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Adenosine triphosphate and diadenosine pentaphosphate induce [Ca 2+ ] i increase in rat basal ganglia aminergic terminals
Author(s) -
Giraldez Lisandro,
DíazHernández Miguel,
GómezVillafuertes Rosa,
Pintor Jesus,
Castro Enrique,
MirasPortugal M. Teresa
Publication year - 2001
Publication title -
journal of neuroscience research
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.72
H-Index - 160
eISSN - 1097-4547
pISSN - 0360-4012
DOI - 10.1002/jnr.1063
Subject(s) - ionotropic effect , biology , receptor , basal ganglia , purinergic receptor , medicine , endocrinology , biochemistry , glutamate receptor , central nervous system
Synaptosomal preparations from rat midbrain exhibit specific responses to both ATP and Ap 5 A, which stimulate a [Ca 2+ ] i increase in the presynaptic terminals via specific ionotropic receptors, termed P2X , and diadenosine polyphosphate receptors. Aminergic terminals from rat brain basal ganglia were characterized by immunocolocalization of synaptophysin and the vesicular monoamine transporter VMAT2 and represent 29% of the total. These aminergic terminals respond to ATP and/or Ap 5 A with an increase in the intrasynaptosomal calcium concentration as measured by a microfluorimetric technique. This technique, which allows single synaptic terminals to be studied, showed that roughly 8.2% ± 1.6% of the aminergic terminals respond to ATP, 16.9% ± 1.3% respond to Ap 5 A, 32.6% ± 0.8% to both, and 42.3% ± 1.5% of them have no response. Immunological studies performed with antibodies against ionotropic ATP receptor subunits showed positive labelling with anti‐P2X 3 antibodies in 39% of the terminals. However, colocalization studies of VMAT and P2X 3 receptor subunit indicate that only 25% of the aminergic terminals also contain this receptor subtype. These results demonstrate that the aminergic terminals from the rat brain basal ganglia are to a large extent under the modulation of presynaptic nucleotide and dinucleotide receptors. J. Neurosci. Res. 64:174–182, 2001. © 2001 Wiley‐Liss, Inc.