Extract of Ginkgo biloba EGb761 Facilitates Extinction of Conditioned Fear Measured by Fear-Potentiated Startle

Abstract

A standard extract of Ginkgo biloba (EGb761) has been used in the treatment of various common geriatric complaints including vertigo, short-term memory loss, hearing loss, lack of attention, or vigilance. We demonstrated that acute systemic administration of EGb761 facilitated the acquisition of conditioned fear. Many studies suggest the neural mechanism underlies extinction is similar to the acquisition. This raises a possibility that EGb761 may modulate and accelerate the fear extinction process. We tested this possibility by using fearpotentiated startle (FPS) on laboratory rats. Acute systemic injection of EGb761 (10, 20, or 50 mg/kg) 30 min before extinction training facilitated extinction in a dose-dependent manner. Intra-amygdaloid infusion of EGb761 (28 ng/side, bilaterally) 10 min before extinction training also facilitated extinction. Control experiments showed that facilitation effect of EGb761 was not the result of impaired expression of conditioned fear or accelerated forgetting. Rats previously injected with EGb761 showed significant FPS after retraining. Extinction of conditioned fear appeared to result from acute drug effects rather than from toxic action. Systemic administration of EGb761 immediately after extinction training did not facilitate extinction, suggested the EGb761 facilitation effect is contributed to the acquisition phase of extinction learning. Western blot results showed that extinction induced amygdaloid extracellular signal-regulated kinase (ERK1/2) phosphorylation was significantly elevated by EGb761 treatment. Intra-amygdala injection of ERK1/2 inhibitor PD98059 completely blocked the EGb761 effect. Therefore, acute EGb761 administration modulated extinction of conditioned fear by activating ERK1/2.

Intra-amygdaloid infusion of Ginkgo biloba leaf extract (EGb761) facilitates fear-potentiated startle in rats

“…We found that EGb761 can enhance fear memory formation rather than serve as an anti-stress buffer . In addition, we also demonstrated that either systemic or intra-amygdaloid administration of EGb761 facilitate conditioned fear extinction in a dose-dependent manner (Yang et al 2007b).…”

“…2a). The doses of EGb761 chosen were based on our previous studies (Yang et al 2007b). ACSF and EGb761 were infused into the BLA 10 min prior to fear conditioning.…”

Chemokine receptor CCR2 contributes to neuropathic pain and the associated depression via increasing NR2B-mediated currents in both D1 and D2 dopamine receptor-containing medium spiny neurons in the nucleus accumbens shell

“…To check if ERK is involved in SNL-induced NR2B phosphorylation, MEK inhibitor PD98059 (0.1 μg each site) [44] was injected into bilateral NAc shell at day 7 after SNL. pNR2B expression was significantly reduced by PD98059 1 h after injection (Fig.…”

Optimal duration of therapy in the recovery period of vestibular diseases

“…Более суще-ственное снижение балла по эмоциональной шкале не было статистически достоверным, однако выявленная тенденция может свидетельствовать о влиянии танакана на эмоцио-нальное состояние пациентов с головокружением. Посколь-ку предположение о способности EGb 761 уменьшать трево-гу выдвигалось и в других исследованиях, как клинических, так и экспериментальных [18,19], целесообразны дальней-шие исследования, оценивающие способность танакана улучшать эмоциональное состояние пациентов, страдающих острыми и хроническими вестибулярными расстройствами. Возможный анксиолитический эффект танакана может быть очень важен в лечении таких пациентов, поскольку тес-ная взаимосвязь вестибулярных нарушений с эмоциональ-ными расстройствами хорошо известна [20][21][22].…”