Reduction in brain tyrosine hydroxylase activity following acetylcholinesterase blockade in rats

Authors:
  • JRJ. Steven Richardson
    J. Steven Richardson
  • FLFriedhelm Lamprecht
    Friedhelm Lamprecht
  • TKTomislav Kazic
    Tomislav Kazic
  • IKIrwin J. Kopin
    Irwin J. Kopin
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Abstract
Activation of cholinergic neurons in the brain is produced by administration of the acetylcholinesterase inhibitors physostigmine and diisopropylfluorophosphate (DFP). This activation has a biphasic effect on tyrosine hydroxylase (EC 1.14.3–) activity. The acute effect of DFP, 1 mg/kg, intraperitoneally, or physostigmine, 0.2 mg/kg, intravenously, or 10 μg, intraventricularly, was a rapid reduction in tyrosine hydroxylase activity in the hypothalamus. The activities of DOPA decarboxylase (EC 4.1.1.28) and dopamine-β-hydroxylase (EC 1.14.17.1) were not changed. In contrast to the acute effect, chronic administration of physostigmine, 0.2 mg/kg, intravenously, twice daily for 7 days produced an increase in tyrosine hydroxylase activity in the hypothalamus. The rapid acute effects may be due to an allosteric inactivation of tyrosine hydroxylase, while the chronic effects may reflect enzyme induction.