Evolution from Darss Hypothesis to Multineuronal Associations with TD

Eventually the DARSS hypothesis was recognized as being too simplistic, and a multineuronal association was invoked to explain the underlying basis of TD (Casey 1987; Jeste and Caligiuri 1993; Waddington 1990; Gunne and Haggstron 1983; Kostrzewa 1995; Gong et al. 1992; Knable et al. 1994; Egan et al. 1995). Cholinergic (Rupniak et al. 1983, 1985; Salamone et al. 1990), ^aminobutyric acid (GABA)-ergic (Mithani et al. 1987; Tamminga et al. 1979; Lloyd et al. 1985; Gunne et al. 1988), and serotoninergic systems (Gong et al. 1992; Gong and Kostrzewa 1992) appeared to also be involved in the production of orofacial dyskinesia. Nevertheless, DA systems were still recognized as crucial in the development of TD. Most intriguing was a finding by Gunne et al that neuroleptic-evoked VCMs in rats were enhanced after partial damage to the frontal cortex (Gunne et al. 1982).

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