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  • Title: The effects of neuroleptics on the GABA receptor of cat primary afferent neurons.
    Author: Higashi H, Inokuchi H, Nishi S, Inanaga K, Gallagher JP.
    Journal: Brain Res; 1981 Oct 05; 222(1):103-17. PubMed ID: 6271332.
    Abstract:
    Butyrophenones (haloperidol and pimozide) at low concentrations (0.05-1.0 micro M) inhibited the GABA-induced depolarization of cat primary afferent neurons, while at high concentrations (greater than 10 micro M) they enhanced the GABA-depolarization. These actions of the butyrophenones were not accompanied by any measurable change in the dissociation constant of the GABA-GABA receptor interaction, whereas their inhibitory and facilitatory influences on the GABA-depolarization were associated with reduction and increase in the cell membrane resistance, respectively. Further analysis showed that the reduction of membrane resistance by low concentrations of butyrophenones was brought about by an increased sodium and potassium conductance and that the increase in membrane resistance by a high concentration of these drugs was caused by a reduced sodium and potassium conductance. In contrast to the butyrophenones, a typical phenothiazine derivative (chlorpromazine) at concentrations of 0.1-100 micro M did not affect the GABA-depolarization. The results suggest that butyrophenones do not mimic the action of GABA as originally proposed by Janssen, but alter the GABA-induced depolarization indirectly by modifying the electrically excitable portion of the cell membrane. Chlorpromazine, a phenothiazine, on the other hand, has no recognizable effects on either the GABA-receptor membrane or the electrically excitable membrane.
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