Honokiol and Magnolol Increased Hippocampal Acetylcholine Release in Freely-Moving Rats

2000 ◽  
Vol 28 (03n04) ◽  
pp. 379-384 ◽  
Author(s):  
Yu-Chi Hou ◽  
Pei-Dawn Lee Chao ◽  
Shiouh-Yi Chen
Keyword(s):  
Acetylcholine Release ◽  
Stem Bark ◽  
High Dose ◽  
M 10 ◽  
Freely Moving Rats ◽  
Freely Moving ◽  
Magnolia Officinalis ◽  
Choline Acetyltransferase Activity

Honokiol and magnolol, phenolic compounds isolated from the stem bark of Magnolia officinalis, have been demonstrated to increase choline acetyltransferase activity, inhibit acetylcholinesterase, promote potassium-induced acetylcholine release and exhibit neurotrophic function in in vitro studies. The objective of the present study was to determine the effect of these compounds on hippocampal acetylcholine release in conscious, freely-moving rats. 10-4 M–10-6 M of honokiol or magnolol was perfused into rat hippocampus via a dialysis probe. The results showed that at 10-4 M concentration, honokiol and magnolol markedly increased extracellular acetylcholine release to 165.5 ± 5.78% and 237.83 ± 9.47% of the basal level, respectively. However, lower concentrations of either compounds failed to elicit significant acetylcholine release. This result suggests that a high dose of honokiol or magnolol may enhance in vivo hippocampal acetylcholine release.

scholarly journals Orexin A suppresses in vivo GH secretion

2004 ◽  
pp. 731-736 ◽  
Author(s):  
LM Seoane ◽  
SA Tovar ◽  
D Perez ◽  
F Mallo ◽  
M Lopez ◽  
...  
Keyword(s):  
Nutritional Status ◽  
Area Under The Curve ◽  
Sleep Regulation ◽  
Gh Secretion ◽  
Neuroendocrine Function ◽  
Freely Moving Rats ◽  
Freely Moving ◽  
The Brain

BACKGROUND/AIMS: Orexins (OXs) are a newly described family of hypothalamic neuropeptides. Based on the distribution of OX neurons and their receptors in the brain, it has been postulated that they could play a role in the regulation of neuroendocrine function. GH secretion is markedly influenced by nutritional status and body weight. To investigate the role OX-A plays in the neuroregulation of GH secretion we have studied its effect on spontaneous GH secretion as well as GH responses to GHRH and ghrelin in freely moving rats. Finally, we also assessed the effect of OX-A on in vitro GH secretion. METHODS: We administered OX-A (10 microg, i.c.v.) or vehicle (10 microl, i.c.v.) to freely moving rats. Spontaneous GH secretion was assessed over 6 h with blood samples taken every 15 min. RESULTS: Administration of OX-A led to a decrease in spontaneous GH secretion in comparison with vehicle-treated rats, as assessed by mean GH levels (means+/-s.e.m. 4.2+/-1.7 ng/ml vs 9.4+/-2.2 ng/ml; P<0.05), mean GH amplitude (3.6+/-0.5 ng/ml vs 20.8+/-5.6 ng/ml; P<0.01) and area under the curve (848+/-379 ng/ml per 4 h vs 1957+/-458 ng/ml per 4 h; P<0.05). In contrast, OX-A failed to modify in vivo GH responses to GHRH (10 microg/kg, i.v.) although it markedly blunted GH responses to ghrelin (40 microg/kg, i.v.) (mean peak GH levels: 331+/-71 ng/ml, vehicle, vs 43+/-11 ng/ml in OX-A-treated rats; P<0.01). Finally, OX-A infusion (10(-7), 10(-8) or 10(-9) M) failed to modify in vitro basal GH secretion or GH responses to GHRH, ghrelin and KCl. CONCLUSIONS: These data indicate that OX-A plays an inhibitory role in GH secretion and may act as a bridge among the regulatory signals that are involved in the control of growth, nutritional status and sleep regulation.

Flexible intravenous microdialysis probe for blood sampling in freely moving rats

1993 ◽  
Vol 74 (1) ◽  
pp. 466-469 ◽  
Author(s):  
P. Rada ◽  
M. Parada ◽  
L. Hernandez
Keyword(s):  
Blood Sampling ◽  
In Vitro Tests ◽  
Microdialysis Probe ◽  
Freely Moving Rats ◽  
Intravenous Microdialysis ◽  
Silastic Tubing ◽  
Freely Moving ◽  
Circulating Levels

A flexible intravenous microdialysis probe was constructed from Silastic tubing (0.5 mm ID and 1.0 mm OD), with a cellulose hollow fiber tip 0.2 mm in diameter and 25 mm long with a 6,000 mol wt cut off. In vitro tests showed relative recovery rates of 39.1 +/- 1.9% for epinephrine. In vivo tests in freely moving rats, 36 h and 7 days after surgery, showed stable amounts of epinephrine and glucose. After intraperitoneal injections of 2-deoxy-D-glucose, circulating levels of epinephrine and glucose increased significantly. Similar results were obtained several days after implantation of the probe. We conclude that in situations where prolonged blood sampling is necessary, the flexible microdialysis probe provides a reliable means of accessing circulating levels of neuroactive compounds, nutrients, metabolites, and drugs.

scholarly journals Suppression of PKCδ/NF-κB Signaling and Apoptosis Induction through Extrinsic/Intrinsic Pathways Are Associated with Magnolol-Inhibited Tumor Progression in Colorectal Cancer In Vitro and In Vivo

2020 ◽  
Vol 21 (10) ◽  
pp. 3527 ◽  
Author(s):  
Chun-Min Su ◽  
Yueh-Shan Weng ◽  
Lin-Yen Kuan ◽  
Jiann-Hwa Chen ◽  
Fei-Ting Hsu
Keyword(s):  
Colorectal Cancer ◽  
Tumor Progression ◽  
Stem Bark ◽  
Treated Group ◽  
Gene Assay ◽  
Fas L ◽  
Magnolia Officinalis ◽  
Ht 29

Magnolol is one of the hydroxylated biphenyl compounds from the root and stem bark of Magnolia officinalis, which shown to possess anti-colorectal cancer (CRC) effects. However, the regulatory mechanism of magnolol on apoptosis and NF-κB signaling in human CRC has not been elucidated. Thus, we investigated the inhibitory mechanism of magnolol on human and mouse CRC (HT-29 and CT-26) in vitro and in vivo. Results from reporter gene assay indicated that both magnolol and rottlerin (PKCδ inhibitor) reduced the endogenous NF-κB activity. In addition, indolactam V (PKCδ activator)-induced NF-κB signaling was significantly suppressed with both magnolol and rottlerin treatment. Results from Western blotting also indicated that phosphorylation of PKCδ and NF-κB -related proteins involved in tumor progression were effectively decreased by magnolol treatment. The invasion capacity of CRC cells was also attenuated by both magnolol and rottlerin. Furthermore, magnolol triggered Fas/Fas-L mediated extrinsic apoptosis and mitochondria mediated intrinsic apoptosis were validated by flow cytometry. Most importantly, tumor growth in both HT-29 and CT-26 bearing mice were suppressed by magnolol, but no pathologic change was detected in mice kidney, spleen, and liver. As confirmed by immunohistochemistry (IHC) staining from tumor tissue, PKCδ/NF-κB signaling and downstream proteins expression were decreased, while apoptotic proteins expression was increased in the magnolol treated group. According to these results, we suggest that the induction of apoptosis through extrinsic/intrinsic pathways and the blockage of PKCδ/NF-κB signaling are associated with the magnolol-inhibited progression of CRC.

Mechanism of the galanin induced increase in acetylcholine release in vivo from striata of freely moving rats

1992 ◽  
Vol 589 (1) ◽  
pp. 33-38 ◽  
Author(s):  
D. Amoroso ◽  
P. Girotti ◽  
G. Fisone ◽  
T. Bartfai ◽  
S. Consolo
Keyword(s):  
Acetylcholine Release ◽  
Freely Moving Rats ◽  
Freely Moving

scholarly journals Ghrelin elicits a marked stimulatory effect on GH secretion in freely-moving rats

2000 ◽  
pp. R7-R9 ◽  
Author(s):  
LM Seoane ◽  
S Tovar ◽  
R Baldelli ◽  
E Arvat ◽  
E Ghigo ◽  
...  
Keyword(s):  
Physiological Control ◽  
Gh Secretion ◽  
Freely Moving Rats ◽  
Anaesthetized Rats ◽  
Freely Moving ◽  
The One ◽  
Plasma Gh ◽  
Different Doses

Ghrelin is a growth hormone-releasing acylated peptide from stomach. The purified peptide consist of 28 amino acids in which the serine 3 residue is n-octanoylated. Ghrelin has been reported to increase in vitro GH secretion as well as in vivo plasma GH levels in pentobarbital anaesthetized rats. The aim of this work was to characterize the stimulatory effect of Ghrelin on in vivo GH secretion in freely-moving rats. Furthermore, we compare the effect of Ghrelin with GHRH. In addition to vehicle, we administered different doses of Ghrelin (3 nmol/Kg, 12 nmol/Kg and 60 nmol/Kg); GHRH (3 nmol/Kg and 12 nmol/kg). Plasma GH levels were measured in blood samples taken at 5, 10, 15, 20, 30 and 45 min after their administration as an i.v. bolus at 0 min. Administration of Ghrelin led to an increase in plasma GH levels at all time-points tested (5, 10, 15, 20 and 30 min, P<0.01; and 45 min, P<0.05) in comparison to control untreated rats. A maximal stimulatory effect on plasma GH was observed following administration of 12 nmol/Kg of Ghrelin, the effect being similar to the one obtained with 60 nmol/Kg in terms of both AUC and mean peak GH levels. At the dose of 3 nmol/Kg GHRH and Ghrelin exhibited a similar stimulatory effect in term of both, AUC and mean peak GH levels. However following administration of a dose of 12 nmol/Kg, the effect of Ghrelin was much greater than the same dose of GHRH in terms of both AUC and mean peak GH levels. In summary, this study provides the first evidences that Ghrelin exert a marked stimulatory effect in plasma GH levels in freely-moving rats and provides further evidences that Ghrelin may play an important role in the physiological control of GH secretion.

Significance of Platelet β-Adrenoceptors for Platelet Responses In Vivo and In Vitro

1992 ◽  
Vol 68 (06) ◽  
pp. 687-693 ◽  
Author(s):  
P T Larsson ◽  
N H Wallén ◽  
A Martinsson ◽  
N Egberg ◽  
P Hjemdahl
Keyword(s):  
Ex Vivo ◽  
High Dose ◽  
Platelet Aggregability ◽  
Adrenoceptor Agonist ◽  
Dose Infusion ◽  
Von Willebrand ◽  
Willebrand Factor ◽  
Factor Antigen

SummaryThe significance of platelet β-adrenoceptors for platelet responses to adrenergic stimuli in vivo and in vitro was studied in healthy volunteers. Low dose infusion of the β-adrenoceptor agonist isoprenaline decreased platelet aggregability in vivo as measured by ex vivo filtragometry. Infusion of adrenaline, a mixed α- and β-adrenoceptor agonist, increased platelet aggregability in vivo markedly, as measured by ex vivo filtragometry and plasma β-thromboglobulin levels. Adrenaline levels were 3–4 nM in venous plasma during infusion. Both adrenaline and high dose isoprenaline elevated plasma von Willebrand factor antigen levels β-Blockade by propranolol did not alter our measures of platelet aggregability at rest or during adrenaline infusions, but inhibited adrenaline-induced increases in vWf:ag. In a model using filtragometry to assess platelet aggregability in whole blood in vitro, propranolol enhanced the proaggregatory actions of 5 nM, but not of 10 nM adrenaline. The present data suggest that β-adrenoceptor stimulation can inhibit platelet function in vivo but that effects of adrenaline at high physiological concentrations are dominated by an α-adrenoceptor mediated proaggregatory action.

Sign in / Sign up

Export Citation Format

Share Document