DOPA is a Causal Factor for Glutamate Release and Delayed Neuron Death by Transient Ischemia in Striatum and Hippocampal CA1 of Conscious Rats

  • Y. Misu
  • Y. Goshima
  • N. Furukawa
  • N. Arai
  • T. Miyamae
Part of the Advances in Behavioral Biology book series (ABBI, volume 53)


DOPA is believed to be an inert amino acid that affects Parkinson’s disease via conversion to dopamine (DA) by aromatic L-amino acid decarboxylase (AADC). We proposed that DOPA is a transmitter and/or modulator as well as a DA precursor.1 DOPA seems to be a transmitter of the primary baroreceptor afferents terminating in the nucleus tractus solitarii (NTS).2 In the NTS, neurons showing immunocytochemically tyrosine hydroxylase-(+), AADC-(-), DOPA-(+) and DA-(-)-reactivity exist.1,2 Such neurons may have DOPA as an end product. DOPA is released by aortic depressor nerve (ADN) stimulation.2 DOPA esters competitively antagonize hypotension and bradycardia by ADN stimulation and by DOPA microinjected.1–3 DOPA cyclohexyl ester (CHE) is the most potent and relatively stable competitive antagonist among DOPA esters.3 Responses to DOPA occur under inhibition of central AADC.1,2


Glutamate Release Nucleus Tractus Solitarii Transient Ischemia Depressor Response Ischemic Neuron 
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© Springer Science+Business Media New York 2002

Authors and Affiliations

  • Y. Misu
    • 1
  • Y. Goshima
    • 2
  • N. Furukawa
    • 2
  • N. Arai
    • 3
  • T. Miyamae
    • 2
  1. 1.Shinobu HospitalFukushimaJapan
  2. 2.Yokohama City University School of MedicineJapan
  3. 3.Tokyo Metropolitan Institute of NeuroscienceTokyoJapan

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