When the d2 receptors are blocked for long periods of time they tend to up regulate. This is what causes tardive dyskinesia.
Why do the newer atypical anti psychotics cause such at a lower rate? Added tables for clarification of receptors I am referring to.
D1 35–118 Antagonist D2 3.00–106 Antagonist D2L 31–38 Antagonist D2S 21–52 Antagonist D3 7.8–91 Antagonist D4 1.6–50 Antagonist D4.2 17–102 Antagonist D4.4 21–60 Antagonist D5 74–90 Antagonist
D1 265–1,170 ND D2 0.45–3.3 Partial agonist D2L 0.34–0.74 Partial agonist D3 0.8–9.7 Partial agonist D4 44–514 Partial agonist D5 95–2,590 ND
D1 (silent antagonist) — Unknown efficiency D5 (silent antagonist) — Unknown efficiency D2 (inverse agonist) — 1.55 nM D3 (inverse agonist) — 0.74 nM