脳および脊髄アストロサイトにおけるアドレナリン作動性突起形成制御とその差異

抄録

Astrocytes are glial cells with numerous processes through which they contact neurons to control functions in the central nervous system (CNS). Astrocytic processes are morphologically heterogeneous throughout the CNS regions and exhibit neuronal activity-induced plasticity. We previously reported that the process formation by cultured spinal cord astrocytes is bidirectionally regulated by β- and α₂-adrenoceptors (ARs). Here, we examined the role of α₁-ARs in process formation and adrenergic regulation of cortical astrocyte processes. We evaluated morphology of cultured astrocytes by phalloidin-cytoskeletal staining.

Noradrenaline (NA) and isoproterenol (β-agonist) induced process formation, which was more potent in cortical astrocytes than in spinal cord astrocytes. Prazosin and atipamezole (α₁- and α₂-antagonist) enhanced NA-induced process formation in spinal cord astrocytes but not in cortical astrocytes. Dexmedetomidine (α₂-agonist), but not phenylephrine (α₁-agonist), inhibited the process formation by both astrocytes. The expression of AR mRNAs was different between both astrocytes, especially less expression of α₁-ARs in cortical astrocytes.

 Adrenergic regulation of astrocyte processes likely depends on the balance of α- and β- ARs, which may be related to astrocytic morphological heterogeneity and functions in the CNS.