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Ca 2+ changes induced by different presynaptic nicotinic receptors in separate populations of individual striatal nerve terminals
Author(s) -
Nayak Sanjay V.,
Dougherty John J.,
McIntosh J. Michael,
Nichols Robert A.
Publication year - 2001
Publication title -
journal of neurochemistry
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.75
H-Index - 229
eISSN - 1471-4159
pISSN - 0022-3042
DOI - 10.1046/j.1471-4159.2001.00197.x
Subject(s) - nicotinic agonist , mecamylamine , nicotinic antagonist , alpha 4 beta 2 nicotinic receptor , chemistry , receptor , acetylcholine receptor , ganglion type nicotinic receptor , synaptosome , agonist , biophysics , nicotinic acetylcholine receptor , neuroscience , endocrinology , biology , biochemistry , central nervous system
Presynaptic nicotinic acetylcholine receptors likely play a modulatory role in the nerve terminal. Using laser‐scanning confocal microscopy, we have characterized physiological responses obtained on activation of presynaptic nicotinic receptors by measuring calcium changes in individual nerve terminals (synaptosomes) isolated from the rat corpus striatum. Nicotine (500 n m ) induced Ca 2+ changes in a subset (10–25%) of synaptosomes. The Ca 2+ responses were dependent on extracellular Ca 2+ and desensitized very slowly (several minutes) on prolonged exposure to agonist. The nicotine‐induced Ca 2+ responses were dose‐dependent and were completely blocked by dihydro‐β‐erythroidine (5 µ m ), differentially affected by mecamylamine (10 µ m ) and α‐conotoxin MII (100 n m ), and not affected by α‐bungarotoxin (500 n m ). Immunocytochemical studies using well‐characterized monoclonal antibodies revealed the presence of the α4 and α3/α5 nicotinic subunits. The nicotine‐induced responses were unaffected by prior depolarization or by a mixture of Ca 2+ channel toxins including ω‐conotoxin MVIIC (500 n m ), ω‐conotoxin GVIA (500 n m ) and agatoxin TK (200 n m ). Our results indicate that nicotinic receptors present on striatal nerve terminals induce Ca 2+ entry largely without involving voltage‐gated Ca 2+ channels, most likely by direct permeation via the receptor channel itself. In addition, at least two subpopulations of presynaptic nicotinic receptors reside on separate terminals in the striatum, suggesting distinct modulatory roles.