## 4 Discussion
It was reported to move the sperm from the seminiferous tubules to the epididymis [30]. DEX administration to Leydig cells isolated from rats inhibited testosterone synthase activities, such as 3\(\beta\)HSD [9]. \(\alpha\)2A-adrenergic receptors and imidazoline receptors are present in the cytoplasm of testicular cells and are thought to be functional. DEX is a stable formulation of dexmedetomidine hydrochloride in saline between pH 4.5 and 7.0. Dexmedetomidine hydrochloride changes to fat-soluble DEX depending on blood pH [31]. Therefore, it is thought that it also reacts with receptors present in the cytoplasm. This study is the first to examine the localization of \(\alpha\)2A-adrenergic receptors and imidazoline receptors in the testis. In this study, a decrease in pituitary LH and FSH mRNA expression after DEX administration was observed. Gonadotropin-releasing hormone (GnRH), which is secreted from the medial preoptic area of the hypothalamus and arcuate nucleus, stimulated the secretion of LH and FSH from the pituitary gland. Hunger stress increased the release of renal corticotropin-releasing hormone (CRH) produced in the paraventricular nucleus via \(\alpha\)2-adrenergic receptors of the hypothalamus and suppressed GnRH [32]. The administration of noradrenaline to the paraventricular nucleus of normal rats reduced LH [33]. Furthermore, the administration of \(\alpha\)2-adrenergic receptor agonists inhibited GnRH and LH in fasting stress-induced LH suppression experiments [34]. These findings suggest that noradrenergic neurons entering the paraventricular nucleus suppress GnRH and LH via CRH [32]. It was reported that the administration of clonidine, an \(\alpha\)2A-adrenergic receptor agonist similar to DEX, to the paraventricular nucleus of the hypothalamus in rats significantly decreased plasma LH concentrations [33; 35; 36]. Therefore, it is thought that LH and FSH mRNA expression also decreased because GnRH was suppressed by noradrenaline and CRH stimulation. GnRH and CRH should also be investigated in the future. The number of \(\alpha\)2-adrenergic receptors is known to be inversely related to noradrenaline levels, as adrenergic receptors are downregulated throughout the brain in the presence of high agonist concentrations [37; 38]. However, in adrenalectomized rats, \(\alpha\)2-adrenergic receptors are decreased in the paraventricular nucleus but increased in the supraoptic nucleus [39]. The short-term and long-term administration of cortisol to tree shrews also decreased the hypothalamic \(\alpha\)2-adrenergic receptor expression in the short term and increased it in the long term [40]. Thus, \(\alpha\)2-adrenergic receptor expression is regulated by adrenal hormones and noradrenaline. Since the expression of \(\alpha\)2-adrenergic receptors differs depending on each part of the brain, the treatment period, and the treatment concentration, it was found that in the case of the pituitary gland in this study, administration of 10 \(\mu\)g/kg DEX increased the mRNA expression of \(\alpha\)2-adrenergic receptors. The absence of changes in \(\alpha\)2-adrenergic receptor mRNA following the administration of 40 \(\mu\)g/kg DEX compared to that of 10 \(\mu\)g/kg DEX may be due to the presence of high concentrations of the agonist [37; 38]. The half-life of DEX in the blood is only 2.36-2.91 h. In mice, the blood concentration of DEX decreased to about 0.1 fmol/mL in 6 h in the 40 \(\mu\) group. Since DEX has such a short half-life, the expression of \(\alpha\)2-adrenergic receptor was transiently increased, while the expression of LH and FSH was decreased, but it recovered quickly. In a study of Leydig cells (0.05 \(\times\) 10\({}^{6}\) cells/well) isolated from rats, DEX administration (approximately 3.6-360 \(\mu\)g/L) inhibited testosterone synthase activity in a dose-dependent manner [9]. It also increased cells undergoing apoptosis [9]. However, in this study, administration of DEX (40 \(\mu\)g/kg) to normal mice had no effect on blood testosterone levels.