Abstract
Background:
The amygdala is a key brain region involved in emotional processing. Activity of its cells is modulated by adenosine, via both A1 and A2A receptors (A1R and A2AR). A1R and A2AR control fear memory, a process critically dependent on NMDA receptors (NMDAR). Thus, we now tested whether A1R and A2AR control NMDAR in the amygdala.
Materials and Methods:
We recorded synaptically evoked NMDAR-mediated excitatory post-synaptic currents (NMDA-EPSCs) in pyramidal cells of the basolateral amygdala, upon stimulation of the lateral amygdala in brain slices from 4- to 6-week-old male Wistar rats.
Results:
Activation of A1R decreased NMDAR-mediated currents. Surprisingly, activation of A2AR with CGS21680 (30 nM) also decreased NMDAR-mediated synaptic currents, an effect prevented by the A1R antagonist 8-cyclopentyl-1,3-dipropylxanthine (DPCPX) rather than by the selective A2AR antagonist SCH58261.
Conclusions:
Our data suggest that adenosine primarily inhibits intra-amygdalar circuits through A1R activation.
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