“…These striatal neurons are primarily GABAergic but other neuropeptides and neurotransmitters such as dynorphin, substance P, neurotensin, CCK (cholecystokinin), and NMDA (N-methyl D-aspartate, a glutamate receptor), and opioid receptors may also contribute to the development of TD (Hyde et al, 2005;Margolese et al, 2005). We discuss two hypotheses, the dopamine supersensitivity hypothesis, including the related D2 binding affinity theory, because they explain at least some of the characteristics of TD, and the neurotoxicity theory which hypothesis is also linked to movement disorders found in neurology.…”