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Suppression of bladder reflex activity in chronic spinal cord injured cats by activation of serotonin 5-HT1A receptors.

机译:通过激活血清素5-HT1A受体抑制慢性脊髓损伤猫的膀​​胱反射活性。

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摘要

The effects of 8-OH-DPAT (5-HT1A receptor agonist) and WAY100635 (5-HT1A receptor antagonist) on reflex bladder activity were investigated in alpha-chloralose anesthetized or conscious chronic spinal cord injured cats. The results were similar in both anesthetized and conscious animals. Cystometrograms revealed that 8-OH-DPAT (0.5 mg/kg, s.c.) significantly increased the bladder volume threshold for eliciting a large amplitude micturition contraction, but only slightly reduced the amplitude of the contractions and did not alter the small amplitude pre-micturition contractions. 8-OH-DPAT also reduced the amplitude of isovolumetric bladder contractions. The inhibitory effect of 8-OH-DPAT was reversed by WAY100635 (0.5 mg/kg) or blocked by pre-treatment with WAY100635. Reflex bladder contractions evoked by tactile stimulation of the perigenital region were not altered by 8-OH-DPAT. These results suggest that the inhibitory effect of 8-OH-DPAT is mediated by an action on interneuronal pathways in the spinal cord or on the C-fiber afferent limb of the spinal micturition reflex and not on bladder smooth muscle or the efferent limb of the reflex pathway. Drugs that activate 5-HT1A receptors might be useful in treating detrusor overactivity after spinal cord injury.
机译:在α-氯代海洛因麻醉或有意识的慢性脊髓损伤的猫中研究了8-OH-DPAT(5-HT1A受体激动剂)和WAY100635(5-HT1A受体拮抗剂)对反射性膀胱活动的影响。在麻醉和清醒动物中,结果相似。膀胱造影图显示,8-OH-DPAT(0.5 mg / kg,sc)显着增加了引起大幅度排尿收缩的膀胱容量阈值,但仅略微减小了收缩幅度,而没有改变小幅度排尿前收缩。 8-OH-DPAT还减少了等容膀胱收缩的幅度。 8-OH-DPAT的抑制作用被WAY100635(0.5 mg / kg)逆转,或被WAY100635预处理阻断。通过触觉刺激生殖器周围区域引起的反射性膀胱收缩不会被8-OH-DPAT改变。这些结果表明8-OH-DPAT的抑制作用是通过对脊髓或排尿反射的C纤维传入肢上神经内通路的作用介导的,而不是对膀胱平滑肌或上肢的传出肢体的作用介导的。反射途径。激活5-HT1A受体的药物可能可用于治疗脊髓损伤后逼尿肌过度活动。

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