Effects of bi-adrenergic receptor blockade during chronic restraint stress on the expression of selected proteins of the glutamatergic transmission in the rat prefrontal cortex

• Autorzy: Zelek-Molik A. , Kowalska M. , Roman A. , Kusmierczyk J. , Bielawski A. , Nalepa I.
• Języki publikacji: EN

Abstrakty

EN

BACKGROUND AND AIMS: The stress impaired the structure and activity ofthe prefrontal cortical(PFC) neurons has been postulated to underlie the pathology of stress related psychiatric disorders. NMDA and AMPA glutamate receptors of PFC were shown to be affected by stress. High level of the noradrenaline release during stress is known to stimulate the β adrenergic receptors (βAR), densely expressed in PFC. The βAR can directly or indirectly, by means of Fyn kinase, regulate glutamatergic receptors activation. Also, evidence have shown that pharmacological blockade of β1AR alleviated anxiety in stress models. The aim of the study wasto evaluate the stressinduced changes in the expression of total- and phospho-(Y1472)GluN2B, (Ser845)GluA1, and (Y530)Fyn proteins in rat dorso-medial (dm) PFC and to assess whether β1AR blockade can modulate it. METHODS: Male Wistar rats underwent the chronic restraint stress procedure applied for 3 hours daily, for 14 days. During the last 7 days rats were treated with betaxolol (1 or 5 mg/kg/po) given immediately after daily stress. Next day after a completion of stress procedure, the rats were decapitated, their dmPFC was dissected and subjected to standard Western blot analysis. RESULTS: Neither stress nor betaxolol treatment changed the expression of studied NMDA and AMPA subunits. Repeated stress increased phosphorylation level of (Y530)Fyn kinase (by 25% vs. non stressed groups) and betaxolol treatment did not influence this effect. CONCLUSIONS: The Fyn kinase is a known regulator of NMDA receptors’membrane stability, on the other hand phosphorylation at Tyr 530 inactivates the kinase. Our results showing the increased phosphorylation of Fyn suggest the inhibition of Fyn activity which can be responsible for disturbed glutamatergic transmission observed in PFC after prolonged stress. This mechanism seems to be independent on β1AR activity in PFC. Supported by statutory funds of the Institute of Pharmacology PAS.

• Wydawca: -
• Czasopismo: Acta Neurobiologiae Experimentalis
• Rocznik: 2015
• Tom: 75
• Numer: Supl.
• Opis fizyczny: p.S82

Twórcy

autor

Zelek-Molik A.

• Department of Brain Biochemistry, Institute of Pharmacology, Polish Academy of Sciences, Krakow, Poland

autor

Kowalska M.

• Department of Brain Biochemistry, Institute of Pharmacology, Polish Academy of Sciences, Krakow, Poland

autor

Roman A.

• Department of Brain Biochemistry, Institute of Pharmacology, Polish Academy of Sciences, Krakow, Poland

autor

Kusmierczyk J.

• Department of Brain Biochemistry, Institute of Pharmacology, Polish Academy of Sciences, Krakow, Poland

autor

Bielawski A.

• Department of Brain Biochemistry, Institute of Pharmacology, Polish Academy of Sciences, Krakow, Poland

autor

Nalepa I.

• Department of Brain Biochemistry, Institute of Pharmacology, Polish Academy of Sciences, Krakow, Poland