scholarly journals Up-regulation of L-Type Ca2+ Channel Associated with the Development of Elevated K+-Mediated Survival of Superior Cervical Ganglion Cells in Vitro

1995 ◽  
Vol 168 (1) ◽  
pp. 166-178 ◽  
Author(s):  
Shuuitsu Tanaka ◽  
Tatsuro Koike
Keyword(s):  
Superior Cervical Ganglion ◽  
Ganglion Cells ◽  
Cervical Ganglion

scholarly journals Nerve Fibers Containing Neuropeptide Y in the Cerebrovascular Bed: Immunocytochemistry, Radioimmunoassay, and Vasomotor Effects

1987 ◽  
Vol 7 (1) ◽  
pp. 45-57 ◽  
Author(s):  
L. Edvinsson ◽  
J. R. Copeland ◽  
P. C. Emson ◽  
J. McCulloch ◽  
R. Uddman
Keyword(s):  
Neuropeptide Y ◽  
Blood Vessels ◽  
Superior Cervical Ganglion ◽  
Cerebral Arteries ◽  
Nerve Fibers ◽  
Calcium Entry Blocker ◽  
Cervical Ganglion ◽  
Prostaglandin F ◽  
6 Hydroxydopamine

Perivascular nerve fibers containing neuropeptide Y (NPY)-like immunoreactivity were identified around cerebral blood vessels of human, cat, guinea pig, rat, and mouse. The major cerebral arteries were invested by dense plexuses; veins, small arteries, and arterioles were accompanied by few fibers. Removal of the superior cervical ganglion resulted in a reduction of NPY-like material in pial vessels and dura mater. Pretreatment with 6-hydroxydopamine or reserpine reduced the number of visible NPY fibers and the concentration of NPY in rat cerebral vessels. Sequential immuno-staining with antibodies toward dopamine-β-hydroxylase (DBH) (an enzyme involved in the synthesis of noradrenaline) and NPY revealed an identical localization of DBH and NPY in nerve cell bodies in the superior cervical ganglion and in perivascular fibers of pial blood vessels, suggesting their coexistence. Administration of NPY in vitro resulted in concentration-dependent contractions that were not modified by a sympathectomy. The contractions induced by noradrenaline, 5-hydroxytryptamine, and prostaglandin F2α and the dilator responses to calcitonin gene-related peptide were not modified by NPY in rat cerebral arteries. However, the constrictor response to NPY was reduced by 70% in the presence of the calcium entry blocker nifedipine, and abolished following incubation in a calcium-free buffer. These data suggest an interaction of NPY at a postsynaptic site, which for induction of contraction may open calcium channels in the sarcolemma of cerebral arteries.

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