Abstract：
:Iontophoretic application of carbachol caused excitation of CA1 neurones and decreased the amplitude of antidromic CA1 population spikes recorded extracellularly. Adenosine, adenosine triphosphate (ATP) and the purine analogues N-ethylcarboxamide adenosine (NECA) and R- and S-phenylisopropyladenosine (PIA) reduced the effects of carbachol on single cell firing and on the population spike. Responses to excitatory amino acids were unaffected by adenosine except for a small depression of kainate and N-methyl-D-aspartate responses at high concentrations. The rank order of potency for the purine reduction of carbachol responses was R-PIA = S-PIA = NECA much greater than adenosine greater than ATP. The actions of purines and purine analogues were antagonized by 8-phenyltheophylline (8-PT) and other xanthine antagonists. Application of 8-PT and other xanthines without prior exposure to purines frequently resulted in marked potentiation of carbachol responses. Thus in the hippocampus, responses to the cholinomimetic carbachol are markedly and selectively reduced by purines acting at the P1 purine receptor type and it appears that endogenous levels of adenosine limit the effects of cholinergic agents.
journal_name
Brain Resjournal_title
Brain researchauthors
Brooks PA,Stone TWdoi
10.1016/0006-8993(88)90501-xsubject
Has Abstractpub_date
1988-08-16 00:00:00pages
106-14issue
1eissn
0006-8993issn
1872-6240pii
0006-8993(88)90501-Xjournal_volume
458pub_type
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