Dopamine sensitivity of hypothalamic arcuate neurons and their role in the regulation of pituitary gonatropic function

1977 ◽  
Vol 84 (5) ◽  
pp. 1534-1537
Author(s):  
V. N. Babichev ◽  
V. Ya. Ignatkov
Keyword(s):  
Arcuate Neurons

Decreased inhibition by leptin of hypothalamic arcuate neurons in neonatally overfed young rats

Neuroreport ◽  
2000 ◽  
Vol 11 (12) ◽  
pp. 2795-2798 ◽  
Author(s):  
Helga Davidowa ◽  
Andreas Plagemann
Keyword(s):  
Young Rats ◽  
Arcuate Neurons

Insulin resistance of hypothalamic arcuate neurons in neonatally overfed rats

Neuroreport ◽  
2007 ◽  
Vol 18 (5) ◽  
pp. 521-524 ◽  
Author(s):  
Helga Davidowa ◽  
Andreas Plagemann
Keyword(s):  
Insulin Resistance ◽  
Arcuate Neurons

Single-Unit Activity of Hypothalamic Arcuate Neurons in Brain Tissue Slices

1986 ◽  
Vol 43 (2) ◽  
pp. 189-196 ◽  
Author(s):  
Jenn-Tser Pan ◽  
Lee-Ming Kow ◽  
Donald W. Pfaff
Keyword(s):  
Brain Tissue ◽  
Unit Activity ◽  
Single Unit ◽  
Single Unit Activity ◽  
Tissue Slices ◽  
Arcuate Neurons

scholarly journals Identification of Neuronal Enhancers of the Proopiomelanocortin Gene by Transgenic Mouse Analysis and Phylogenetic Footprinting

2005 ◽  
Vol 25 (8) ◽  
pp. 3076-3086 ◽  
Author(s):  
Flávio S. J. de Souza ◽  
Andrea M. Santangelo ◽  
Viviana Bumaschny ◽  
María Elena Avale ◽  
James L. Smart ◽  
...  
Keyword(s):  
Energy Homeostasis ◽  
Significant Quantitative Trait Locus ◽  
Phylogenetic Footprinting ◽  
Transcriptional Unit ◽  
Human Populations ◽  
Chromosome 2 ◽  
Loss Of Function ◽  
Trait Locus ◽  
Genomic Regions ◽  
Arcuate Neurons

ABSTRACT The proopiomelanocortin (POMC) gene is expressed in the pituitary and arcuate neurons of the hypothalamus. POMC arcuate neurons play a central role in the control of energy homeostasis, and rare loss-of-function mutations in POMC cause obesity. Moreover, POMC is the prime candidate gene within a highly significant quantitative trait locus on chromosome 2 associated with obesity traits in several human populations. Here, we identify two phylogenetically conserved neuronal POMC enhancers designated nPE1 (600 bp) and nPE2 (150 bp) located approximately 10 to 12 kb upstream of mammalian POMC transcriptional units. We show that mouse or human genomic regions containing these enhancers are able to direct reporter gene expression to POMC hypothalamic neurons, but not the pituitary of transgenic mice. Conversely, deletion of nPE1 and nPE2 in the context of the entire transcriptional unit of POMC abolishes transgene expression in the hypothalamus without affecting pituitary expression. Our results indicate that the nPEs are necessary and sufficient for hypothalamic POMC expression and that POMC expression in the brain and pituitary is controlled by independent sets of enhancers. Our study advances the understanding of the molecular nature of hypothalamic POMC neurons and will be useful to determine whether polymorphisms in POMC regulatory regions play a role in the predisposition to obesity.

Adenosine Modulation of Calcium Currents and Presynaptic Inhibition of GABA Release in Suprachiasmatic and Arcuate Nucleus Neurons

1997 ◽  
Vol 77 (6) ◽  
pp. 3035-3047 ◽  
Author(s):  
Gong Chen ◽  
Anthony N. van den Pol
Keyword(s):  
Presynaptic Inhibition ◽  
Receptor Agonist ◽  
Arcuate Nucleus ◽  
Gaba Release ◽  
Calcium Currents ◽  
Whole Cell ◽  
Adenosine A1 ◽  
A1 Receptor ◽  
Arcuate Neurons ◽  
A2 Receptors

Chen, Gong and Anthony N. van den Pol. Adenosine modulation of calcium currents and presynaptic inhibition of GABA release in suprachiasmatic and arcuate nucleus neurons. J. Neurophysiol. 77: 3035–3047, 1997. Adenosine modulation of calcium channel currents and synaptic γ-aminobutyrate (GABA) release was investigated with whole cell voltage-clamp recordings in rat suprachiasmatic nucleus (SCN) and arcuate nucleus cultures ( n = 94). In SCN cultures, ∼70% of the neurons showed a reversible inhibition of whole cell barium currents on the application of adenosine or its analogues. Adenosine at 1 μM reduced the amplitude of the barium currents by ∼27%. In contrast to the significant reduction in the amplitude, the rising and decaying phases of the barium currents, and the inverted bell shape of the current-voltage curve of the barium currents, were not changed by adenosine. The adenosine A1 receptor agonist N6-cyclopentyladenosine (CPA; 100 nM) and the adenosine A2 receptor agonist N6-[2-(3,5-dimethoxyphenyl)-ethyl]adenosine (DPMA; 100 nM) inhibited the barium currents by 21% and 16%, respectively, in SCN neurons, indicating both A1 and A2 receptor actions. The A1 receptor antagonist 8-cyclopentyl-1,3-dipropylxanthine (100 nM) significantly reduced the effect of CPA but did not change the effect of DPMA on the barium currents. In the presence of tetrodotoxin to block action potentials, the frequency, but not the amplitude, of miniature inhibitory postsynaptic currents was significantly reduced (46%) by 1 μM adenosine, suggesting a presynaptic mechanism of adenosine action. In support of this suggestion, the postsynaptic GABA receptor responses were not influenced by 1 μM adenosine in the majority of SCN neurons. Most solitary self-innervating SCN neurons in microisland cultures were GABAergic. In these cells, the evoked autaptic GABA release (inhibitory postsynaptic current) was significantly inhibited by adenosine (37%), CPA (27%), and DPMA (28%), indicating that both A1 and A2 receptors were present in presynaptic axons. Similar to the effect in SCN neurons, adenosine inhibited both barium currents and GABA release in arcuate neurons. The reduction of whole cell barium currents by adenosine (1 μM), CPA (100 nM), and DPMA (100 nM) was 24, 17, and 19%, respectively. In solitary self-innervating arcuate neurons, adenosine inhibited the evoked GABA release (inhibitory postsynaptic current) by ∼48%. We conclude that both adenosine A1 and A2 receptors are present in the SCN and arcuate nucleus of the hypothalamus. Adenosine inhibits calcium currents and presynaptically reduces inhibitory GABA neurotransmission.

Increase of galanin-like immunoreactivity in rat hypothalamic arcuate neurons after peripheral nerve injury

2004 ◽  
Vol 368 (1) ◽  
pp. 102-106 ◽  
Author(s):  
Hiroki Imbe ◽  
Tetsuya Abe ◽  
Keiichiro Okamoto ◽  
Makoto Sato ◽  
Hiroki Ito ◽  
...  
Keyword(s):  
Peripheral Nerve ◽  
Nerve Injury ◽  
Peripheral Nerve Injury ◽  
Arcuate Neurons
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