Carbachol reduces IK,baclofen, but not IK,GABA in guinea pig hippocampal slices.
In the presence of bicuculline and/or picrotoxin (-)-baclofen and gamma-aminobutyric acid (GABA) induced outward currents (IBac and IGABA) at holding potentials of -55 to -75 mV in guinea pig CA3 neurones of hippocampal slices. Zero potentials for these currents were at the K-equilibrium potential indicating that they were carried by K-ions (IK.Bac, IK.GABA). IK.Bac was strongly reduced by carbachol (Cch) in low concentration (0.1 0.3 microM), while IK.GABA was not affected by Cch concentrations even up to 20 microM. The K-dependent late inhibitory postsynaptic potential (IPSP) was reduced significantly by Cch concentrations higher than 1 microM, but with these concentrations the early, Cl-dependent IPSP was reduced as well. The baclofen-derivative phaclofen, considered a selective antagonist of both the postsynaptic action of baclofen and the bicuculline - and picrotoxin - resistant action of GABA, exhibited, in our hands, partial agonistic effects and effects on non-transmitter gated K-currents. Our findings cast some doubt on the assumption that IK.Bac, IK.GABA and the late IPSP are all mediated by the same receptor and generated by the same mechanism.
Müller
W
W
Abteilung Neurophysiologie, Max-Planck-Institut für Psychiatrie, Martinsried, F.R.G.
Misgeld
U
U
D000818:Animals; D001418:Baclofen / Q000378:metabolism*; D002217:Carbachol / Q000494:pharmacology*; D004594:Electrophysiology; D006168:Guinea Pigs; D006624:Hippocampus / Q000187:drug effects*; D008564:Membrane Potentials; D009474:Neurons / Q000187:drug effects / Q000502:physiology*; D005680:gamma-Aminobutyric Acid / Q000378:metabolism*
D005680:gamma-Aminobutyric Acid; D002217:Carbachol; D001418:Baclofen