Strahlendorf J C, Lee M, Netzeband J G, Strahlendorf H K
Department of Physiology, Texas Tech University Health Sciences Center, School of Medicine, Lubbock 79430.
Neuroscience. 1988 Oct;27(1):107-15. doi: 10.1016/0306-4522(88)90222-9.
The ability of pentobarbital to modify the direct effects of iontophoretically ejected serotonin on the firing rates of cerebellar Purkinje cells was examined. Serotonin elicited inhibition, excitation, or a biphasic effect on cerebellar Purkinje cells. With continuous application of iontophoretic pentobarbital at currents found to potentiate GABA-induced inhibition, serotonin-mediated inhibitions were also augmented consistently. When application of serotonin elicited excitation, including a late component of biphasic responses, iontophoretic pentobarbital converted the effect to, primarily, inhibition. Besides increasing the magnitude of serotonin-mediated inhibition, iontophoretic pentobarbital increased the duration of this effect. In another series of experiments using pentobarbital rather than urethan as the anesthetic, serotonin-mediated inhibition was significantly augmented for all ejection currents tested. The GABA antagonists bicuculline, pentylenetetrazole and picrotoxin attenuated pentobarbital augmentation of serotonin-elicited inhibition. We conclude that serotonin-mediated inhibition of Purkinje cells is modifiable by pentobarbital and this effect bears a strong semblance to the actions of barbiturates on GABAergic neurotransmission.
