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Effects of the nootropic drug nefiracetam on the GABAA receptor-channel complex in dorsal root ganglion neurons.

Abstract：

:The effects of nefiracetam on GABA-induced chloride currents were studied with rat dorsal root ganglion neurons in primary culture using the whole-cell patch-clamp technique. The dose-response curve for GABA-induced currents was shifted by 16 microM to lower concentrations by 10 microM nefiracetam while the maximal response was reduced by 22.84 +/- 0.68%. Thus at a low concentration (10 microM) of GABA, the chloride currents were potentiated by nefiracetam in a concentration-dependent manner. With 10 microM nefiracetam, the potentiation occurred slowly and the recovery after washout was also slow. The desensitization of the GABAA receptor at high concentration (100 microM) of GABA was accelerated by nefiracetam. The recovery process of chloride currents from desensitization was not affected by nefiracetam. KT 5720 (0.56 microm), a specific protein kinase A (PKA) inhibitor, blocked the transient potentiation of GABA-activated currents by nefiracetam, but did not affect the acceleration of desensitization. Nefiracetam suppression of GABA-induced currents was also abolished by KT 5720 or the pertussis toxin. Thus, nefiracetam may inhibit Gi/G(o) proteins leading to a cascade of events that increase the intracellular cAMP level, activate the PKA system, and suppress GABA-induced currents. Nefiracetam-induced transient potentiation and acceleration of desensitization of GABA-induced currents may involve other pathways. The nefiracetam modulation of the GABAA receptor function will result in a nootropic effect on the central nervous system through modification of synaptic transmission.

journal_name

Neuropharmacology

journal_title

Neuropharmacology

authors

Huang CS,Ma JY,Marszalec W,Narahashi T

doi

10.1016/s0028-3908(96)00074-3

subject

Has Abstract

pub_date

1996-01-01 00:00:00

pages

1251-61

issue

9-10

eissn

0028-3908

issn

1873-7064

journal_volume

35

pub_type

杂志文章

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