Presumed DA Receptor Supersensitivity in TD

From the 1970s DA receptor supersensitivity (DARSS) had been invoked as the underlying neural basis for development of TD (Klawans 1973; Chiu et al. 1981).

Because acute or long-term D2 antagonist treatment produced orofacial dyskinesias, and because D1 agonists acutely had that effect in rats, it was reasonable to conclude that VCMs and TD might be the product of endogenous DA acting at supersensitized DA D1 receptors (Waddington 1990; Kostrzewa 1995). However, as we later showed, a DA D1 receptor antagonist failed to attenuate spontaneous orofacial dyskinesias in rodents being treated for 1 year with a D2 receptor antagonist (Kostrzewa et al. 2007).

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