Anaesthetics in a bind?

Article Abstract:

Recent molecular studies on interactions between general anaesthetics and transmitter-gated ion channels add to knowledge on the mechanism of their action. Transmitter-gated ion channels have been observed to be particularly sensitive targets of anaesthetic action. The subunit composition of transmitter-gated ion channels has been found to affect allosteric regulation by some anaesthetic agents, with two recent studies using these interactions to locate single amino acid residues that influence sensitivity to general anaesthetics.

---

Allosteric modulation of 5-HT3 receptors: focus on alcohols and anaesthetic agents

Article Abstract:

Previous studies have elucidated the function of the serotonin (5-HT3) receptor as an ion channel. Pharmacological data from electrophysiological experiments have shown that 5-HT3 receptor function is directly modulated by certain alcohols such as ethanol, trichloroethanol, methanol, propanol and butanol, and anaesthetic agents such as ketamine, isoflurane and halothane. Responses induced by these agents differed between the receptor subtype, indicating the 5-HT3 receptor complex comprises of multiple modulatory sites.

Alcohols, Drug receptors

---

Recent advances in the electrophysiological characterization of 5-HT3 receptors

Article Abstract:

Electrophysiological studies show that 5-HT3 receptors control neurotransmitter release and promote rapid inotropic neurotransmission in the CNS. Results show that different 5-HT3 receptor preparations give varying ion channel conductance levels. Moreover, the success of cloning a 5-HT3 receptor subunit provides new information in the function and behavior of receptors. 5-HT3 receptors are found to exhibit interspecies pharmacological differences.

Analysis, Electrophysiology

Similar abstracts:

• Abstracts: G protein regulation of adenylate cyclase. Receptor sites for Ca2+ channel antagonists. Direct regulation of cardiac Ca2+ channels by G proteins: neither proven nor necessary?

This website is not affiliated with document authors or copyright owners. This page is provided for informational purposes only. Unintentional errors are possible.