PUBLICATION

Modulation of adenosine signaling prevents scopolamine-induced cognitive impairment in zebrafish

Authors
Bortolotto, J.W., Melo, G.M., Cognato, G.D., Vianna, M.R., Bonan, C.D.
ID
ZDB-PUB-141210-8
Date
2015
Source
Neurobiology of learning and memory   118: 113-9 (Journal)
Registered Authors
Bonan, Carla Denise, Vianna, Mônica Ryff Moreira Roca
Keywords
Adenosine, Inhibitory avoidance, Memory, Scopolamine, Zebrafish
MeSH Terms
  • Adenine/analogs & derivatives
  • Adenine/pharmacology
  • Adenosine/metabolism*
  • Adenosine Deaminase Inhibitors/pharmacology
  • Animals
  • Avoidance Learning/drug effects
  • Cognition Disorders/chemically induced*
  • Dipyridamole/pharmacology
  • Disease Models, Animal
  • Motor Activity/drug effects
  • Muscarinic Antagonists/pharmacology*
  • Nucleoside Transport Proteins/antagonists & inhibitors
  • Purinergic P1 Receptor Antagonists/pharmacology
  • Scopolamine/pharmacology*
  • Signal Transduction/drug effects*
  • Social Behavior
  • Zebrafish
PubMed
25490060 Full text @ Neurobiol. Learn. Mem.
Abstract
Adenosine, a purine ribonucleoside, exhibits neuromodulatory and neuroprotective effects in the brain and is involved in memory formation and cognitive function. Adenosine signaling is mediated by adenosine receptors (A1, A2A, A2B, and A3); in turn, nucleotide and nucleoside-metabolizing enzymes and adenosine transporters regulate its levels. Scopolamine, a muscarinic cholinergic receptor antagonist, has profound amnesic effects in a variety of learning paradigms and has been used to induce cognitive deficits in animal models. This study investigated the effects of acute exposure to caffeine (a non-selective antagonist of adenosine receptors A1 and A2A), ZM 241385 (adenosine receptor A2A antagonist), DPCPX (adenosine receptor A1 antagonist), dipyridamole (inhibitor of nucleoside transporters) and EHNA (inhibitor of adenosine deaminase) in a model of pharmacological cognitive impairment induced by scopolamine in adult zebrafish. Caffeine, ZM 241385, DPCPX, dipyridamole, and EHNA were acutely administered independently via i.p. in zebrafish, followed by exposure to scopolamine dissolved in tank water (200 μM). These compounds prevented the scopolamine-induced amnesia without impacting locomotor activity or social interaction. Together, these data support the hypothesis that adenosine signaling may modulate memory processing, suggesting that these compounds present a potential preventive strategy against cognitive impairment.
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