The effect of intracerebroventricular treatment of mice with pertussis toxin (PTX) on pain perception and 3H-nitrendipine binding was examined to study a possible change in the GTP-binding proteins in morphine tolerant rodents. It was observed that both PTX treatment and chronic administration of morphine cause hyperalgesia in the acetic acid-induced writhing test. Analgesic effects brought by the acute administration of morphine or nifedipine, a calcium antagonist, were not affected by PTX treatment. In synaptic membrane fractions prepared from mice treated with PTX or morphine chronically, specific binding of 3H-nitrendipine was enhanced approximately 41.8% and 35.7%, respectively, without alteration in its affinity. Chronic administration of morphine followed by PTX treatment did not display further increases in 3H-nitrendipine binding. These results suggest that the PTX-sensitive GTP-binding proteins may not be involved in the manifestation of the analgesic effect of morphine in mice.

Acetates↗

PubMedDate not supplied

In vitro production and release of opioid peptides in the tooth pulp induced by bradykinin.

A possible relationship between met-enkephalin (ME)-like peptides and bradykinin (BK) in the rat incisor pulp was examined in in vitro experiments using whole pulp. ME-like peptide content in the pulp was increased by BK at a concentration of 1 microM, but not in higher concentrations, while the release of ME-like peptides from the pulp into the incubation medium was increased dose-dependently by BK. These effects of BK were inhibited by Des-Arg9-[Leu8]-BK, a potent BK-antagonist, suggesting that the effects of BK were mediated through a specific BK-receptor in the pulp. On the other hand, high K+ did not induce any increased release of ME-like peptides from the pulp and the BK effects were influenced neither in Ca++-free medium nor in the presence of ouabain. These results suggested that ME-like peptide releasing effect of BK was not due to depolarization of the cell membrane and was not active. In addition, kyotorphin, and enkephalin-releaser, could not only elicit a release of ME-like peptides from the pulp, but also a marked increase of the peptide content in the pulp. However, a combination of BK and kyotorphin attenuated the effect of BK or kyotorphin each other. These results suggested that there might be two kinds of mechanisms of ME-like peptide production in the pulp and those mechanisms might interfere mutually.

Analgesics↗

PubMedDate not supplied

Influences of bradykinin and substance P on the met-enkephalin-like peptide content in the rat incisor pulp.

The present study was aimed to examine possible influences of bradykinin (BK) and substance P (SP) on met-enkephalin (ME)-like peptide content in the rat incisor pulp. Des-Arg9-[Leu8]-BK, a potent BK-antagonist, significantly reduced the increased content of ME-like peptides induced by noxious stimulation, while the effect of BK-antagonist was reversed in combination with BK. Morphine decreased the increased content of ME-like peptides. Ethylketocyclazocine, a kappa-agonist, also decreased the increased content of the peptides. From these results, it was suggested that BK might be a trigger in the increase of ME-like peptide content induced by noxious stimulation and, in contrast, ME-like peptides in the pulp might inhibit BK release from the pulp in a negative feedback mechanism. On the other hand, [D-Pro2,D-Trp7,9]-SP, a potent SP-antagonist, did not show any significant influence to ME-like peptide content in the pulp. Furthermore, the content was not changed following cutting of inferior alveolar nerve. From these results, it was suggested that ME-like peptides in the pulp cells might be independent on SP-containing nerves in the pulp.

Animals↗

PubMedDate not supplied

Effect of ethanol on hippocampal GABA receptors in the rat brain.

The effect of ethanol on GABA receptors was studied in hippocampal slices and membrane preparations of the rat brain. In slice preparation, ethanol enhanced the GABA inhibition of the population spikes evoked in CA 1 pyramidal cells by Schaffer collateral stimulation. The effect of ethanol was dose-dependent being observed with minimal concentration of 70 mM. In 3H-GABA binding experiments, ethanol enhanced the binding to fresh membranes with no change in the affinity. Maximal stimulation was observed at ethanol concentration of 70 mM. In hippocampal slices or membrane preparations obtained from ethanol- or barbital-administered rats chronically, ethanol failed to enhance GABA function. Thus, the present study demonstrated the involvement of GABA in central effect of ethanol. Also suggested in GABA was the involvement in the development of cross-tolerance between ethanol and barbiturates.

Action Potentials↗

PubMedDate not supplied

Inhibitory effect of Apernyl on production of bradykininlike substance in pulp.

In the Formalin-induced pulpitis of rats and the electrically stimulated pulps of dogs, a bradykininlike substance developed by the pulps and released into a saline pool on the exposed pulps disappeared after a local application of Apernyl solution. This suggests that the possible pain-reducing or anti-in-flammatory effect of Apernyl is a result of its inhibiting bradykinin production.

Animals↗