Objective To explore the effects of exercise on dentate gyrus (DG) neLuogenesis and the ability of learning and memory in hippocampus-lesioned adult rats.Methods Hippocampus lesion was produced by intrahippocampal microinjection of kainic acid (KA).Bromodeoxyuridine (BrdU) was used to label dividing cells.Y mae test was used to evaluate the ability of learning and memory.Exercise was conducted in the form of forced running in a motor-driven running wheel.The speed of wheel revolution was regulated at 3 kinds of intensity:lightly running, modemtely running,or heavily running.Resutts Hippocampus lesion could increase the number of BrdU-labeled DG cells,moderately running after lesion could further enhance the number of BrdU-laheled cells and decrease the error number (EN) in Y maze test,while neither lightly running,nor heavily running had such effects.There was a negative conelation beiween the numberof DG BrdU-labeled cells and the EN in the Y maze test after running.Condusion Moderate exercise could enhance the DG neurogenesis and ameliorate the ability of learning and memory in hippocampus-lesioned rats.

To explore the potential role of norepinephrine (NE) and nitric oxide (NO)in activities of rat hypothalamus arginine vasopressin (AVP) neurons in response to immune challenge, we observed the effect of prazosin,an antagonist of α1-adrenergic receptor, and the specific nitric oxide synthase (NOS) inhibitor Nwnitro-L-arginine-methylester (L-NAME) on the Fos expression in AVP neurons induced by systemic lipopolysaccharide (LPS) using double immunohistochemistry. Intravenous (i.v.) injection of LPS induced Fos expression in AVP neurons mainly in the hypothalamus paraventricular nucleus (PVN) and in the supraoptic nucleus (SON).The percentage of Fos-positive AVP neurons was dose-dependent. Pretreatment with prazosin (5mg/kg) effectively suppressed the Fos expression induced by LPS (5μg/kg), whereas L-NAME(30 mg/kg)did not influence the Fos expression in the AVP neurons induced by LPS (0.25,0.5,1,5μg/kg). Our results suggest that the activation of central AVP neurons caused by systemic LPS may be mediated by NE through α1-adrenergic receptors, but could not be changed by NO.

The effect of peripheral hypertonic stimulation on the neurons of hypothalamic paraventricular nucleus(PVN)was investigated in the present study with both electrophysiological and immunocytochemical methods.The discharge frequency of the neurons with phasic activity in PVN could be increased by intraperitoneal (i.p.)injection of hypertonic saline (HS,1.5M NaCl)(from 2.8±0.5 Hz to 5.4±0.9 Hz,P<0.001).The Fos expression in PVN could be enhanced (from 21.2±12.9 to 217.3±38.5 Fos-positive neurons,P<0.001)by i.p.HS and the majority of AVP-positive neurons expressing Fos (91.7±3.6%) was in magnocellular subdivision of PVN. After intracerebroventricular(i.c.v.)injection of losartan, angiotensin Ⅱtype 1(AT1) receptor antagonist(5μg/μl),the excitatory effect of peripheral hypertonic stimulation on PVN neurons with phasic activity was inhibited significantly, and the number of the neurons co-expressing Fos and AVP in PVN decreased significantly (P<0.001) as well.The result demonstrated that the vasopressinergic neurons in PVN could be excited by peripheral hypertonic stimulation, and this excitation might be mediated by angiotensin Ⅱ fibers projecting from subfornical organ to PVN.

目的 用6-OHDA分别选择性地损毁外周和中枢的去甲肾上腺素（NE）能系统，探讨去甲肾上腺素能系统在冷应激诱导大鼠NK细胞活性下降中的作用。方法 大鼠置于4℃的冷室4h。腹腔和侧脑室分别注射6-OHDA。采用YAC-1细胞51Cr释放法测定脾脏NK细胞的活性。用免疫细胞化学法观察下丘脑室旁核（PVN）和脑干蓝斑（LC）中的Fos表达，以及Fos表达阳性的神经元的性质。用放射免疫法测定血浆CORT的浓度。结果 脑室注射6-OHDA能部分翻转冷应激诱导的血浆CORT浓度的升高，减少PVN和LC中Fos的表达，同时使脾脏NK细胞活性不再下降。同样，腹腔注射6-OHDA也能翻转冷应激诱导NK细胞活性的下降，但对脑内Fos表达没有明显影响。另外，双染实验表明，PVN中有少量的Fos阳性的神经元同时表达精氨酸加压素（AVP）或催产素（OT），而LC中大多数Fos阳性的神经元同时表达酪氨酸羟化酶（TH）。结论 冷应激诱导大鼠NK细胞活性下降的可能机制是：一方面通过中枢去甲肾上腺素能系统去激活HPA轴;另一方面介导外周交感神经系统。最后两者共同作用于脾脏NK细胞，导致其活性下降。

The aim of the present study is to investigate the mechanisms of suppression of splenic natural killer(NK)cytotoxicity caused by cold stress, using 6-hydroxydopamine (6-OHDA) as chemical sympathectomy. The NK activity was measured by 51chromium release assay.Central sympathectomy with intracerebroventricular (i.c.v.) injection of 6-OHDA reduced significantly the elevation of plasma corticosterone level, the expression of Fos in hypothalamic paraventricular nucleus and in locus coeruleus, as well as the suppression of NK activity induced by cold stress at 4℃ for 4h. Peripheral sympathectomy with intraperitoneal (i.p.)injection of 6-OHDA and blockade of β- adrenergic receptor with i.p. injection of propranolol also reversed the cold stress-induced suppression of NK cytotoxicity, but without significant effect on Fos expression in brain. The results suggest that the activation of hypothalamic–pituitary–adrenal axis induced by cold stress might be mediated, at least partially, by central noradrenergic system, and that the cold stress-induced suppression of NK cytotoxicity might be mediated by the activation of peripheral sympathetic nerve.