Iuvone P M, Besharse J C
J Neurochem. 1986 Jan;46(1):82-8. doi: 10.1111/j.1471-4159.1986.tb12928.x.
The possible involvement of calcium in the regulation of retinal serotonin N-acetyltransferase (NAT) activity was investigated using eye cups of Xenopus laevis cultured in defined medium. Omitting CaCl2 from the culture medium completely inhibited the dark-dependent increase of NAT activity at night. Approximately 10(-4)-10(-3) M free Ca2+ was found to be required for the maximal increase of NAT activity in the dark. Other divalent cations--Ba2+, Sr2+, and Mn2+--did not substitute for Ca2+. Antagonists of voltage-sensitive calcium channels, including nifedipine, methoxyverapamil (D600), Co2+, and Mg2+, were found to be effective inhibitors of the dark-dependent increase of retinal NAT activity. Trifluoperazine also decreased retinal NAT activity. These studies indicate that the increase of retinal NAT activity in the dark is mediated by a specific Ca2+-dependent process and that Ca2+ influx through voltage-sensitive calcium channels is involved.
利用在特定培养基中培养的非洲爪蟾眼杯,研究了钙在视网膜5-羟色胺N-乙酰基转移酶(NAT)活性调节中的可能作用。从培养基中去除氯化钙完全抑制了夜间NAT活性的暗依赖性增加。发现大约10⁻⁴ - 10⁻³ M的游离Ca²⁺是黑暗中NAT活性最大增加所必需的。其他二价阳离子——Ba²⁺、Sr²⁺和Mn²⁺——不能替代Ca²⁺。包括硝苯地平、甲氧基维拉帕米(D600)、Co²⁺和Mg²⁺在内的电压敏感性钙通道拮抗剂被发现是视网膜NAT活性暗依赖性增加的有效抑制剂。三氟拉嗪也降低了视网膜NAT活性。这些研究表明,黑暗中视网膜NAT活性的增加是由特定的Ca²⁺依赖性过程介导的,并且涉及通过电压敏感性钙通道的Ca²⁺内流。