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Involvement of CRF but not NPY in the anxiety regulation via NMDA receptors
Joanna M Wierońska1, Bernadeta Szewczyk, Agnieszka Pałucha
1Department of Neurobiology, Institute of Pharmacology, Polish Academy of Sciences, Smetna 12, PL 31-343 Kraków, Poland.
Abstract:
The study attempts to evaluate whether neuropeptide Y (NPY) and corticotropin-releasing factor (CRF) are involved in anxiogenic and anxiolytic reactions induced by NMDA receptor ligands. The animals were given MK-801 (1 mg/kg, ip), a non-competitive NMDA-receptor antagonist, which acts as anxiolytic agent, or NMDA (15 mg/kg, ip), which has an anxiogenic effect. The anxiogenic or anxiolytic actions of these compounds were evaluated in the plus-maze test. The animals, which were given MK-801, were administered BIBO 3304 (130 ng/0.5 microl/site) intraamygdalarly and the animals which were given NMDA were administered alpha-helical CRF (500 ng/0.5 microl/site). BIBO 3304 did not attenuate MK-801-induced anxiolysis and alpha-helical CRF abolished NMDA-induced anxiogenesis. Our results show that anxiogenic effect of NMDA is mediated via CRF1 receptors and anxiolytic action of MK-801 is not dependent on Y1 receptors.
Insights
Neuropeptide Y (NPY) and corticotropin-releasing factor (CRF) roles in NMDA receptor-induced anxiety were studied. NMDA
Area of Science:
- Neuroscience
- Pharmacology
- Anxiolytic and Anxiogenic Mechanisms
Background:
- NMDA receptor ligands can induce anxiety-like behaviors.
- Neuropeptide Y (NPY) and corticotropin-releasing factor (CRF) are implicated in stress and anxiety.
- Understanding the specific roles of NPY and CRF in NMDA receptor-mediated anxiety is crucial.
Purpose of the Study:
- To investigate the involvement of NPY and CRF in the anxiogenic effects of NMDA and the anxiolytic effects of MK-801.
- To determine if CRF1 receptors mediate NMDA-induced anxiogenesis.
- To assess if Y1 receptors mediate MK-801-induced anxiolysis.
Main Methods:
- Administered NMDA (anxiogenic) and MK-801 (anxiolytic) to animals.
- Evaluated anxiogenic/anxiolytic effects using the plus-maze test.
- Administered CRF1 antagonist BIBO 3304 and CRF antagonist alpha-helical CRF intraamygdalarly.
Main Results:
- Alpha-helical CRF abolished NMDA-induced anxiogenesis, indicating CRF1 receptor mediation.
- BIBO 3304 did not attenuate MK-801-induced anxiolysis, suggesting Y1 receptor independence.
- NMDA's anxiogenic effect is mediated by CRF1 receptors.
Conclusions:
- The anxiogenic effects of NMDA are mediated through CRF1 receptors.
- The anxiolytic effects of MK-801 are not dependent on Y1 receptors.
- This study elucidates specific receptor pathways involved in NMDA receptor ligand-induced anxiety.
