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Differentiation of tyrosine hydroxylase‐synthesizing and/or aromatic L ‐amino acid decarboxylase‐synthesizing neurons in the rat mediobasal hypothalamus: Quantitative double‐immunofluorescence study
Author(s) -
Ershov Petr V.,
Ugrumov Michael V.,
Calas André,
Krieger Monique,
Thibault Jean
Publication year - 2002
Publication title -
journal of comparative neurology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.855
H-Index - 209
eISSN - 1096-9861
pISSN - 0021-9967
DOI - 10.1002/cne.10173
Subject(s) - aromatic l amino acid decarboxylase , tyrosine hydroxylase , biology , immunofluorescence , endocrinology , medicine , population , hypothalamus , arcuate nucleus , dopamine , tyrosine , neuron , antibody , neuroscience , biochemistry , immunology , environmental health
In this double‐immunofluorescence study, we first quantified the neurons of the arcuate nucleus as immunoreactive (+) for tyrosine hydroxylase (TH) and/or aromatic L ‐amino acid decarboxylase (AADC) in rats at embryonic day 21 (E21), at postnatal day 9 (P9), and in adulthood by using conventional fluorescent or confocal microscopy. On E21, monoenzymatic (TH + AADC immunonegative (−) and TH − AADC + ) neurons and bienzymatic (TH + AADC + ) neurons accounted for 99% and 1%, respectively, of the whole neuron population expressing enzymes of dopamine synthesis. Further development was characterized by the dramatic increase in TH + AADC − dorsomedial and TH + AADC + dorsomedial populations from E21 to P9 as well as by the increase in the TH + AADC + dorsomedial population (in females) and a drop in the TH + AADC − ventrolateral and TH + AADC − dorsomedial (in males) populations from P9 to adulthood. In contrast to TH + AADC − (in males) and TH + AADC + neurons, the TH − AADC + neurons did not change in number from E21 to adulthood. Thus, in rat fetuses, the neurons synthesizing TH and/or AADC were mainly monoenzymatic, whereas during postnatal life the fraction of bienzymatic neurons increased by up to 60%. J. Comp. Neurol. 446:114–122, 2002. © 2002 Wiley‐Liss, Inc.