Calbindin‐D_28K in the basal ganglia of patients with parkinsonism

Abstract

An immunohistochemical study was carried out to investigate the topographic distribution of calbindin-D28k in the human basal ganglia and substantia nigra and its alterations in patients with idiopathic Parkinson's disease (PD), parkinsonism-dementia complex on Guam, progressive supranuclear palsy, and striatonigral degeneration. In normal control subjects, calbindin-D28k immunoreactivity was identified in the medium-sized neurons and neuropil of the matrix compartment of the striatum, the woolly fiber arrangements of the globus pallidus, and the fiber structures of the pars reticulata of the substantia nigra. Calbindin-D28k expression in the basal ganglia of patients with PD and parkinsonism-dementia on Guam was not different from that of control subjects, suggesting that the matrical output pathway is spared in these disorders. In contrast, its disruption is inferred from the observed disorganization of woolly fibers in the globus pallidus of patients with progressive supranuclear palsy and the reduced calbindin-D28k reactivity in the putaminal matrix and the pars reticulata of the substantia nigra of subjects with striatal degeneration. Thus, our results indicate that calbindin-D28k is a useful marker for the projection system from the matrix compartment and that its expression is modified in patients with progressive supranuclear palsy and striatal degeneration.

Neurochemical architecture of the human striatum

“…A ventral-to-dorsal gradient of intensity of calbindin immunostaining in the striatum has been described in monkeys, cats, rats, and humans Ito et al, 1992;De Las Heras et al, 1994;Francois et al, 1994). A similar ventral-to-dorsal gradient in immunostaining intensity has been described for SP and enkephalin immunoreactivities in the human striatum (Graybiel and Ragsdale, 1983;Ito et al, 1992;Kowall et al, 1993).…”

“…Ito et al (1992) found that calbindin and enkephalin immunoreactivities have similar distribution patterns in the ventral striatum of the human. Hurd and Herkenham (1995) found that AChE-poor zones corresponded to mu opiate receptor-rich zones in much of the human striatum but not in the nucleus accumbens.…”

Calcium, Bioenergetics, and Neuronal Vulnerability in Parkinson's Disease

“…However, there are reasons to doubt whether this type of cellular stress alone is responsible for PD pathology. For example, there is considerable regional variability in the vulnerability of DA neurons in PD, with some DA neurons in the brain being devoid of pathology (19,(21)(22)(23)(24). Moreover, many of the neurons showing signs of pathology in PD do not use DA as a transmitter (e.g.…”

Physiological Phenotype and Vulnerability in Parkinson's Disease

“…However, there are reasons to doubt whether this type of cellular stress alone is responsible for the loss of DA neurons in PD. For example, there is considerable regional variability in the vulnerability of DA neurons in PD, with some areas being devoid of pathological markers (Matzuk and Saper 1985;Kish et al 1988;Saper et al 1991;Ito et al 1992;Damier et al 1999). Moreover, Ldopa administration (which relieves symptoms by elevating DA levels in PD patients) does not accelerate disease progression (Fahn 2005), suggesting that DA itself is not a significant source of reactive oxidative stress, at least in the short term.…”