Polychlorocycloalkane insecticide-induced convulsions in mice in relation to disruption of the GABA-regulated chloride ionophore☆
References (15)
- et al.
Life Sci.
(1984) - et al.
Pestic. Biochem. Physiol.
(1985) - et al.
Comp. Biochem. Physiol.
(1982) - et al.
Biochem. Biophys. Res. Commun.
(1985) - et al.
Neuroscience Lett.
(1983) - et al.
Neuropharmacol.
(1984) - et al.
Life Sci.
(1984)
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2020, NeuroToxicologyCitation Excerpt :The basis for the high in vivo seizurogenic potency of TETS is not understood. TETS is markedly more potent than PTZ, but not substantially more potent than PTX, in displacing the GABAAR ligand [35S]t-butylbicyclophosphorothionate in rat brain membranes (Cole and Casida, 1986; Esser et al., 1991; Ratra et al., 2001; Squires et al., 1984). TETS and picrotoxin are similarly potent in inhibiting GABAAR-mediated GABA-activated chloride ion uptake by membrane vesicles from rat cerebral cortex (Obata et al., 1988).
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2015, Handbook of Clinical NeurologyCitation Excerpt :GABAA receptors are members of the superfamily of ligand-gated ion channels that contain a chloride ionophore; by binding to these receptors, endogenous GABA causes the opening of chloride channels resulting in hyperpolarization of the membrane. Lindane and cyclodienes bind to a specific site (the picrotoxin site) on the chloride channel, thereby blocking its opening and thus antagonizing the “inhibitory” action of GABA (Cole and Casida, 1986; Eldefrawi and Eldefrawi, 1987; Narahashi et al., 2007). Treatment of acute poisoning is symptomatic; phenobarbital and diazepam can be used as anticonvulsants.
The environmental pollutant endosulfan disrupts cerebral cortical function at low doses
2011, NeuroToxicologyCitation Excerpt :In addition, a wide array of molecular targets of this insecticide have been discovered in the endocrine (Wozniak et al., 2005) and immunological systems (Aggarwal et al., 2008). The mechanism of neurotoxicity of endosulfan appears to be dominated by its capacity to inhibit non-competitively the GABA-A type of receptors (Cole and Casida, 1986; Chen et al., 2006) although other targets are believed to exist (Sunol et al., 2008; Paul et al., 1994; Vale et al., 2003). GABA-A receptors are pentameric proteins formed by various combinations of 19 receptor subunits in mammals, each attributed to a different gene (Simon et al., 2004).
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This research was supported in part by NIH grant P01 ES00049.