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大鼠腹侧或背侧海马体损伤会延迟青春期、卵泡生长和性类固醇激素的分泌。

Lesion of the ventral or dorsal hippocampus in the rat delays puberty, follicular growth and secretion of sex steroid hormones.

作者信息

Castillo Estrella Del Mar, Quiróz Ubaldo, Milflores Lorena, Reyes Rosalina, Flores Gonzalo

机构信息

Laboratorio de Histofisiología, Facultad de Ciencias Biológicas, Benemérita Universidad Autónoma de Puebla, Puebla, Mexico.

Laboratorio de Biología Oral, Facultad de Estudios Superiores Zaragoza, Universidad Nacional Autónoma de México (UNAM), Ciudad de Mexico, Mexico.

出版信息

Front Endocrinol (Lausanne). 2025 Apr 16;16:1530692. doi: 10.3389/fendo.2025.1530692. eCollection 2025.

DOI:10.3389/fendo.2025.1530692
PMID:40309443
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC12040663/
Abstract

INTRODUCTION

The hypothalamus-pituitary-gonad axis is controlled by gonadotropins and by a direct neural pathway to the gonads. New evidence suggests the existence of neural connection from the hippocampus to the hypothalamus that can regulate its function. It could be a new control on the well-regulated hormonal and neural connection to the gonads and hence in reproduction. The objective of this study was to analyze the effects of independent lesion of the dorsal or ventral hippocampus in the female rat on the onset of puberty, follicular growth and serum concentration of sex steroid and gonadotropins.

METHODS

Prepubertal female rats of the CII-ZV strain, 21 days old, were used. Ventral (VH-L) or dorsal (DH-L) hippocampus lesions by the administration of ibotenic acid were performed using stereotaxic surgery. Controls were sham-operated (VH-Sham and DH- Sham), a fifth group was used as absolute control. At 30 days of age all groups underwent novel object recognition tests (NORT).

RESULTS

Data from memory using NORT showed a decrease both in short- and long-term memory in the animals in the VH- L and DH-L groups compared to their respective sham-operated controls and the absolute control group. Similarly, injured rats presented delayed vaginal opening and in first vaginal estrus, a decrease in the number of healthy ovarian follicles and an increase in follicular atresia. The ventral or dorsal hippocampus lesions also caused a significant decrease in the secretion of estradiol and progesterone, an increased plasma testosterone. Only DH-L group showed a significant decrease in serum FSH concentrations compared to their respective control groups.

DISCUSSION

These results show for the first time that the hippocampus participates in a stimulatory manner, that could overcome the gonadotropic control by acting by a neural connection to the gonads giving a novel integrative mechanism between learning processes with neuroendocrine mechanism regulating the ovary function.

摘要

引言

下丘脑 - 垂体 - 性腺轴受促性腺激素以及一条通向性腺的直接神经通路控制。新证据表明存在从海马体到下丘脑的神经连接,该连接可调节下丘脑功能。这可能是对与性腺之间调节良好的激素和神经连接的一种新控制,进而影响生殖。本研究的目的是分析雌性大鼠背侧或腹侧海马体独立损伤对青春期启动、卵泡生长以及性类固醇和促性腺激素血清浓度的影响。

方法

使用21日龄的CII - ZV品系青春期前雌性大鼠。通过立体定位手术,给予鹅膏蕈氨酸以造成腹侧(VH - L)或背侧(DH - L)海马体损伤。对照组为假手术组(VH - Sham和DH - Sham),第五组作为绝对对照组。在30日龄时,所有组均进行新物体识别测试(NORT)。

结果

使用NORT进行记忆测试的数据显示,与各自的假手术对照组和绝对对照组相比,VH - L组和DH - L组动物的短期和长期记忆均有所下降。同样,受伤大鼠出现阴道开口延迟和首次阴道发情延迟,健康卵巢卵泡数量减少,卵泡闭锁增加。腹侧或背侧海马体损伤还导致雌二醇和孕酮分泌显著减少,血浆睾酮增加。与各自对照组相比,仅DH - L组血清促卵泡生成素(FSH)浓度显著降低。

讨论

这些结果首次表明,海马体以刺激的方式参与其中,通过与性腺的神经连接发挥作用,可能克服促性腺激素的控制,从而在学习过程与调节卵巢功能的神经内分泌机制之间形成一种新的整合机制。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5cd2/12040663/3ce063653a0e/fendo-16-1530692-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5cd2/12040663/f967ce572c35/fendo-16-1530692-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5cd2/12040663/0214b5890434/fendo-16-1530692-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5cd2/12040663/81cccb1fe940/fendo-16-1530692-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5cd2/12040663/e743c2b04250/fendo-16-1530692-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5cd2/12040663/3ce063653a0e/fendo-16-1530692-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5cd2/12040663/f967ce572c35/fendo-16-1530692-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5cd2/12040663/0214b5890434/fendo-16-1530692-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5cd2/12040663/81cccb1fe940/fendo-16-1530692-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5cd2/12040663/e743c2b04250/fendo-16-1530692-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5cd2/12040663/3ce063653a0e/fendo-16-1530692-g005.jpg

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