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Tyrosine hydroxylase-negative, dopaminergic neurons are targets for transmitter-depleting action of haloperidol in the snail brain

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Summary

  1. 1.

    The effects of long term administration of micromolar concentrations of the D2 antagonist haloperidol upon monoaminergic neurons in the snailLymnaea stagnalis was investigated.

  2. 2.

    Treatment by bath application with 0.5–2.0 micromolar haloperidol, caused a significant, continuous depletion of dopamine levels in the nervous system as revealed by high performance liquid chromatography.

  3. 3.

    A transient depletion of serotonin was also observed, but DOPA and norepinephrine levels were unaffected. Similar depletion of dopamine was observed after the land snail,Achatina fulica, was injected with haloperidol on each of 4 consecutive days.

  4. 4.

    The depletion of dopamine as revealed with glyoxylate-induced fluorescence inLymnaea appears to be restricted to a subpopulation of catecholaminergic neurons which are immuno-negative for tyrosine hydroxylase, the synthetic enzyme responsible for the conversion of tyrosine to DOPA.

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Sakharov, D.A., Voronezhskaya, E.E., Nezlin, L. et al. Tyrosine hydroxylase-negative, dopaminergic neurons are targets for transmitter-depleting action of haloperidol in the snail brain. Cell Mol Neurobiol 16, 451–461 (1996). https://doi.org/10.1007/BF02150226

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  • DOI: https://doi.org/10.1007/BF02150226

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