{'fraction_non_alphanumeric': 0.037037037037037035, 'fraction_numerical': 0.021164021164021163, 'mean_word_length': 6.170616113744076, 'pattern_counts': {'":': 0, '<': 0, '<?xml version=': 0, '>': 0, 'https://': 0, 'lorem ipsum': 0, 'www.': 0, 'xml': 0}, 'pii_count': 0, 'substrings_counts': 0, 'word_list_counts': {'cursed_substrings.json': 0, 'profanity_word_list.json': 0, 'sexual_word_list.json': 0, 'zh_pornsignals.json': 0}}
Protein Kinase C‐Mediated Suppression of the Presynaptic Adenosine A1 Receptor by a Facilitatory Metabotropic Glutamate Receptor

Abstract: KCl‐evoked glutamate exocytosis from cerebrocortical synaptosomes can be inhibited by the adenosine A1 receptor agonist cyclohexyladenosine (CHA). Inhibition is associated with a decreased KCl‐evoked Ca2+ level elevation, and the effect of the agonist is occluded by prior incubation with the Agelenopsis aperta neurotoxin ω‐agatoxin‐IVA at 250 nM. The inhibition is suppressed in the presence of 3 nM phorbol dibutyrate (PDBu) or by activation of the protein kinase C (PKC)‐coupled metabotropic glutamate receptor by 100 µM (1S,3R)‐1‐aminocyclopentane‐1,3‐dicarboxylate [(1S,3R)ACPD]. A tonic inhibition of release by leaked exogenous adenosine can be reversed by adenosine deaminase or by PDBu addition. The CHA‐induced inhibition can be enhanced by the PKC inhibitor Ro 31‐8220. The mechanism for the suppression of the adenosine A1 receptor‐mediated inhibition is distinct from that previously described for the (1S,3R)ACPD‐evoked, PKC‐mediated, facilitatory pathway, which enhances phosphorylation of the MARCKS protein, 4‐aminopyridine‐induced action potentials, and release of glutamate because the latter requires at least 100 nM PDBu [or the combination of (1S,3R)ACPD and arachidonic acid] and is not seen following KCl depolarization. Both PKC‐mediated pathways may be involved in the presynaptic events associated with the establishment of synaptic plasticity.