Neuropeptide Y blocks anxiogenic-like behavioral action of corticotropin-releasing factor in an operant conflict test and elevated plus maze

Neuropeptide Y blocks anxiogenic-like behavioral action of corticotropin-releasing factor in an... Central administration of neuropeptide Y (NPY) produces anxiolytic-like behavioral effects in rat models of anxiety. Because previous evidence has suggested a relationship between NPY and corticotropin-releasing factor (CRF) in the brain, we have focused on the interaction of these neuropeptide systems in emotional responsiveness to stressful stimuli. Intracerebroventricular administration of CRF produced a marked response suppression in an operant incremental shock conflict paradigm. NPY ((1 μg, intracerebroventricularly (i.c.v.)) significantly antagonized the response-suppressing effects of CRF (0.75 μg, i.c.v.) on punished responding in the conflict test at doses that produced little or no behavioral effect when administered alone. Central administration of the CRF antagonist (D-Phe 12 , Nle 21,38 ,C α MeLeu 37 )CRF (D-Phe CRF 12–41 ) alone did not alter punished or unpunished responding in the conflict test. However, pretreatment with the CRF antagonist before a subthreshold dose of NPY (1 μg, i.c.v.) produced a significant potentiation of the release of punished responding relative to NPY alone and untreated controls. NPY also antagonized the “anxiogenic-like” behavioral effects of CRF in the elevated plus maze. These findings support the hypothesis that NPY and CRF may reciprocally modulate an animal’s behavioral response to stressful stimuli. http://www.deepdyve.com/assets/images/DeepDyve-Logo-lg.png Peptides Elsevier

Neuropeptide Y blocks anxiogenic-like behavioral action of corticotropin-releasing factor in an operant conflict test and elevated plus maze

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Publisher
Elsevier
Copyright
Copyright © 2000 Elsevier Science Inc.
ISSN
0196-9781
DOI
10.1016/S0196-9781(99)00169-2
Publisher site
See Article on Publisher Site

Abstract

Central administration of neuropeptide Y (NPY) produces anxiolytic-like behavioral effects in rat models of anxiety. Because previous evidence has suggested a relationship between NPY and corticotropin-releasing factor (CRF) in the brain, we have focused on the interaction of these neuropeptide systems in emotional responsiveness to stressful stimuli. Intracerebroventricular administration of CRF produced a marked response suppression in an operant incremental shock conflict paradigm. NPY ((1 μg, intracerebroventricularly (i.c.v.)) significantly antagonized the response-suppressing effects of CRF (0.75 μg, i.c.v.) on punished responding in the conflict test at doses that produced little or no behavioral effect when administered alone. Central administration of the CRF antagonist (D-Phe 12 , Nle 21,38 ,C α MeLeu 37 )CRF (D-Phe CRF 12–41 ) alone did not alter punished or unpunished responding in the conflict test. However, pretreatment with the CRF antagonist before a subthreshold dose of NPY (1 μg, i.c.v.) produced a significant potentiation of the release of punished responding relative to NPY alone and untreated controls. NPY also antagonized the “anxiogenic-like” behavioral effects of CRF in the elevated plus maze. These findings support the hypothesis that NPY and CRF may reciprocally modulate an animal’s behavioral response to stressful stimuli.

Journal

PeptidesElsevier

Published: Jan 1, 2000

References

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