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The Journal of Neuroscience, December 15, 2000, 20(24):9224-9234
Association of Cocaine- and Amphetamine-Regulated
Transcript-Immunoreactive Elements with Thyrotropin-Releasing
Hormone-Synthesizing Neurons in the Hypothalamic Paraventricular
Nucleus and Its Role in the Regulation of the
Hypothalamic-Pituitary-Thyroid Axis during Fasting
Csaba
Fekete1, 2,
Emese
Mihály1,
Lu-Guang
Luo3,
Joseph
Kelly1,
Jes Thorn
Clausen4,
QuanFu
Mao3,
William M.
Rand5,
Larry Gene
Moss1,
Michael
Kuhar7,
Charles H.
Emerson8,
Ivor M. D.
Jackson3, and
Ronald M.
Lechan1, 6
1 Tupper Research Institute and Department of Medicine,
Division of Endocrinology, Diabetes, Metabolism and Molecular Medicine,
New England Medical Center, Boston, Massachusetts 02111, 2 Department of Neurobiology, Institute of Experimental
Medicine, Hungarian Academy of Sciences, Budapest, Hungary 1083, 3 Division of Endocrinology, Rhode Island Hospital and
Brown University, Providence, Rhode Island 02903, 4 Novo
Nordisk A/S, Department of Assay and Cell Technology, Novo Alle,
DK-2880 Bagsvaerd, Denmark, Departments of 5 Community
Health and 6 Neuroscience, Tufts University School of
Medicine, Boston, Massachusetts 02111, 7 Yerkes Regional
Primate Center, Emory University, Atlanta, Georgia 30329, and
8 Department of Medicine, Division of Endocrinology,
University of Massachusetts Medical School, Worcester, Massachusetts
01655
Because cocaine- and amphetamine-regulated transcript (CART)
coexists with  -melanocyte stimulating hormone (-MSH) in
the arcuate nucleus neurons and we have recently demonstrated that -MSH innervates TRH-synthesizing neurons in the hypothalamic paraventricular nucleus (PVN), we raised the possibility that CART may
also be contained in fibers that innervate hypophysiotropic thyrotropin-releasing hormone (TRH) neurons and modulate TRH gene expression. Triple-labeling fluorescent in situ
hybridization and immunofluorescence were performed to reveal the
morphological relationships between pro-TRH mRNA-containing
neurons and CART- and -MSH-immunoreactive (IR) axons. CART-IR axons
densely innervated the majority of pro-TRH mRNA-containing neurons in
all parvocellular subdivisions of the PVN and established asymmetric
synaptic specializations with pro-TRH neurons. However, whereas all
-MSH-IR axons in the PVN contained CART-IR, only a portion of
CART-IR axons in contact with pro-TRH neurons were immunoreactive for
-MSH. In the medial and periventricular parvocellular subdivisions
of the PVN, CART was co-contained in ~80% of pro-TRH neuronal
perikarya, whereas colocalization with pro-TRH was found in <10% of
the anterior parvocellular subdivision neurons. In addition, >80% of
TRH/CART neurons in the periventricular and medial parvocellular
subdivisions accumulated Fluoro-Gold after systemic administration,
suggesting that CART may serve as a marker for hypophysiotropic TRH
neurons. CART prevented fasting-induced suppression of pro-TRH in the
PVN when administered intracerebroventricularly and increased
the content of TRH in hypothalamic cell cultures. These studies
establish an anatomical association between CART and pro-TRH-producing
neurons in the PVN and demonstrate that CART has a stimulatory effect on hypophysiotropic TRH neurons by increasing pro-TRH gene expression and the biosynthesis of TRH.
Key words:
thyrotropin-releasing hormone; thyroid axis; CART; -MSH; fasting; leptin
Copyright © 2000 Society for Neuroscience 0270-6474/00/20249224-11$05.00/0
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