Cross-talk signals in the CNS Role of neurotrophic and hormonal factors adhesion molecules and intercellular signaling agents in luteinizing hormone-releasing hormone LHRH -astroglial interactive network

10.2741/a177 ◽  
1997 ◽  
Vol 2 (4) ◽  
pp. d88-125 ◽  
Author(s):  
B. Marchetti
Keyword(s):  
Luteinizing Hormone ◽  
Adhesion Molecules ◽  
Cross Talk ◽  
Intercellular Signaling ◽  
Hormonal Factors ◽  
Luteinizing Hormone Releasing Hormone ◽  
Releasing Hormone ◽  
Interactive Network

Gender, Neuroendocrine-Immune Interactions and Neuron-Glial Plasticity: Role of Luteinizing Hormone-Releasing Hormone (LHRH)

2006 ◽  
Vol 917 (1) ◽  
pp. 678-709 ◽  
Author(s):  
BIANCA MARCHETTI ◽  
FRANCESCO GALLO ◽  
ZELINDA FARINELLA ◽  
CATALDO TIROLO ◽  
NUCCIO TESTA ◽  
...  
Keyword(s):  
Luteinizing Hormone ◽  
Luteinizing Hormone Releasing Hormone ◽  
Releasing Hormone

Vitamin E Stimulates Luteinizing Hormone-Releasing Hormone and Ascorbic Acid Release from Medial Basal Hypothalami of Adult Male Rats

2003 ◽  
Vol 228 (7) ◽  
pp. 779-785 ◽  
Author(s):  
S. Karanth ◽  
W.H. Yu ◽  
C.A. Mastronardi ◽  
S.M. McCann
Keyword(s):  
Ascorbic Acid ◽  
Vitamin E ◽  
Luteinizing Hormone ◽  
Adult Male ◽  
Male Rats ◽  
Soluble Form ◽  
Luteinizing Hormone Releasing Hormone ◽  
Releasing Hormone ◽  
Lhrh Release

Vitamin E, a dietary factor, is essential for reproduction in animals. It is an antioxidant present in all mammalian cells. Previously, we showed that ascorbic acid (AA) acted as an inhibitory neurotransmitter in the hypothalamus by scavenging nitric oxide (NO). Earlier studies have shown the antioxidant synergism between vitamin E and ascorbic acid (AA). Therefore, it was of interest to evaluate the effect of vitamin E on luteinizing hormone-releasing hormone (LHRH) and AA release. Medial basal hypothalami from adult male rats of the Sprague Dawley strain were incubated with Krebs-Ringer bicarbonate buffer or graded concentrations of a water soluble form of vitamin E, tocopheryl succinate polyethylene glycol 1000 (TPGS, 22–176 μM) for 1 hr. Subsequently, the tissues were incubated with vitamin E or combinations of vitamin. E + N-methyl-D-aspartic acid (NMDA), an excitatory amino acid for 30 min to study the effect of prior and continued exposure to vitamin E on NMDA-induced LHRH release. AA and LHRH released into the incubation media were determined by high-performance liquid chromatography and radioimmunoassay, respectively. Vitamin E stimulated both LHRH and AA release. The minimal effective concentrations were 22 and 88 μM, respectively. NMDA stimulated LHRH release as previously shown and this effect was not altered in the combined presence of vitamin E plus NMDA. However, AA release was significantly reduced in the combined presence of vitamin E plus NMDA. To evaluate the role of NO in vitamin E-induced LHRH and AA release, the tissues were incubated with vitamin E or combinations of vitamin E + NG-monomethyl-L-arginine (NMMA), a competitive inhibitor of NO synthase. NMMA significantly suppressed vitamin E-induced LHRH and AA release indicating a role of NO in the release of both LHRH and AA. The data suggest that vitamin E plays a role in the hypothalamic control of LHRH and AA release and that the release is mediated by NO.

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