Posted by Larry Hoover on July 31, 2004, at 11:57:56
In reply to Re: good to know, posted by SLS on July 31, 2004, at 11:37:45
> People often forget about those cute little glial cells. They only outnumber neurons by a factor of 9 to 1! Now, I understand that they are capable of not only modulating the excitability of neurons, but also of sending each other messages using calcium and ATP. Just when you think you've got it all figured out...
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> - ScottYa, glial cells are the worker bees of the brain.
Also, there's more to ginkgo than that, vis a vis stress and mood.
Cell Mol Biol (Noisy-le-grand). 2002 Sep;48(6):633-9.
Use of ginkgolide B and a ginkgolide-activated response element to control gene transcription: example of the adrenocortical peripheral-type benzodiazepine receptor.
Amri H, Drieu K, Papadopoulos V.
Department of Cell Biology, Georgetown University Medical Center, Washington, DC, USA.
Identification of the molecular switch controlling glucocorticoid synthesis might facilitate the development of pharmacological tools to control circulating cortisol levels. The transport of cholesterol from intracellular sources to the inner mitochondrial membrane represents the rate-determining step in the cascade of reactions leading to cortisol synthesis. A key element in this step is the peripheral-type benzodiazepine receptor (PBR). Several studies have indicated the beneficial effects of Ginkgo biloba on memory and stress control. Using pharmacological, biochemical and proteomic methods, we demonstrated that the standardized Ginkgo biloba extract EGb 761 and its isolated component ginkgolide B (GKB) inhibit PBR ligand binding and protein expression, resulting in decreased serum corticosterone levels. We further demonstrated that EGb 761- and GKB-induced inhibition of PBR protein is preceded by a decrease in mRNA-levels due to transcriptional suppression of PBR gene expression. Further studies indicated that the action of GKB is mediated by a transcription factor binding to the PBR gene promoter, thereby regulating PBR gene expression. These data indicate that EGb 761-induced inhibition of glucocorticoid production is due to specific transcriptional suppression of the adrenal PBR gene by GKB, and suggest that EGb 761 and GKB might serve as pharmacological tools to control excess glucocorticoid
formation.
Int Immunopharmacol. 2003 Jan;3(1):75-80.Effect of Ginkgo biloba extract, EGb 761, on the cellular immune response in a hypothalamic-pituitary-adrenal axis activation model in the rat.
Puebla-Perez AM, Lozoya X, Villasenor-Garcia MM.
Laboratorio de Inmunofarmacologia de Productos Naturales, Centro de Investigacion Biomedica de Occidente, Mexico. ampuebla@cencar.udg.mx
We evaluated the effects of Ginkgo biloba extract (EGb 761) on the cellular immune response of rats with immunosuppression induced by activation of the hypothalamic-pituitary-adrenal (HPA) axis. Groups of five rats were subjected to chronic stress by the application of daily electric shocks (ES) over 7 days. This stress produced a significant decrement in the delayed-type hypersensitivity response (DTH) to dinitrofluorobenzene (DNFB), and a decrease in the proliferation index of splenocytes. Treatment with oral doses of the phytopharmaceutical EGb 761 (100 mg/kg per day over 7 days) restored both the DTH response to DNFB and the proliferation index. EGb 761 has stress-alleviating properties through its moderation of corticosterone levels. It also possesses antioxidant activity that may contribute to its effects on the immune response. Our observations indicate that the phytopharmaceutical EGb 761 possesses immunostimulatory properties.
poster:Larry Hoover
thread:372598
URL: http://www.dr-bob.org/babble/alter/20040718/msgs/372630.html