Expression of the MYL2 gene in the development of rat testis tissue / 中华男科学杂志

<p><b>Objective</b>To study the expression of the gene of myosin regulatory light chain-2 (MYL2) in the development of rat testis tissue.</p><p><b>METHODS</b>Using real-time PCR and immunohistochemistry, we determined the mRNA transcription level and protein expression of MYL2 in the rat testis.</p><p><b>RESULTS</b>The mRNA expression of the MYL2 gene changed in an age-dependent manner, reaching the highest value on postnatal day (PND) 2, then dropped rapidly till PND 8, increased slowly on PNDs 10 and 12, decreased on PND 14, rose slightly from PND 15 and rapidly on PNDs 20 and 25, and declined slowly from PND 65. Immunohistochemistry showed that the MYL2 protein was mainly expressed in testicular sperm cells.</p><p><b>CONCLUSIONS</b>The MYL2 gene may be involved in the proliferation of spermatogonial stem cells and the process of sperm cells developing into mature sperm.</p>

Effect of dopamine receptor agonist apomorphine on scopolamine induced memory deficits in mice / 中国应用生理学杂志

<p><b>OBJECTIVE</b>To research the mechanism of dopamine (DA) controlled memory in mice.</p><p><b>METHODS</b>Mice received i.p. injection of scopolamine (0.3 mg/kg, SCOP 0.3, and 3.0mg/kg, SCOP 3.0, respectively, n = 10) and saline (NS, n = 10) for 60 days in experiment 1. Memory of mice was detected by dark avoidance behavior in the 53" d and the 60"' d. Animals were sacrificed after the memory test; brain tissues were processed for Fos-ir and TH-ir by immunohistochemistry. Mice were divided into four groups according results of expri-ment 1, they received i.p. injection of apomorphine (0.1 mg/kg, APO 0.1, 0.5 mg/kg, APO 0.5, and 2.0 mg/kg, APO2.0 respectively, n = 10).</p><p><b>RESULTS</b>Memory was inhibited in mice injected scopolamine 3.0 mg/kg. Latency was significantly less than in NS group, only 1/ 4 that of NS group (P > 0.05). The number of mistake of SCOP 3.0 group increased about four times than that of NS group (P > 0.05). But there was no difference of latency and number of mistake between SCOP 0.3 and NS group in expriment 1. Scopolamine-induced memory deficit was associated with decreased cellular activation, indicated by Fos immunoreactive (ir) staining, in NAcc CA1 and CA3 (P < 0.05), and also associated with decreases in the number of cells labeled for tyrosine hydroxylase (TH-ir), the rate limiting enzyme for dopamine conversion (P < 0.01) and the number of cells co-labeled for TH-ir/Fos-ir (P <0.01) in the ventral tegmental area(VTA), apomorphine lessened scopolamine-induced memory deficit in experiment 2. The number of cells co-labeled for TH-ir/Fos-ir (P <, 0.05) was increased in VTA after apomorphine treatment.</p><p><b>CONCLUSION</b>Apomorphine lessened scopolamine-induced memory deficit in mice by increasing DA activities in VTA.</p>