Posted by undopaminergic on June 5, 2008, at 11:10:00
In reply to Re: Nitrous Oxide, posted by yxibow on June 5, 2008, at 4:12:20
More trivia:
Nitrous oxide (N2O) is an antagonist of the NMDA-glutamate receptor and thus has some pharmacological similarity to memantine and ketamine. This property of N2O is likely to account for the dissociative effects sometimes associated with its use.
N2O also has some GABAergic activity. It has anxiolytic efficacy that is antagonised by benzodiazepine-receptor antagonists such as flumazenil.
By some mechanism, N2O interacts with the endogenous opioid system, but the details are unclear. There are conflicting reports as to whether the effects of N2O are diminished by opioid-antagonists such as naloxone. One paper reports that rats tolerant to the analgesic effects of N2O do not exhibit cross-tolerance to morphine, whereas, in contrast, morphine-tolerant rats have reduced sensitivity to the analgesic effects of N2O.
Possibly via stimulating the release of endogenous opioids, N2O activates brain stem noradrenergic neurons, which results in enhanced noradrenaline release in the spinal cord. Apparently, spinal alpha2B-adrenergic receptors mediate N2O-analgesia, as the analgesic - but not sedative - effects of N2O in animals lacking alpha2B-adrenoceptors are abolished.
Animals that develop tolerance to N2O upon long-term exposure are reportedly cross-tolerant to alcohol, and conversely, animals tolerant to alcohol have reduced sensitivity to the analgesic effects of N2O.
However, N2O-tolerant animals are reportedly not cross-tolerant to barbiturates.
N2O depletes the cyanocobalamine form of vitamin B12 by oxidising it to an inactive compound, and chronic use of N2O can result in vitamin B12-deficiency.
poster:undopaminergic
thread:832870
URL: http://www.dr-bob.org/babble/20080528/msgs/833092.html