[THE DAMAGING EFFECTS AT AN EARLY AGE ALTER PAIN SENSITIVITY IN ADULT FEMALE RATS, CORRECTION WITH BUSPIRONE].

I P Butkevich, V A Mikhailenko
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Abstract

Most studies on the damaging effects of pain and stress impacts in the neonatal period of development on pain sensitivity were performed on individuals of the male sex. In the present study, we investigated the influence of inflammatory pain and/or stress of isolation from the mother in newborn female rats to pain sensitivity when they reached adulthood; an attempt was undertaken to correct identified deviations using 5-HT1A-receptor agonist buspirone. Adult females exposed to early pain displayed increased hypoalgesia in the hot plate test and rats subjected to stress of isolation from the mother showed increased hyperalgesia in the formalin test. The pain and subsequent isolation from the mother did not change pain sensitivity in the adult females. The chronic injection of buspirone from 25 th to 39 th day of life to females subjected to inflammatory pain and isolation from the mother in the neonatal period caused the normalization of pain sensitivity when they reached adulthood. It is found that the prepubertal period is a critical period for the correction of deviations caused by damaging impacts in neonatal rata in the functional activity of the nociceptive system.

[早期的破坏性影响改变了成年雌性大鼠的疼痛敏感性,用丁螺环酮纠正]。
大多数关于新生儿发育阶段疼痛和应激对疼痛敏感性的破坏性影响的研究都是在男性个体上进行的。在本研究中,我们研究了新生雌性大鼠炎症性疼痛和/或与母亲分离的压力对成年后疼痛敏感性的影响;尝试使用5- ht1a受体激动剂丁螺环酮纠正已确定的偏差。暴露于早期疼痛的成年雌性在热板试验中表现出增加的痛觉减退,而与母亲隔离应激的大鼠在福尔马林试验中表现出增加的痛觉过敏。疼痛和随后与母亲的隔离并没有改变成年雌性的疼痛敏感性。新生儿期炎性疼痛和与母亲分离的雌性小鼠在出生后第25 ~ 39天长期注射丁螺环酮,可使其成年后疼痛敏感性恢复正常。研究发现,青春期前是纠正新生儿损伤性影响对伤害感觉系统功能活动的影响的关键时期。
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