L-DOPA elicits non-vesicular releases of serotonin and dopamine in hemiparkinsonian rats in vivo

Eur Neuropsychopharmacol. 2016 Aug;26(8):1297-309. doi: 10.1016/j.euroneuro.2016.05.004. Epub 2016 May 24.

Abstract

The control of the secretory activity of serotonergic neurons has been pointed out to reduce motor and non-motor side effects of the antiparkinsonian drug L-DOPA. This strategy deserves further investigation because it is presently unclear whether L-DOPA promotes a non-vesicular release of dopamine and serotonin from serotonergic neurons. To get a full neurochemical picture compatible with the existence of such a mechanism, we combined multisite intracerebral microdialysis, post mortem tissue measurement and single unit extracellular recordings in the dorsal raphe nucleus from hemiparkinsonian rats. L-DOPA (3-100mg/kg, ip.) non-homogeneously decreased extracellular serotonin levels in the striatum, substantia nigra pars reticulata, hippocampus and prefrontal cortex and homogenously serotonin tissue content in the striatum, cortex and cerebellum. L-DOPA (12mg/kg) did not modify the firing rate or pattern of serotonergic-like neurons recorded in the dorsal raphe nucleus. When focusing on serotonin release in the prefrontal cortex and the hippocampus, we found that L-DOPA (12 or 100mg/kg) enhanced serotonin extracellular levels in both regions upon Ca(2+) removal. Concomitantly, L-DOPA-stimulated dopamine release partly persisted in the absence of Ca(2+) in a region-dependent manner. Local application of the serotonin reuptake inhibitor citalopram (1µM) blunted the responses to L-DOPA (3-12mg/kg), measured as extracellular dopamine levels, most prominently in the hippocampus. These data stress that L-DOPA, already at low to moderate doses, promotes non-vesicular releases of serotonin and dopamine in a region-dependent manner.

Keywords: Electrophysiology; Exocytosis; Hippocampus; Intracerebral microdialysis; Prefrontal cortex; Tissue measurement.

MeSH terms

  • Action Potentials / drug effects
  • Animals
  • Antiparkinson Agents / administration & dosage
  • Antiparkinson Agents / pharmacology
  • Antiparkinson Agents / therapeutic use*
  • Cholestanols
  • Citalopram / pharmacology
  • Disease Models, Animal*
  • Dopamine Agents / administration & dosage
  • Dopamine Agents / pharmacology
  • Dopamine Agents / therapeutic use
  • Dopaminergic Neurons / drug effects*
  • Dopaminergic Neurons / metabolism
  • Dose-Response Relationship, Drug
  • Hippocampus / drug effects
  • Hippocampus / metabolism
  • Hippocampus / physiopathology
  • Hydroxyindoleacetic Acid / metabolism
  • Levodopa / administration & dosage
  • Levodopa / metabolism
  • Levodopa / pharmacology
  • Levodopa / therapeutic use*
  • Male
  • Organ Specificity
  • Parkinson Disease / drug therapy*
  • Parkinson Disease / physiopathology
  • Prefrontal Cortex / drug effects
  • Prefrontal Cortex / metabolism
  • Prefrontal Cortex / physiopathology
  • Rats, Sprague-Dawley
  • Selective Serotonin Reuptake Inhibitors / pharmacology
  • Serotonergic Neurons / drug effects*
  • Serotonergic Neurons / metabolism
  • Serotonin / metabolism*
  • Single-Cell Analysis
  • Synaptic Transmission / drug effects

Substances

  • Antiparkinson Agents
  • Cholestanols
  • Dopamine Agents
  • Serotonin Uptake Inhibitors
  • microdiplane
  • Citalopram
  • Serotonin
  • Levodopa
  • Hydroxyindoleacetic Acid