Immunocytochemical studies of substance P and met-enkephalin in the basal ganglia and substantia nigra in Hungtingtonʼs, Parkinsonʼs and Alzheimerʼs disease

Differential loss of striatal projection systems in Huntington’s disease: a quantitative immunohistochemical study

“…Other RIA studies of HD brain have, however, not reported greater preservation of SP in GPi than ENK in GPe (Emson et al, 1980;Storey and Beal, 1993). The present findings on SP and ENK loss from pallidum of HD victims are also in apparent conflict with some prior immunohistochemical studies (Marshall et al, 1983;Grafe et al, 1985;Zech and Bogerts, 1985), which reported equal loss of striatal projection systems. The discrepancy between studies that did not and those that did find greater preservation of SP in GPi than ENK in GPe may, in large part, be explained by the fact that they were carried out prior to the Vonsattel et al (1985) neuropathological grading system for HD.…”

“…Our finding that the SP+ striatal projection to substantia nigra is progressively lost beginning early in HD, culminating with extensive loss by late HD, is consistent with prior immunohistochemical findings (Marshall et al, 1983;Grafe et al, 1985;Zech and Bogerts, 1985;Reiner et al, 1988;Albin et al, 1990aAlbin et al, , 1990bAlbin et al, , 1992. Earlier biochemical studies of SP, dynorphin, GABA, or GAD also indicated that striatal input to nigra is severely depleted in HD (Gale et al, 1977;Kanazawa et al, 1977Kanazawa et al, , 1979Emson et al, 1980;Spokes, 1980;Spokes et al, 1980;Buck et al, 1981), as have more recent ones (Seizinger et al, 1986;Ellison et al, 1987;Beal et al, 1988;Storey and Beal, 1993).…”

“…Other studies, however, have reported no difference in the relative loss of immunoreactivity for SP and ENK in striatal terminals in GPe and GPi, as detected by immunohistochemistry (Marshall et al, 1983;Zech and Bogerts, 1985;Ferrante et al, 1990) or radioimmunoassay (Storey and Beal, 1993), while yet others have reported a more marked loss of SP than ENK (Grafe et al, 1985;Emson et al, 1980). Biochemical studies of GABA and its synthesizing enzyme, glutamic acid decarboxylase (GAD), have also been used to characterize projection neuron loss in HD (Spokes, 1980;Spokes et al, 1979;Reynolds and Pearson, 1990;Storey and Beal, 1993).…”

Bilateral 6‐Hydroxydopamine‐induced Lesion of the Nigrostriatal Dopamine Pathway Reproduces the Effects of Unilateral Lesion on Substance P but not on Enkephalin Expression in Rat Basal Ganglia

“…In contrast to the consistent results obtained in the hemiparkinsonian rat model concerning enkephalin and substance P expression, the available data from idiopathic parkinsonism in this regard are contradictory. Indeed, different studies report unchanged or decreased concentrations and immunoreactivity of substance P and enkephalin in the striatum and its targets (Taquet et al, 1983;Llorens-Cortes et al, 1984;Grafe et al, 1985;Fernandez et al, 1992); in addition, recent in situ hybridization studies show no change in substance P mRNA expression but increased or unchanged enkephalin mRNA expression (Levy et al, 1995, Nisbet et al, 1995. Previous studies have investigated the possible interference of the pharmacological dopamine replacement therapies used in Parkinson's disease with the responses to dopamine denervation in the hemiparkinsonian rat model and MPTP-treated primates.…”

Caffeine as a psychomotor stimulant: mechanism of action

“…In contrast, the expression of mRNA for preproenkephalin, a selective marker for striato-Gpe neurons [65], is increased in Parkinsonian patients [143,144], as well as in experimental animals treated with 6-hydroxydopamine (6-OHDA) [145] or 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) [146], two toxins that cause a selective disruption of dopaminergic transmission. These changes in the activity of striatal projection pathways are thought to result in the motor dysfunctions typical of Parkinson's disease [65].…”