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  • 1
    Electronic Resource
    Electronic Resource
    Springer
    Experimental brain research 9 (1969), S. 63-72 
    ISSN: 1432-1106
    Keywords: Noradrenaline and 5-hydroxytryptamine nerve terminals ; Cortex cerebelli ; Rat
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary The monoamine innervation of the cerebellum of the rat has been studied by both in vivo and in vitro techniques using the histochernical fluorescence method for the demonstration of catecholamines (CA) and certain tryptamines. By way of a pharmacological approach using inter alia protriptyline, which acts mainly by blocking the membrane pump of the noradrenaline (NA) neurons, evidence was obtained that CA nerve terminals in the cerebellum mainly represent NA nerve terminals. These were found to innervate practically all parts of the cerebellar cortex with a patchy innervation pattern and with an innervation of especially the anterior and posterior lobes. The terminals mainly seem to make axodendritic contacts in the molecular and granular layers without any strict localization of the terminal plexus to any special plane of the cerebellar folia. The fibers enter the cerebellum via the inferior cerebellar peduncle and run in the white matter of the cortex cerebelli. Incubation studies with 6-hydroxytryptamine indicate that there exists also a 5-hydroxytryptamine (5-HT) innervation of the cortex cerebelli, although not as pronounced as the NA innervation. The 5-HT nerve terminals are very fine, varicose fibers and innervate mainly the molecular layer, especially of the anterior lobe. The terminals run mainly in the transverse plane of the folium parallel to the surface. Thus, the pattern of innervation of these 5-HT afferents is different from that of the NA nerve terminals. In the uvula, structures which may represent the “rosettes” of the mossy fibers or golgi axon terminals in the granular layer take up and accumulate monoamines after incubation with amine in vitro. The exact nature of these structures remains to be elucidated.The cerebellar nuclei receive a very low to low degree of innervation of NA and 5-HT nerve terminals.
    Type of Medium: Electronic Resource
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  • 2
    ISSN: 1432-1106
    Keywords: In vivo microdialysis ; Astrocytic reaction ; Gliosis ; Brain lesion ; Rat
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract In vivo microdialysis is an established tool for sampling extracellular fluid compartments. However, microdialysis faces the problem that the implantation of the probe damages the microenvironment from which measurements are derived. In this study, we examined the expression of basic fibroblast growth factor mRNA and protein at the cellular level after implantation of a microdialysis probe into the dorsal hippocampus and found that 8 h after inserting the probe bFGF mRNA was markedly increased in a relatively large area centered around the probe, involving both the dorsal hippocampus and the overlying cerebral cortex, as revealed by radioactive in situ hybridization. Using nonradioactive in situ hybridization with digoxigenin-labelled riboprobes, combined with immunohistochemistry for glial fibrillary acidic protein we demonstrated that bFGF mRNA was exclusively increased in astrocytes at the probe insertion site. Using immunohistochemistry we also found that bFGF-like immunoreactivity was increased after implantation of the probe close to the lesion site, as shown by an increased number of bFGF immunoreactive nuclear glial profiles. These results provide evidence that the implantation of a microdialysis probe into the brain induces activation of bFGF gene expression in astrocytes associated with nuclear bFGF-like immunoreactivity. We conclude that lesion-induced effects have to be considered when evaluating microdialysis data, and that mechanical trauma to the brain will activate astroglial trophism, as seen from the increased density of astroglial profiles demonstrating bFGF mRNA and protein levels.
    Type of Medium: Electronic Resource
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  • 3
    ISSN: 1432-2072
    Keywords: Adenosine A2 receptor ; Dopamine D2 receptor ; Methylxanthine ; Tardive dyskinesias ; Receptor-receptor interaction ; Rat
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract Stimulation of adenosine A2 receptors (with the selective adenosine A2 agonist CGS 21680) in rat striatal membrane preparations, produces a decrease in both the affinity of D2 receptors and the transduction of the signal from the D2 receptor to the G protein. This intramembrane A2-D2 interaction might be responsible for the behavioural depressant effects of adenosine agonists and for the behavioural stimulant effects of adenosine antagonists such as caffeine and theophylline. Dopamine denervation induces an increase in the intramembrane A2-D2 interaction, which may underlie the observed higher sensitivity to the behavioural effects induced by adenosine antagonists found in these animals. The present study was designed to examine if chronic treatment with haloperidol, which also produces dopamine receptor supersensitivity, is also associated with an increase in the intramembrane A2-D2 interaction in the neostriatum and with a higher sensitivity to the behavioural effects induced by adenosine antagonists. The data showed that: (i) haloperidol pretreatment causes a higher binding of the D2 antagonist [3H] raclopride in striatal membrane preparations due to an increase in the number of D2 receptors without changes in their affinity for the antagonist (increase in Bmax without changes in kd); (ii) GCS 21680 decreases the affinity of dopamine for the D2 receptor, by increasing the equilibrium dissociation constants of high (Kh) and low affinity (K1) dopamine D2 binding sites and increases the proportion of high affinity binding sites (Rh); (iii) a low dose of CGS 21680 (3 nM), which is ineffective in membrane preparations from neostriatum of nontreated animals, is effective in membranes from the striatum of haloperidol-pretreated animals; (iv) the nonselective adenosine antagonist theophylline (20 mg/kg SC) causes a higher motor activation in rats pretreated with haloperidol. The possible relevance of these results for the pathophysiology and treatment of tardive dyskinesias is discussed.
    Type of Medium: Electronic Resource
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