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The Journal of Neuroscience, January 15, 2002, 22(2):377-388
Modulatory Mechanism of the Endogenous Peptide Catestatin on
Neuronal Nicotinic Acetylcholine Receptors and Exocytosis
Carlos J.
Herrero1,
Eva
Alés1,
Antonio J.
Pintado1,
Manuela G.
López1,
Esther
García-Palomero1,
Sushil K.
Mahata2,
Daniel T.
O'Connor2,
Antonio G.
García1, and
Carmen
Montiel1
1 Departamento de Farmacología and Instituto
Teófilo Hernando, Facultad de Medicina, Universidad
Autónoma de Madrid, 28029 Madrid, Spain, and
2 Department of Medicine and Center for Molecular Genetics,
University of California at San Diego, San Diego, California 92161
The catestatin fragment of chromogranin A is the first known
endogenous compound able to inhibit catecholamine release elicited by
the activation of neuronal nicotinic acetylcholine receptors (nAChRs)
of different animal species and catecholaminergic cell types. However,
how catestatin regulates the receptor activity, which subunit
combination of the heteropentameric forms of receptor is better blocked
by the peptide, or how it affects the different stages of the
exocytotic process have not yet been evaluated. To address these
questions, we have assayed the effects of catestatin: (first) on the
inward currents elicited by ACh
(IACh) in voltage-clamped oocytes
expressing different combinations of nAChR subunits; and (second) on
the cytosolic Ca2+ concentration,
[Ca2+]c, and quantal release of
catecholamines simultaneously monitored in single adrenal chromaffin
cells stimulated with ACh. Catestatin potently blocks all the subtypes
of nAChRs studied. Furthermore, it inhibits the
 3 4 current in a reversible,
noncompetitive, voltage-, and use-dependent manner, a behavior
compatible with open-channel blockade. In fura-2-loaded single
chromaffin cells, the peptide reduced the
[Ca2+]c signal and the total release
of catecholamines elicited by ACh; however, catestatin did not modify
the kinetics or the last step of the exocytotic process. Our results
suggest that catestatin might play an autocrine regulatory role in
neuroendocrine secretion through its interaction with different native
nAChR subtypes; the extent of receptor blockade by the peptide could be
acutely regulated by the intensity and duration of the presynaptic stimulus.
Key words:
catestatin; chromogranin A; 34 nAChRs; 7 nAChRs; 42 nAChRs; 32 nAChRs; exocytosis; Xenopus
oocytes; chromaffin cells
Copyright © 2002 Society for Neuroscience 0270-6474/02/222377-12$05.00/0
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