PUBLICATION

Interactions between serotonin and glutamate-nitric oxide pathways in zebrafish scototaxis

Authors
Herculano, A.M., Puty, B., Miranda, V., Lima, M.G., Maximino, C.
ID
ZDB-PUB-141224-1
Date
2015
Source
Pharmacology, biochemistry, and behavior   129: 97-104 (Journal)
Registered Authors
Lima, Monica Gomes, Maximino, Caio
Keywords
5-HT(1A) receptor, Glutamate, Nitric oxide, Scototaxis, Serotonin, Zebrafish
MeSH Terms
  • 5-Hydroxytryptophan/pharmacology
  • Animals
  • Anxiety/metabolism*
  • Glutamic Acid/metabolism*
  • N-Methylaspartate/pharmacology
  • Nitric Oxide/metabolism*
  • Nitric Oxide Donors/pharmacology
  • Piperazines/pharmacology
  • Pyridines/pharmacology
  • Serotonin/metabolism*
  • Zebrafish
PubMed
25536532 Full text @ Pharmacol. Biochem. Behav.
Abstract
NMDA receptors have been implicated in the acute response to stress, possibly mediated the nitric oxide pathway; serotonin has also been implicated in these responses, and has recently been shown to modulate the nitric oxide pathway via 5-HT1 and 5-HT2 receptors. In this work, we compare the effects of NMDA and a 5-HT1A receptor ligands on light/dark preference in adult zebrafish, and investigate whether nitric oxide mediates the effects of such drugs. The noncompetitive NMDA receptor antagonist MK-801 decreased dark preference (scototaxis), while NMDA increased it; the effects of NMDA were completely blocked by pretreatment with the nitric oxide synthase (NOS) antagonist L-NAME. SNP, a nitric oxide donor, produced a bell-shaped dose-response profile on scototaxis. Treatment with 5-HTP increased scototaxis, an effect which was potentiated by pre-treatment with NMDA, but not MK-801, and partially blocked by L-NAME. The 5-HT1A receptor antagonist WAY 100,635 decreased scototaxis, an effect which was completely blocked by L-NAME. These results suggest that tonic NOS inhibition is an important downstream effector of 5-HT1A receptors in the regulation of dark preference behavior in zebrafish, and that NOS is also under phasic independent control by NMDA receptors.
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