sodium-oxybate and Glioma

sodium-oxybate has been researched along with Glioma* in 1 studies

Other Studies

1 other study(ies) available for sodium-oxybate and Glioma

Article	Year
Lack of effect of gamma-hydroxybutyrate on mu, delta and kappa opioid receptor binding. Neuroscience letters, 1996, Jul-05, Volume: 212, Issue:1 gamma-Hydroxybutyrate (GHB) and morphine induce a number of similar effects. Moreover, the effects they elicit can be reversed by the opiate antagonist naloxone (NX), suggesting that GHB may produce at least some of its central effects by acting as an opiate agonist. The present study considered this possibility by examining the effect of GHB on mu, delta, and kappa-opioid receptor binding in concentrations of 1 nM-0.1 mM. GHB was inactive in each instance, at every dose examined. GHB is consequently not a direct opiate receptor agonist. It is also unlikely to be an indirect (enkephalin or dynorphin release-stimulating) agonist. The mechanism of action involved whereby NX can reverse the effects of GHB must therefore not involve opioid mechanisms; at least not directly. Topics: Adjuvants, Anesthesia; Analgesics; Animals; Diprenorphine; Enkephalin, Ala(2)-MePhe(4)-Gly(5)-; Enkephalins; Etorphine; Glioma; Guinea Pigs; Naloxone; Narcotic Antagonists; Narcotics; Neuroblastoma; Receptors, Opioid; Receptors, Opioid, delta; Receptors, Opioid, kappa; Receptors, Opioid, mu; Sodium Oxybate; Tritium; Tumor Cells, Cultured	1996

Article

Year

Lack of effect of gamma-hydroxybutyrate on mu, delta and kappa opioid receptor binding.

Neuroscience letters, 1996, Jul-05, Volume: 212, Issue:1

gamma-Hydroxybutyrate (GHB) and morphine induce a number of similar effects. Moreover, the effects they elicit can be reversed by the opiate antagonist naloxone (NX), suggesting that GHB may produce at least some of its central effects by acting as an opiate agonist. The present study considered this possibility by examining the effect of GHB on mu, delta, and kappa-opioid receptor binding in concentrations of 1 nM-0.1 mM. GHB was inactive in each instance, at every dose examined. GHB is consequently not a direct opiate receptor agonist. It is also unlikely to be an indirect (enkephalin or dynorphin release-stimulating) agonist. The mechanism of action involved whereby NX can reverse the effects of GHB must therefore not involve opioid mechanisms; at least not directly.

Topics: Adjuvants, Anesthesia; Analgesics; Animals; Diprenorphine; Enkephalin, Ala(2)-MePhe(4)-Gly(5)-; Enkephalins; Etorphine; Glioma; Guinea Pigs; Naloxone; Narcotic Antagonists; Narcotics; Neuroblastoma; Receptors, Opioid; Receptors, Opioid, delta; Receptors, Opioid, kappa; Receptors, Opioid, mu; Sodium Oxybate; Tritium; Tumor Cells, Cultured

1996