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Next Article 
Volume 17, Number 12,
Issue of June 15, 1997
pp. 4509-4516
Copyright ©1997 Society for Neuroscience
Endogenous Adenosine Mediates the Presynaptic Inhibition Induced
by Aglycemia at Corticostriatal Synapses
Received Jan. 8, 1997; revised March 24, 1997; accepted March 26, 1997.
Paolo Calabresi1,
Diego Centonze1,
Antonio Pisani1, 2, and
Giorgio Bernardi1, 2
1 Clinica Neurologica, Universitá di Roma Tor
Vergata, Dipartimento Sanitá, 00173 Rome, Italy, and 2 Ospedale
Santa Lucia, Rome, Italy
Energy deprivation, as a result of aglycemia, leads to
depression of the central synaptic transmission. Endogenous adenosine has been implicated in this depressant effect. We have studied the
possible involvement of endogenous adenosine in the depression of
corticostriatal excitatory transmission induced by glucose deprivation
by using intracellular recordings in brain slices. After stimulation of
corticostriatal fibers, EPSPs were recorded from striatal spiny
neurons. Adenosine (3-300 µM) or brief periods (5-10
min) of aglycemia reduced the EPSP amplitude but did not alter the
membrane potential and the resistance of the recorded cells. These
inhibitory effects were not associated with an alteration of the
postsynaptic sensitivity to exogenous glutamate but were coupled with
an increased paired-pulse facilitation, suggesting the involvement of
presynaptic mechanisms. A delayed postsynaptic membrane
depolarization/inward current was detected after 15-20 min of glucose
deprivation. The presynaptic inhibitory effects induced by adenosine
and aglycemia were both antagonized either by the nonselective
adenosine receptor antagonist caffeine (2.5 mM) or by the
A1 receptor antagonists 8-cyclopentyl-1,3-dimethylxanthine (CPT, 1 µM) and 1,3-dipropyl-8-cyclopentylxanthine (CPX, 300 nM). Conversely, these antagonists affected neither the
delayed membrane depolarization/inward current nor the underlying
conductance increase produced by glucose deprivation. The
ATP-sensitive potassium channel blockers tolbutamide (1 mM)
and glipizide (100 nM) had no effect on the
aglycemia-induced decrease of EPSP amplitude. Our data demonstrate that
endogenous adenosine acting on A1 receptors mediates the presynaptic
inhibition induced by aglycemia at corticostriatal synapses, whereas
ATP-dependent potassium channels do not play a significant role in this
presynaptic inhibition.
Key words:
adenosine;
aglycemia;
ischemia;
excitatory amino acids;
synaptic transmission;
glutamate
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