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Journal of Neuroscience, Vol 14, 3628-3634, Copyright © 1994 by Society for Neuroscience
Adenosine acting at an A1 receptor decreases N-type calcium current in mouse motoneurons
M Mynlieff and KG Beam
Department of Physiology, Colorado State University, Fort Collins 80523.
The neuromodulator adenosine is known to decrease neurotransmitter release
at the neuromuscular junction by activation of an A1 adenosine receptor
coupled to a pertussis toxin-sensitive G protein. Among the mechanisms that
could contribute to the depression of neurotransmitter release is reduced
entry of calcium through channels located in the presynaptic terminal. In
the present study, we have examined the effects of adenosine on
high-voltage-activated (HVA) calcium currents in motoneurons, the
presynaptic cells of the neuromuscular junction. The motoneurons were
isolated from embryonic mice, placed in primary tissue culture for 16 hr,
and analyzed by means of the whole-cell patch- clamp technique. Adenosine
(40 microM) reduced both transient and sustained components of HVA calcium
current. This effect was blocked by the A1 antagonist
8-cyclopentyltheophylline (CPT; 100 nM) and was mimicked by the A1 agonist
N6-cyclohexyladenosine (CHA; 50 nM to 10 microM) but not by the A2a agonist
2-p-(2-carboxyethyl)phenethylamino- 5'-N-ethylcarboxamido adenosine
(CGS-21680; 1 micron). Pretreatment with pertussis toxin (200 ng/ml, >
16 hr) abolished the depression of HVA calcium current by adenosine
receptor activation. Brief (3 min) exposure of the cells to 10 microM
omega-conotoxin GVIA irreversibly blocked a part of the HVA current, which
can therefore be attributed to N-type channels; the remaining current was
unaffected by adenosine receptor activation. Hence, it appears that
adenosine decreases only the N-current portion of HVA current and that this
inhibition occurs via an A1 receptor linked to a pertussis toxin-sensitive
G protein. Other investigators have shown that N-type channels do not play
a primary role in eliciting transmitter release at the mammalian
neuromuscular junction. Thus, it is uncertain what motoneuronal functions
are influenced by adenosine modulation of N-type channels.
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