Fig. 3.

Hypothetical schema for estrogenic influences on compensatory mechanisms in striatal terminals of surviving neurons in the damaged nigrostriatal dopaminergic system. (A) As indicated by the arrows, in females, but not in males, estradiol (E2) enhances dopamine synthesis, release and turnover, whilst suppressing DAT levels and re-uptake of the neurotransmitter from the synaptic cleft. (B) This preserves striatal function when lesion size is small/moderate (⩽50%), but fails to do so as lesions increase, allowing motor symptoms to become manifest. This action of E2 in females may render them more able to delay progression, or even onset, of disease.