PubMed · 13007296
The source did not provide an abstract. Follow the original record for more information.
Explore connections, maps & timelines
P M DESBARAX. 1952. [Divinyl ether].. https://pubmed.ncbi.nlm.nih.gov/13007296/
Cite the original work for its findings. Save a collection to share your selection of sources.
KEEP EXPLORING
Several general anesthetics reduce dopamine (DA) neuronal activity and release. However, anesthetic-induced alterations in DA transporter (DAT) function are unclear. We used high-speed chronoamperometry to examine how urethane, chloral hydrate and ethanol affected clearance of locally-applied DA in the dorsal striatum of unrestrained rats. Maximal DA signal amplitudes (A(max)) and signal decay rate constants (k) were monitored continuously from the awake to anesthetized state. Urethane did not significantly change A(max) or k. Chloral hydrate and ethanol potentiated A(max) by 32% and 37%, respectively, over baseline, indicative of DAT inhibition. These effects were not additive. Only ethanol increased k, an effect blocked by chloral hydrate. These results suggest differential effects of anesthetics on striatal DAT function, with chloral hydrate and ethanol significantly altering DAT activity but urethane producing only minimal effects.
The effects of general anaesthetics and temperature on carbachol-evoked gamma oscillations in the rat hippocampal brain slice preparation were investigated. The frequency of the oscillations was found to be dependent on temperature in the range 32-25 degrees C, with a linear reduction in frequency from 40-17 Hz over this temperature range. The volatile anaesthetics isoflurane and halothane, and the intravenous anaesthetics thiopental, propofol and R(+)-etomidate caused a reduction in the frequency of the oscillations, in a concentration-dependent manner, over a range of clinically relevant concentrations. On the other hand, the intravenous agent ketamine and the "inactive" S(-)-isomer of etomidate had no significant effect on the oscillation frequency. The oscillations were markedly asymmetric over one cycle with a relatively rapid "rising" phase followed by a slower "decaying" phase. The decrease in oscillation frequency was due to an increase in the time-course of the "decaying phase" of the oscillation with little effect on the "rising" phase, consistent with the idea that carbachol-evoked gamma oscillations are trains of GABAergic inhibitory postsynaptic potentials and that the anaesthetics are acting postsynaptically at the GABA(A) receptor.
General anesthesia is a complex behavioral state provoked by the pharmacological action of a broad range of structurally different hydrophobic molecules called general anesthetics (GAs) on receptor members of the genetically linked ligand-gated ion channel (LGIC) superfamily. This superfamily includes nicotinic acetylcholine (AChRs), type A and C gamma-aminobutyric acid (GABAAR and GABACR), glycine (GlyR), and type 3 5-hydroxytryptamine (5-HT3R) receptors. This review focuses on recent advances in the localization of GA binding sites on conformationally and compositionally distinct AChRs. The experimental evidence outlined in this review suggests that: 1. Several neuronal-type AChRs might be targets for the pharmacological action of distinct GAs. 2. The molecular components of a specific GA binding site on a certain receptor subtype are different from the structural determinants of the locus for the same GA on a different receptor subtype. 3. There are unique binding sites for distinct GAs in the same receptor protein. 4. A GA can activate, potentiate, or inhibit an ion channel, indicating the existence of more than one binding site for the same GA. 5. The affinity of a specific GA depends on the conformational state of the receptor. 6. GAs inhibition channels by at least two mechanisms, an open-channel-blocking and/or an allosteric mechanism. 7. Certain GAs may inhibit AChR function by competing for the agonist binding sites or by augmenting the desensitization rate.