Evidence for GABA as the transmitter for early cortically evoked inhibition of cat caudate neurons.
Bicuculline methochloride derived from (+) bicuculline was applied by microiontophoresis to intracellularly recorded cat caudate neurons during stimulation of the cortico-caudate pathway. This resulted in a distinct increase of the duration and amplitude of the evoked excitatory postsynaptic potentials and an increase of the delay to the following hyperpolarizations. In most cases, however, a residual hyperpolarization remained even after prolonged applications of bicuculline methochloride. Iontophoretic application of GABA usually reduced the amplitude of the cortically evoked depolarizations. Very similar effects were seen if bicuculline methochloride was applied to dorsal hippocampal neurons while the fimbria/fornix was stimulated, an augmentation of the evoked depolarizations with a concomitant reduction of the following evoked inhibition. From these observations it was concluded that GABA is very probably the transmitter for the early part of cortically evoked hyperpolarizations in cat caudate neurons and that one of its functions is to regulate the strength of cortically evoked excitation.
D000818:Animals; D001640:Bicuculline / Q000031:analogs & derivatives / Q000494:pharmacology; D002415:Cats; D002421:Caudate Nucleus / Q000187:drug effects / Q000502:physiology*; D002540:Cerebral Cortex / Q000502:physiology*; D005071:Evoked Potentials / Q000187:drug effects; D005260:Female; D006624:Hippocampus / Q000502:physiology*; D008297:Male; D009433:Neural Inhibition; D009434:Neural Pathways / Q000502:physiology; D009435:Synaptic Transmission / Q000187:drug effects; D005680:gamma-Aminobutyric Acid / Q000502:physiology*
D005680:gamma-Aminobutyric Acid; C006749:bicuculline methochloride; D001640:Bicuculline