Oliveros L, Forneris M, Aguado L
Laboratorio de Biología de la Reproducción, Facultad de Química, Bioquímica y Farmacia, Universidad Nacional de San Luis, San Luis, Chacabuco y Pedernera, 5700 San Luis, Argentina.
Medicina (B Aires). 2001;61(1):35-40.
There are evidences for modulation of immune function by the sympathetic nervous system and its principal neurotransmitter norepinephrine (NE) through superior ovarian nerve (SON)-coeliac ganglion-noradrenergic postganglionic innervation of the spleen. Seven days after SON transection at 53 days of age, the rat splenocytes were isolated and then cultured for 48 h. These culture media, used to stimulate ovaries from 60-day-old intact rats (neither SON-transected nor sham-operated) at diestrus 2 stage, in in vitro incubations, showed a decrease in progesterone release, an increase in estradiol release and no change in androstenedione release in relation to splenocyte culture media from control (sham-operated) rats. When splenocytes from SON transected (SON-t) rats were treated with vasoactive intestinal peptide (VIP) or neuropeptide Y (NPY), both at 10(-6) M for 24 h, their secretions increased the progesterone release while decreasing the estradiol release from the intact ovaries, compared with the secretions of untreated splenocytes from SON-t rats. Although the secretions of splenocytes treated with VIP decrease the androstenedione release from the ovaries, the treatment with NPY produced no change in hormone release. In the present paper the ovarian steroidogenic response, which was modified by the effects of an in vivo SON transection on spleen cells, was reverted by an in vitro system in which the splenocytes were treated with VIP or NPY. This could indicate that the spleen of SON-t rats does not receive those neuropeptides by neural route however, when they are added to splenocyte culture in vitro, the cell secretions revert the profile of steroid hormones released from the intact ovary. We also present functional evidence for modulation of the immune function by sympathetic nervous system and neurotransmitters other than NE.
有证据表明，交感神经系统及其主要神经递质去甲肾上腺素（NE）通过卵巢上神经（SON）-腹腔神经节-脾的去甲肾上腺素能节后神经支配来调节免疫功能。在53日龄时进行SON横断术后7天，分离大鼠脾细胞，然后培养48小时。这些培养基用于在体外孵育中刺激处于动情后期2阶段的60日龄完整大鼠（既未进行SON横断也未进行假手术）的卵巢，与来自对照（假手术）大鼠的脾细胞培养基相比，显示孕酮释放减少、雌二醇释放增加且雄烯二酮释放无变化。当用血管活性肠肽（VIP）或神经肽Y（NPY）处理来自SON横断（SON-t）大鼠的脾细胞时，二者均以10(-6) M处理24小时，与未处理的SON-t大鼠脾细胞的分泌物相比，它们的分泌物增加了完整卵巢的孕酮释放，同时减少了雌二醇释放。尽管用VIP处理的脾细胞分泌物减少了卵巢的雄烯二酮释放，但用NPY处理对激素释放没有影响。在本文中，体内SON横断对脾细胞的影响所改变的卵巢类固醇生成反应，在体外系统中通过用VIP或NPY处理脾细胞而得以恢复。这可能表明，SON-t大鼠的脾脏没有通过神经途径接收那些神经肽，然而，当它们在体外添加到脾细胞培养物中时，细胞分泌物恢复了完整卵巢释放的类固醇激素谱。我们还提供了交感神经系统和NE以外的神经递质调节免疫功能的功能证据。
