Summary
1.Various drugs were applied intravenously or into the fourth ventricle and their effects upon the inhibition exerted by Purkinje cell axons were appraised by both extra- and intracellular recording from Deiters neurones. Strychnine, picrotoxin, pentamethylenetetrazol, β-methyl-β-ethylglutarimide, noradrenaline, dopamine, dibenamine and nethalide did not affect this inhibition. 2.γ-aminobutyric acid (GABA) and inhibitors of GABA transaminase were applied iontophoretically into the vicinity of Deiters neurones through an outer barrel of coaxial electrodes, the effects being observed either intra- or extracellularly through an inner barrel. 3. GABA depressed both inhibitory and excitatory postsynaptic potentials and often blocked the spike potentials, while it increased the membrane conductance. 4. GABA also produced a membrane hyperpolarization of 3–8 mV. Concomitantly both the spike potential and after-depolarization increased in amplitude and the after-hyperpolarization decreased. 5. In a few cases hydroxylamine but not amino-oxyacetic acid potentiated the inhibition, there being an increase in the inhibitory postsynaptic potentials thereby induced. 6. These effects were considered in connection with the possibility that GABA acts as a natural transmitter.
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Obata, K., Ito, M., Ochi, R. et al. Pharmacological properties of the postsynaptic inhibition by Purkinje cell axons and the action of γ-aminobutyric acid on Deiters neurones. Exp Brain Res 4, 43–57 (1967). https://doi.org/10.1007/BF00235216
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DOI: https://doi.org/10.1007/BF00235216