Ketamine potentiates the responses of the rat superior cervical ganglion to GABA.
The responses of the rat superior cervical ganglion to gamma-aminobutyric acid (GABA) were recorded in vitro using extracellular electrodes. Ketamine was found to increase the amplitude of these responses by up to 100%. This potentiation was seen at ketamine concentrations as low as 18 microM, reached maximum at 180 microM and then declined as the concentration was raised further. Ketamine (90 microM and over) depressed the nicotinic responses of the ganglia. The log concentration-effect curve to GABA was shifted to the left, and the maximum response increased, by ketamine. Inhibition of glial uptake of GABA did not prevent the effect of ketamine. The effects of 3-aminopropane sulphonic acid, which has a very low affinity for this GABA uptake mechanism, were also increased by ketamine. We conclude that ketamine, at concentrations which are found during general anaesthesia, potentiates the responses of the ganglion to GABA, by a mechanism other than inhibition of uptake, and suggest this may be due to action at the GABA receptor site.
D000818:Animals; D004357:Drug Synergism; D005727:Ganglia, Spinal / Q000187:drug effects*; D007649:Ketamine / Q000494:pharmacology*; D008297:Male; D009539:Nicotinic Acids / Q000502:physiology; D009557:Nipecotic Acids / Q000494:pharmacology; D011392:Proline / Q000031:analogs & derivatives*; D051381:Rats; D011919:Rats, Inbred Strains; D013654:Taurine / Q000031:analogs & derivatives / Q000494:pharmacology; D005680:gamma-Aminobutyric Acid / Q000494:pharmacology*
D009539:Nicotinic Acids; D009557:Nipecotic Acids; D013654:Taurine; C030278:nipecotic acid; D005680:gamma-Aminobutyric Acid; C001355:tramiprosate; D007649:Ketamine; D011392:Proline; C010983:homoproline