Caglar Ozgur, Aydin Mehmet Dumlu, Aydin Nazan, Ahiskalioglu Ali, Kanat Ayhan, Aslan Remzi, Onder Arif
Department of Pediatric Surgery, Medical Faculty of Ataturk University, Erzurum, Turkey.
Department of Neurosurgery, Medical Faculty of Ataturk University, Erzurum, Turkey.
Rev Int Androl. 2022 Jan-Mar;20(1):1-10. doi: 10.1016/j.androl.2020.05.011. Epub 2021 Feb 5.
We previously postulated that orgasmic sensation may occur through recently discovered genital taste bud-like structures. The interaction between the pudendal nerve and Onuf's nucleus may be important for developing orgasmic information. The study aims to investigate whether ischemic damage to Onuf's nucleus-pudendal network following spinal subarachnoid hemorrhage (SAH) causes taste bud degeneration or not.
The study was conducted on 22 fertile male rabbits who were divided into three groups: control (GI; n=5), SHAM (GII; n=5) and study (GIII; n=12). Isotonic solution, .7cm, for the SHAM, and .7cm homologous blood was injected into spinal subarachnoid spaces at S2 level of the study group. Two weeks later, Onuf's nucleus, pudendal ganglia and the taste bud-like structures of the penile urethra were examined histopathologically. Degenerated neuron densities of Onuf's nucleus, pudendal ganglia and atrophic taste bud-like structures were estimated per mm and the results analyzed statistically.
The mean degenerated neuron densities of taste bud-like structures, Onuf's nucleus and pudendal ganglia were estimated as 2±1/mm, 5±1/mm, 6±2/mm in GI; 12±4/mm, 35±9/mm, 188±31/mm, in GII and 41±8/mm, 215±37/mm, 1321±78/mm, in GIII. Spinal SAH induced neurodegeneration in Onuf's nucleus, pudendal ganglia and taste bud atrophy was significantly different between GI/GII (p<.005); GII/GIII (p<.0005) and GI/GIII (p<.0001).
Ischemic neuronal degenerations of Onuf's nucleus and pudendal ganglia following spinal SAH lead to genital taste bud-like structure atrophy. This mechanism may be responsible for sexual anhedonia and sterility in cases with spinal cord injury, which has not been documented so far. More studies are needed.
我们之前推测性高潮感觉可能通过最近发现的生殖器味蕾样结构产生。阴部神经与奥努夫核之间的相互作用对于性高潮信息的形成可能很重要。本研究旨在调查脊髓蛛网膜下腔出血(SAH)后奥努夫核 - 阴部神经网络的缺血性损伤是否会导致味蕾退化。
对22只可育雄性兔子进行研究,将其分为三组:对照组(GI;n = 5)、假手术组(GII;n = 5)和研究组(GIII;n = 12)。假手术组在S2水平的脊髓蛛网膜下腔注射等渗溶液0.7cm,研究组注射0.7cm同源血液。两周后,对奥努夫核、阴部神经节和阴茎尿道的味蕾样结构进行组织病理学检查。每毫米估计奥努夫核、阴部神经节的退化神经元密度以及萎缩的味蕾样结构,并对结果进行统计学分析。
GI组味蕾样结构、奥努夫核和阴部神经节的平均退化神经元密度估计分别为2±1/mm、5±1/mm、6±2/mm;GII组分别为12±4/mm、35±9/mm、188±31/mm;GIII组分别为41±8/mm、215±37/mm、1321±78/mm。脊髓SAH诱导的奥努夫核神经变性、阴部神经节和味蕾萎缩在GI/GII组之间(p <.005);GII/GIII组之间(p <.0005)以及GI/GIII组之间(p <.0001)有显著差异。
脊髓SAH后奥努夫核和阴部神经节的缺血性神经元变性导致生殖器味蕾样结构萎缩。这种机制可能是脊髓损伤患者性快感缺失和不育的原因,目前尚未有相关文献记载。需要更多的研究。