Effects of repeated treatments with an extract of Ginkgo biloba (EGb 761) on cerebral glucose utilization in the rat: an autoradiographic study

• Published in: General pharmacology 1995-10, Vol.26 (6), p.1375-1383
• Main Authors: Duverger, Danielle, Defeudis, Francis V., Drieu, Katy
• Format: Article
• Language: English
• Subjects: 2-deoxy- d[1- 14C]glucose; Administration, Oral; Animals; Autoradiography; Blood Pressure - drug effects; Body Weight - drug effects; Cerebral Cortex - drug effects; cerebral glucose utilization; Free Radical Scavengers - pharmacology; Ginkgo biloba; Ginkgo biloba extract (EGb 761); Glucose - metabolism; Male; Plant Extracts - pharmacology; rat; Rats; Rats, Sprague-Dawley; somatosensory processing; Time Factors; vestibular mechanisms
• ISSN: 0306-3623; 1879-0011
• DOI: 10.1016/0306-3623(94)00309-B

1. l. The autoradiographic method based on 2-deoxy- d[1- 14C]glucose ([ 14C]DG) was used to determine glucose utilization in 49 discrete structures of rat brain under control conditions and after the animals had received repeated treatment with an extract of Ginkgo biloba (EGb 761). 2. 2. Oral administration of EGb 761 (50 or 150 mg/kg/day) to adult male rats for 15 days did not modify body weight, mean arterial blood pressure, the concentrations of glucose or hemoglobin in blood, blood gases or arterial pH. 3. 3. EGb 761 treatments produced only slight-to-moderate changes in glucose utilization in the various brain structures; i.e. decreases to an extent not exceeding 18.4% at the 50 mg/kg dose or 11.7% at the 150 mg/kg dose. 4. 4. Glucose utilization was significantly decreased only in the frontoparietal somatosensory cortex, nucleus accumbens, cerebellar cortex and pons and only with the 50 mg/kg dose of EGb 761. 5. 5. Although the four brain structures affected by EGb 761 treatment do not, in themselves, constitute a specific functional system of the CNS, these effects appear useful in explaining mechanisms underlying the clinical use of EGb 761 in treating problems associated with deficient somatosensory processing (e.g. impairment of “vigilance”) and vestibular mechanisms (e.g. vertiginous syndromes).