Читать книгу Current Concepts in Movement Disorder Management - Группа авторов - Страница 34

It is likely that other structures and feedback loops, such as those involving the centromedian nucleus (CM) contribute to the abnormalities of discharge that are found in the basal ganglia output nuclei. Thus, the CM-striatal projection is known to degenerate in PD patients and in experimental animals, along with a loss of glutamatergic terminals in the striatum (discussed in ref. [8]). Structural changes in other glutamatergic systems are also prominent, including a loss of corticostriatal projections, and a loss of glutamatergic inputs to the STN [9]. Some of these changes are also seen in animals with lesions of the dopaminergic nigrostriatal tract, suggesting that they arise as a consequence of dopamine loss in the basal ganglia, or because of circuit dysfunction which may trigger secondary changes in glutamatergic synapses.

Another area of significant interest in recent times has been the PPN. This nucleus is a heterogeneous entity, consisting of cholinergic and non-cholinergic components, with multiple interactions with the basal ganglia. It is believed that reduced or abnormal PPN activity, specifically its non-cholinergic neurons, contributes to akinesia and gait problems in PD (e.g., ref. [10]).