) in serum was induced by restraint stress in mice and rats, and suppressed lymphocyte proliferation induced by concanavalin A. It was also found that the generation of the serum suppressive factor was under the control of the central nervous system. The present work was designed to investigate the role of interleukin-1 (IL-1) in the brain in the serum suppressive factor. IL-1 receptor antagonist (IL-1ra) was injected intracerebroventricularly in mice and the generation of the serum suppressive factor was found to be significantly decreased in a dose-dependent manner. When the dose of IL-1ra reached 5 micrograms, the generation of the suppressive factor was almost totally abolished. Intracerebroventricular injection of IL-1 beta (1.0 pg) enhanced the generation of the suppressive factor. Taken together, these results indicate the involvement of IL-1 in the brain in mediating generation of the suppressive factor.
Extracts from lymph node and spleen in mice and rats subjected to restraint stress significantly suppressed lymphocyte proliferation, but extracts from brain, skeletal muscle, and thymus gland had no effect on lymphocyte proliferation, suggesting that a suppressive factor for lymphocyte proliferation might selectively be induced in lymph node and spleen. Further experiments showed that biochemical properties, molecular weight, correlation between suppressive factors in serum and in extract of the lymph tissue from stressed animals, and control of the generation, all indicated that under the conditions of restraint stress and under the control of central nervous system a suppressive factor was generated in peripheral lymph tissue and then released into the blood-stream, which acted as a strong suppressor of lymphocyte proliferation.