Abstract
The recent introduction of powerful neuroanatomical techniques combined with extracellular recordings of neurones in the basal ganglia of normal animals and experimental models of basal ganglia diseases, have led to the construction of models that specify the hodology, chemistry and relative activity of the interconnected structures in the basal ganglia-thalamocortical circuits (see Albin et al., 1989; Alexander and Crutcher, 1990; DeLong, 1990 for reviews). According to these models, the information flow is transmitted along a “direct” and an “indirect” routes to the output structures of the basal ganglia, i.e. the internal segment of the globus pallidus (GPi) and the substantia nigra pars reticulata (SNr). The “direct” pathway arises largely from the GABA/substance P spiny neurones in the striatum that send an inhibitory projection to GPi and SNr. On the other hand, the “indirect” pathway arises from the GABA/enkephalin spiny neurones in the striatum that send an inhibitory projection to the external pallidum (GPe). The latter gives rise to a GABAergic input to the subthalamic nucleus which in turn sends a glutamatergic excitatory projection to GPe, GPi and SNr. Then, the pallidal and nigral output cells send the information to the thalamocortical neurones in the ventrolateral nucleus of the thalamus and to the tegmental pedunculopontine nucleus. A series of recent anatomical findings suggest that the inhibitory output from the GPe reaches the output structures of the basal ganglia, not only via the intercalated subthalamic nucleus, but also directly (Kitai and Kita, 1987b; Staines, 1988; Smith et al., 1988; Hazrati et al., 1990; Kincaid et al., 1990; Bolam and Smith, 1992; Smith et al., 1992). Furthermore, ultrastructural findings obtained in rodents suggest that the terminals from the globus pallidus (homologue of GPe in primates) occupy a strategic position on the perikaryon and the proximal dendrites of neurones in the entopeduncular nucleus (homologue of GPi in primates) and the SNr (Smith and Bolam, 1990, 1991; Bolam and Smith, 1992). However, because they were thought to exert a minor influence over the activity in GPi and SNr, the GPe-GPi and GPe-SNr projections were not included in the scheme of the basal ganglia circuitry described above (Albin et al., 1989; Alexander and Crutcher, 1990; DeLong, 1990).
Published Version
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