| In vitro: |
| Neuroscience Letters, 1981, 25(1):83-88. | | Anisatin, a potent GABA antagonist, isolated from Illicium anisatum.[Reference: WebLink] |
METHODS AND RESULTS:
The neuropharmacological properties of anisatin were tested on the frog spinal cord and the crude synaptic membrane from rat brain. Anisatin (10−5 M) reduced the amplitude of dorsal root potentials induced by stimulation of the adjacent dorsal root and presynaptic inhibition of the ventral root reflex. Anisatin shifted the dose-response curve for GABA-induced depolarization in the primary afferent terminal to the right and also reduced the maximum response to GABA. [3H]Muscimol binding to the crude synaptic membrane was not inhibited by anisatin.
CONCLUSIONS:
These results indicate that anisatin is a picrotoxin-like, non-competititve GABA-antagonist. | | British journal of pharmacology, 1999,127(7):1567-1576. | | Anisatin modulation of the gamma-aminobutyric acid receptor-channel in rat dorsal root ganglion neurons.[Reference: WebLink] | 1. Anisatin, a toxic, insecticidally active component of Sikimi plant, is known to act on the GABA system. In order to elucidate the mechanism of anisatin interaction with the GABA system, whole-cell and single-channel patch clamp experiments were performed with rat dorsal root ganglion neurons in primary culture.
METHODS AND RESULTS:
2. Repeated co-applications of GABA and anisatin suppressed GABA-induced whole-cell currents with an EC50 of 1.10 microM. No recovery of currents was observed after washout with anisatin-free solution. 3. However, pre-application of anisatin through the bath had no effect on GABA-induced currents. The decay phase of currents was accelerated by anisatin. These results indicate that anisatin suppression of GABA-induced currents requires opening of the channels and is use-dependent. 4. Anisatin suppression of GABA-induced currents was not voltage dependent. 5. Picrotoxinin attenuated anisatin suppression of GABA-induced currents. [3H]-EBOB binding to rat brain membranes was competitively inhibited by anisatin.
CONCLUSIONS:
These data indicated that anisatin bound to the picrotoxinin site. 6. At the single-channel level, anisatin did not alter the open time but prolonged the closed time. The burst duration was reduced and channel openings per burst were decreased indicating that anisatin decreased the probability of openings. |
|
Cell. 2018 Jan 11;172(1-2):249-261.e12. doi: 10.1016/j.cell.2017.12.019.IF=36.216(2019)
Cell Metab. 2020 Mar 3;31(3):534-548.e5. doi: 10.1016/j.cmet.2020.01.002.IF=22.415(2019)
Mol Cell. 2017 Nov 16;68(4):673-685.e6. doi: 10.1016/j.molcel.2017.10.022.IF=14.548(2019)
ACS Nano. 2018 Apr 24;12(4): 3385-3396. doi: 10.1021/acsnano.7b08969.IF=13.903(2019)
Nature Plants. 2016 Dec 22;3: 16206. doi: 10.1038/nplants.2016.205.IF=13.297(2019)
Sci Adv. 2018 Oct 24;4(10): eaat6994. doi: 10.1126/sciadv.aat6994.IF=12.804(2019)
