Fuxe K, Von Euler G, Agnati L F, Merlo Pich E, O'Connor W T, Tanganelli S, Li X M, Tinner B, Cintra A, Carani C
Department of Histology and Neurobiology, Karolinska Institutet, Stockholm, Sweden.
Ann N Y Acad Sci. 1992;668:186-204. doi: 10.1111/j.1749-6632.1992.tb27350.x.
Evidence has been presented that behavioral actions of NT, inducing its neuroleptic-like action, can be explained on the basis of NT-D2 intramembrane receptor-receptor interactions in the basal ganglia, unrelated to the coexistence phenomenon, leading to reduced affinity and transduction of the D2 agonist binding site. By reducing selectively D2 receptor transduction at the pre- and postsynaptic level, the NT receptor appears capable of switching the DA synapses towards a D1 receptor-mediated transduction, illustrating how receptor-receptor interactions can increase the functional plasticity of central synapses (FIG. 12).
已有证据表明，神经降压素（NT）的行为作用，即诱导其类抗精神病药物作用，可基于基底神经节中NT-D2膜内受体-受体相互作用来解释，这与共存现象无关，会导致D2激动剂结合位点的亲和力和转导降低。通过在突触前和突触后水平选择性降低D2受体转导，NT受体似乎能够将多巴胺（DA）突触转向由D1受体介导的转导，这说明了受体-受体相互作用如何能够增加中枢突触的功能可塑性（图12）。
