Abstract：
:Electrophysiological recordings in rat brain slices have been used to study the actions of adenosine on striatal neurons and striatal excitatory amino acid neurotransmission originating in the cortex or the thalamus. Adenosine had no effects on membrane properties of striatal neurons. Adenosine and the A1 agonist N6-Cyclopentyl adenosine reduced EPSPs of both cortical and thalamic origin by more than 50%. Depression of EPSPs was associated with an increase in paired-pulse facilitation, suggesting a presynaptic locus of action. EPSP depression was blocked by the A1 antagonist, 8-Cyclopentyl-1,3-dipropyl xanthine. The A2 agonist 5'-(N-cyclopropyl)-carboxamidoadenosine had no effect on excitatory amino acid neurotransmission. The A1 antagonist alone enhanced the synaptic component of the evoked field potential (23 +/- 12%). These results indicate that endogenous adenosine, acting via A1 receptors, limits striatal glutamatergic neurotransmission, serving a modulatory and neuroprotective role.
journal_name
Brain Resjournal_title
Brain researchauthors
Flagmeyer I,Haas HL,Stevens DRdoi
10.1016/s0006-8993(97)01060-3subject
Has Abstractpub_date
1997-12-05 00:00:00pages
178-85issue
1eissn
0006-8993issn
1872-6240pii
S0006-8993(97)01060-3journal_volume
778pub_type
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