文拉法辛对慢性应激抑郁大鼠前额区可塑性相关蛋白mRNA表达的影响

目的：探讨文拉法辛对慢性应激抑郁大鼠前额区3种可塑性相关蛋白mRNA表达的影响。方法：用慢性不可预见应激（CUS）方法建立抑郁大鼠模型，给予2种剂量（5mg／kg和10mg／kg）的抗抑郁药物文拉法辛14d或28d，用逆转录-聚合酶链反应检测大鼠前额区脑源性神经营养因子（BDNF）、转录因子环磷腺苷反应元件结合蛋白（CREB）和神经细胞粘附分子（NCAM）mRNA表达的变化。结果：抑郁模型大鼠体质量增加量，蔗糖水消耗量和行为学测试均较正常组明显下降，提示抑郁模型大鼠在第28天建立成功。CUS28d后前额区BDNF、CREB和NCAM mRNA表达均较正常组明显降低（P〈0．05），5mg／kg文拉法辛组明显增加抑郁模型大鼠前额区3种可塑性相关蛋白mRNA的表达，10mg／kg文拉法辛组轻度降低抑郁模型大鼠前额区3种可塑性相关蛋白mRNA的表达。结论：文拉法辛在调节前额区神经可塑性时具有剂量依赖性，BDNF、CREB和NCAM在抑郁症病因和治疗中可能发挥着重要作用。     

不同剂量文拉法辛对抑郁模型大鼠海马区pCREB和BDNF表达的影响

目的探讨不同剂量文拉法辛对慢性应激抑郁大鼠海马区磷酸化转录因子环磷腺苷反应元件结合蛋白(pCREB)和脑源性神经营养因子(BDNF)表达的影响。方法用慢性不可预见应激(CUS)方法建立大鼠抑郁模型,按处理措施不同实验大鼠共分8组各10只,即正常对照组(NC)、抑郁模型组注射生理盐水0 d组(MD0)、14d组(MD1)及28 d组(MD2)、小剂量(5 mg/kg)抗抑郁剂文拉法辛治疗14 d组(LV1)及28 d组(LV2)、大剂量(10mg/kg)文拉法辛治疗14 d组(HV1)及28 d组(HV2)。用免疫组织化学和Western Blot方法检测大鼠海马区pCREB和BDNF表达的情况。结果抑郁模型组(MD0、MD1、MD2)大鼠海马区pCREB和BDNF阳性细胞数目和积分光密度(IOD)均显著低于NC组(P均<0.05),5 mg/kg文拉法辛明显增加大鼠海马区pCREB和BDNF的表达(P<0.05),但10 mg/kg文拉法辛对海马区pCREB和BDNF表达的影响无统计学意义(P>0.05)。结论文拉法辛在5 mg/kg剂量时调节海马区的神经可塑性,pCREB和BDNF可能在抑郁症发生机制中发挥重要的作用。     

文拉法辛对抑郁症模型大鼠海马神经元细胞凋亡的影响

目的 探讨文拉法辛对抑郁症模型大鼠海马神经元细胞凋亡相关基因表达的影响.方法 将SD大鼠随机分为抑郁模型组、文拉法辛干预组和正常对照组.以慢性轻度不可预见性的应激结合孤养建立抑郁症动物模型,应激同时文拉法辛干预组给予文拉法辛(15mg/kg)、抑郁模型组给予蒸馏水灌胃干预.采用敞箱实验和糖水消耗实验观察大鼠行为改变.用逆转录聚合酶链反应(RT-PCR)检测海马神经元细胞凋亡相关基因Bax、Bel-xl mRNA表达情况.结果 抑郁模型组与正常对照组比较,抑郁模型组海马神经元细胞Bax mRNA表达升高[(1.97±0.79)vs(1.28 4±0.49),P<0.01],Bcl-xl mRNA表达降低[(1.06 4±0.42)vs(1.51±0.48),P<0.01];与抑郁模型组比较,文拉法辛干预组海马神经元细胞Bax mRNA表达降低[(1.61±0.68)vs(1.97±0.79),P<0.05],Bcl-xl mRNA表达升高[(1.39±0.51)vs(1.06±0.42),P<0.05].结论 抑郁症模型大鼠存在海马损害,而文拉法辛对Bax mRN和Bcl-xl mBNA的表达具有干预作用,这可能为文拉法辛对抑郁症海马损害具有保护作用的机制之一.     

银杏叶提取物联合盐酸文拉法辛对抑郁大鼠海马BDNF表达及行为学改变的影响

目的　进一步研究抑郁的发病机制 ,探讨银杏叶提取物 (EGb)及盐酸文拉法辛 (venlafaxine)在抑郁治疗中的作用及机理。方法　采用慢性综合应激法建立抑郁大鼠模型。观察抑郁大鼠经不同药物治疗前后的行为学变化及脑源性神经营养因子 (BDNF)的免疫组织化学改变。结果　抑郁大鼠海马CA3区BDNF表达显著减弱 ,开场行为中探究行为减少 ,排便增多 ;EGb及venlafaxine联合给药 2 8天后 ,与其他给药组相比 ,大鼠海马CA3区BDNF表达增强 ,探究行为增多 ,排便量减少。结论　慢性综合应激致抑郁大鼠存在脑损伤 ,EGb及venlafaxine联合用药可能通过保护神经元、减轻脑损伤而达到抗抑郁作用。     

山奈酚对阿尔茨海默病模型大鼠的治疗作用及CREB/BDNF信号通路的影响

目的 探究山奈酚对阿尔茨海默病模型大鼠的治疗作用及环磷酸腺苷(Cyclic adenosine monophosphate, cAMP)反应元件结合蛋白(Response element binding protein, CREB)/脑源性神经营养因子(Brain-derived neurotrophic factor, BDNF)信号通路的影响。方法 构建阿尔茨海默病模型大鼠，将建模成功的48只大鼠随机分为模型组、山奈酚低(25 mg/kg)、高(50 mg/kg)剂量组、盐酸多奈哌齐(0.9 mg/kg)组，每组各12只，另选取12只健康大鼠作为对照组，各组大鼠每天给予相应药物干预1次，连续28 d;检测大鼠行为学表现、海马组织病理学变化、海马组织中肿瘤坏死因子(Tumor necrosis factor, TNF)-α、白细胞介(Interleukin, IL)-1β、IL-6,CREB,BDNF信使RNA(Messenger RNA,mRNA)和蛋白水平。结果 对照组大鼠海马组织神经元结构正常，排列规则；与对照组比较，模型组大鼠海马神经元排列紊乱，核固缩，大量神经元变性坏死，逃...     

成年大鼠局灶脑缺血/再灌注后海马BDNFmRNA和bFGF mRNA的动态变化研究

目的观察局灶脑缺血/再灌注大鼠海马脑源性神经营养因子(brain derived neurotrophic factor,BDNF)mRNA和碱性成纤维生长因子(basic fibroblast growth factor,b FGF)mRNA的动态表达。方法将108只雄性Wistar大鼠随机分为正常组(NC组)、假手术组(SC组)、模型组(I/R组),每组再于缺血1h后再灌注于1,3,7,14,21,28d六个时间点进行观察,正常组和假手术组于相应时间点同步观察。采用线栓法制备大鼠右侧大脑中动脉局灶脑缺血/再灌注模型。应用原位杂交法检测大鼠缺血再灌注后1,3,7,14,21,28d缺血侧海马BDNF mRNA和b FGF mRNA表达。结果正常海马区可见少量BDNF mRNA和b FGF mRNA的阳性表达。BDNF mRNA阳性反应主要集中于齿状回颗粒细胞以及CA2、CA3中的锥体细胞胞浆中,b FGF mRNA主要位于海马锥体细胞层、CA1、CA2区。局灶脑缺血/再灌注后,I/R组缺血侧海马BDNF mRNA表达增加,主要见于齿状回颗粒细胞层和锥体细胞层。缺血/再灌注后1d时BDNF mRNA阳性反应即有增多,3d时达到高峰(P0.01),阳性产物染色较深,7d后迅速下降(P0.01),28d时接近正常水平。局灶脑缺血/再灌注后,I/R组缺血侧海马可见b FGF mRNA的强阳性表达,1d时开始增加(P0.05),3d即达一小高峰(P0.01),7d开始下降,21d时明显下降,28d时降到正常水平(P0.05)。结论局灶脑缺血/再灌注可上调BDNF mRNA和b FGF mRNA的表达,有利于脑缺血后神经功能恢复,具有神经保护作用。     

氟西汀对卒中后抑郁大鼠海马脑源性神经营养因子表达的影响

目的 分析卒中后抑郁（post-stroke depression，PSD）模型大鼠海马脑源性神经营养因子（Brainderived neurotrophic factor，BDNF）蛋白及mRNA表达水平，及抗抑郁剂氟西汀干预后BDNF表达水平的变化，初步探讨BDNF在PSD发生中的作用。方法 大脑中动脉阻塞（Middle cerebral artery occlusion，MCAO）法建立局灶脑缺血模型，加用慢性不可预见温和应激（Chronic unpredictable mild stress，CUMS）结合孤养，建立PSD大鼠模型，并予以氟西汀干预。应用蛋白免疫印迹（Western-blot）、Real time-PCR分别检测应激18、28 d时海马BDNF蛋白及mRNA表达水平。结果 与对照组相比，应激14d后PSD组较对照组大鼠体重与糖水消耗比例降低，水平、垂直试验得分下降（P <0.05或P <0.01）。氟西汀干预组糖水消耗比例，水平、垂直试验得分均较PSD组显著增加（P <0.05或P <0.01）。第18、28天，PSD组BDNF蛋白水平较对照组均显著下降（P <0.05或P <0.01）。PSD组BDNF mRNA的表达在应激18d时较正常组有下降趋势，但无统计学意义；至28 d时，表达含量明显下降，差异有统计学意义（P <0.01）。第18、28天，氟西汀干预组BDNF蛋白及mRNA水平均较PSD组显著增加（P <0.01）。结论 应用MCAO模型联合CUMS加孤养模型制备的PSD大鼠模型在神经功能缺损的同时，表现快感缺乏和探索行为减少的抑郁核心症状，并且体重的增长幅度显著减慢。PSD大鼠海马BDNF蛋白及mRNA表达水平显著降低，氟西汀干预后BDNF表达水平上升，初步提示BDNF在卒中后抑郁发生中的作用。     

慢性应激抑郁大鼠海马CA1神经元突触可塑性研究

目的 探讨慢性轻度不可预见应激(chronic unpredictable mild stress,CUMS)抑郁模型大鼠海马CA1区神经元的突触可塑性改变.方法 将20只雄性Sprague-Dawley (SD)大鼠随机等分为CUMS组和对照组,前者连续28天每天随机接受不同的应激,对照组同样条件下饲养但不给应激,至第28天进行行为测评后处死,在日立(H7500)透射电镜下测量海马CA1神经元突触界面结构参数.结果 CUMS抑郁大鼠海马CA1神经元突触活性区长度(216.64±20.19 nm)及突触后致密物厚度(42.4±5.23 nm)显著小于对照组(321.58±12.27nm,69.6±4.77 nm),差异有统计学意义(P＜0.05),突触界面曲率及宽度与对照组差异无统计学意义(P＞0.05).结论 慢性应激性抑郁大鼠存在海马CA1区神经元突触可塑性的改变.这提示抑郁症的发病机制可能与海马神经元突触可塑性相关.     

5-羟色胺1A受体激动剂8-OH-DPAT对癫痫合并抑郁大鼠的干预作用及其机制研究

目的 探讨5-羟色胺1A(5-HT1A)受体激动剂8-OH-DPAT对癫痫合并抑郁大鼠的干预作用及其机制.方法 成年级SD大鼠160只,随机选取8只为正常对照组,其余大鼠采用匹罗卡品诱导慢性癫痫大鼠模型.25 d后通过体质量与摄食量测量及旷场试验筛选出癫痫合并抑郁模型大鼠32只,随机分为模型组、卡马西平(CBZ)组、CBZ+ 8-OH-DPAT低剂量组(8-OH-DPAT低剂量组)及CBZ+ 8-OH-DPAT高剂量组(8-OH-DPAT高剂量组);分别给予CBZ 100 mg/kg、CBZ +8-OH-DPAT 0.1mg/(kg·d)、CBZ+ 8-OH-DPAT 1 mg/(kg·d).连续治疗7d后,进行癫痫发作的Racine分级、体质量、摄食量测量及旷场试验;采用荧光实时定量聚合酶链反应测定大鼠海马齿状回神经生长因子(NGF) mRNA表达,免疫组化染色观察苔藓纤维出芽(M FS).结果 治疗后,与正常对照组比较,模型组、CBZ组、8-OH-DPAT低、高剂量组的体质量与摄食量明显下降,海马NGF mRNA表达与Timm评分明显增高(均P＜0.05).与模型组比较,CBZ组、8-OH-DPAT低、高剂量组的体质量、摄食量及旷场试验评分明显提高,Racine分级、海马NGF mRNA表达与Timm评分明显下降(均P＜0.05);其中8-OH-DPAT高剂量组上述改变更明显(均P＜0.05).结论 高剂量的5-HT1A受体激动剂8-OH-DPAT能抑制癫痫合并抑郁大鼠海马齿状回的MFS和神经生长因子的表达,促进海马神经重塑.这可能是5-HT1A受体激动剂抗癫痫、抗抑郁的分子机制之一.     

远志总皂苷对阿尔茨海默病模型大鼠海马脑源性神经营养因子及酪氨酸蛋白激酶B表达的影响

目的观察远志总皂苷对阿尔茨海默病模型大鼠海马CA1区脑源性神经营养因子(BDNF)及其特异性受体酪氨酸蛋白激酶B(TrkB)表达的影响,探讨远志总皂苷对阿尔茨海默病的干预作用机制。方法雄性Wistar大鼠被随机分为生理盐水组(正常对照组)、阿尔茨海默病模型组(模型组),以及远志总皂苷低剂量(12.50 mg/ml)和高剂量(37.50 mg/ml)组;采用D-半乳糖致衰老联合鹅膏覃氨酸损毁基底前脑Meynert核法建立阿尔茨海默病大鼠模型,免疫组织化学染色检测大鼠海马CA1区BDNF及其受体TrkB表达水平。结果 BDNF和TrkB阳性物质呈棕黄色,主要表达于海马CA1区神经元胞膜。模型组大鼠海马CA1区BDNF及其受体TrkB表达水平为0.30±0.02和0.21±0.07,低于正常对照组的0.47±0.02和0.46±0.05(均P=0.000);与模型组相比,远志总皂苷低剂量组(0.35±0.05,0.32±0.07)和高剂量组(0.43±0.05,0.37±0.03)大鼠海马CA1区BDNF及其受体TrkB表达水平均显著升高(均P=0.000),但以高剂量组升高更为显著(均P=0.000)。结论远志总皂苷可以显著升高阿尔茨海默病模型大鼠海马CA1区BDNF及其受体TrkB表达水平,且具有剂量依赖性,这可能是其改善认知功能的机制之一。     

Regulation of brain-derived neurotrophic factor (BDNF) in the chronic unpredictable stress rat model and the effects of chronic antidepressant treatment

Chronic unpredictable stress (CUS) is a widely used animal model of depression. The present study was undertaken to investigate behavioral, physiological and molecular effects of CUS and/or chronic antidepressant treatment (venlafaxine or imipramine) in the same set of animals. Anhedonia, a core symptom of depression, was assessed by measuring consumption of a palatable solution. Exposure to CUS reduced intake of a palatable solution and this effect was prevented by chronic antidepressant treatment. Moreover, chronic antidepressant treatment decreased depressive-like behavior in a modified forced swim test in stressed rats. Present evidence suggests a role for brain-derived neurotrophic factor (BDNF) in depression. BDNF mRNA levels in the ventral and dorsal hippocampus were assessed by in situ hybridization. Exposure to CUS was not correlated with a decrease but rather with an increase in BDNF mRNA expression in both the dentate gyrus of the dorsal hippocampus and the CA3 region of the ventral hippocampus indicating that there is no simple link between depression-like behaviors per se and brain BDNF levels in rats. However, a significant increase in BDNF mRNA levels in the dentate gyrus of the dorsal hippocampus correlated with chronic antidepressant treatment emphasizing a role for BDNF in the mechanisms underlying antidepressant activity.     

Chronic Administration of Bacopa Monniera Increases BDNF Protein and mRNA Expressions: A Study in Chronic Unpredictable Stress Induced Animal Model of Depression

Objective

The present study aimed to investigate whether graded doses of Bacopa Monniera (BM) extract could produce antidepressant-like effects in chronic unpredictable stress (CUS) induced depression in rats and its possible mechanism(s).

Methods

Rats were subjected to an experimental setting of CUS. The effect of BM extract treatment in CUS-induced depression was examined using behavioral tests including the sucrose consumption, open field test and shuttle box escape test. The mechanism underlying the antidepressant-like action of BM extract was examined by measuring brain-derived neurotrophic factor (BDNF) protein and mRNA expression in brain tissues of CUS-exposed rats.

Results

Exposure to CUS for 4 weeks caused depression-like behavior in rats, as indicated by significant decreases in sucrose consumption, locomotor activity and escape latency. In addition, it was found that BDNF protein and mRNA levels in the hippocampus and frontal cortex were lower in CUS-treated rats, as compared to controls. Daily administration of the graded doses of BM extract during the 4-week period of CUS significantly suppressed behavioral changes and attenuated the CUS-induced decrease in BDNF protein and mRNA levels in the hippocampus and frontal cortex.

Conclusion

The results suggest that BM extract alleviates depression induced by CUS. Present study also confirms that 80-120 mg/kg doses of BM extract have significantly higher antidepressant-like activity.     

Synergetic effects of quetiapine and venlafaxine in preventing the chronic restraint stress-induced decrease in cell proliferation and BDNF expression in rat hippocampus

Clinical studies show better response rates of patients with depression and schizophrenia to combinations of atypical antipsychotics and antidepressants, compared to responses to either type of drugs alone. Animal studies demonstrate that some antipsychotics and antidepressants increase neurogenesis and BDNF expression in the hippocampus, which is reduced in volume in patients with depression or schizophrenia. We hypothesized that the better therapeutic effects of combined treatment seen in schizophrenia and depression patients are related to the additive or synergistic effects of combined treatment on hippocampal neurogenesis and BDNF expression. To test this hypothesis, we investigated the effects of chronic administration of quetiapine, venlafaxine, and their combination, on hippocampal cell proliferation and BDNF expression in rats, when subjected to chronic restraint stress (CRS) during the last 2 weeks of a 3-week drug administration period. We found (1) CRS decreased hippocampal cell proliferation and BDNF expression; (2) chronic administration of quetiapine or venlafaxine dose-dependently prevented these decreases in hippocampal cell proliferation and BDNF expression caused by CRS (6 h/day for 14 days); (3) the combination of lower doses of quetiapine (5 mg/kg) and venlafaxine (2.5 mg/kg) increased hippocampal cell proliferation and prevented BDNF decrease in stressed rats, whereas each of the drugs exerted mild or no effects; (4) individual higher doses of quetiapine (10 mg/kg) or venlafaxine (5 mg/kg) exerted effects comparable to those produced by their combination. These results support our hypothesis and can lead to future studies to develop new therapeutic approaches for treatment-resistant depression and the negative symptoms of schizophrenia.     

脑缺血与慢性应激对依赖海马的学习记忆的影响

目的 对比脑缺血与慢性应激所致认知损害及海马病变的强弱,为临床改善脑卒中后认知障碍(poststroke cognitive impairment,PSCI)提供参考.方法 40只成年雄性SD大鼠平均分为4组:对照组、应激组、缺血组与缺血加应激组,缺血手术采用改良的选择性大脑中动脉栓塞术;应激处理采用连续3周的慢性不可预见性温和应激;Moms水迷宫实验评价依赖海马的学习记忆功能;免疫组织化学染色及半定量RT-PCR观察海马CA3区脑源性神经营养因子(brain-derived neurotrophic factor,BDNF)的表达变化.结果 应激或缺血均可使大鼠学习功能明显下降,表现为与同时点对照组比较,逃避潜伏期显著延长,二者的综合作用更明显.慢性应激对学习功能的影响强于脑缺血损伤.应激或缺血均减弱记忆功能,但二者的作用差异无统计学意义.与对照相比,缺血显著增加海马CA3区BDNF的表达(27.0±2.5与20.1±2.1),应激降低BDNF的表达(15.2±1.8与20.1±2.1),二者综合作用仍显著降低BDNF的表达(8.2±1.5),差异均具有统计学意义(F=52.87,P＜0.05).结论 缺血与应激均降低大鼠学习记忆功能,应激对认知功能的损害高于缺血,而缺血与应激的综合作用对认知功能损害与抑制BDNF表达作用更明显,提示进行PSCI的综合治疗时,要重视心理社会应激干预和抑郁状态的改善.     

The effects of fluoxetine on oligodendrocytes in the hippocampus of chronic unpredictable stress-induced depressed model rats

Depression is a mental illness which is harmful seriously to the society. This study investigated the effects of fluoxetine on the CNPase⁺ oligodendrocytes in hippocampus of the depressed rats to explore the new target structure of antidepressants. Male Sprague–Dawley rats were used to build chronic unpredictable stress (CUS) depressed model of rats. Then, the depressed rats were divided into the CUS standard group and the CUS + fluoxetine (CUS/FLX) group. The CUS/FLX group was treated with fluoxetine at dose of 5 mg/(kg·d) from the fifth week to seventh week. After 7 weeks CUS intervention, the sucrose preference of the CUS standard group was significantly lower than that of the control group and the CUS/FLX group. The stereological results showed that the total number of the CNPase⁺ cells in the CA1, CA3, and DG subfield of the hippocampus in the CUS standard group were significantly decreased, when compared with the CNPase⁺ cells in the control group. However, the total number of the CNPase⁺ cells in the CA1 and CA3 subfield of the hippocampus in the CUS standard group was significantly decreased when it compared with CNPase⁺ cells in the CUS/FLX group. Therefore, fluoxetine might prevent the loss of CNPase⁺ oligodendrocytes in CA1 and CA3 subfields of hippocampus of the depressed rats. The oligodendrocytes in hippocampus may play an important role in the pathogenesis of depression. The current result might provide structural basis for the future studies that search for new antidepressant strategies.     

Exercise restores levels of neurotrophins and synaptic plasticity following spinal cord injury

We have conducted studies to determine the potential of exercise to benefit the injured spinal cord using neurotrophins. Adult rats were randomly assigned to one of three groups: (1) intact control (Con); (2) sedentary, hemisected at a mid-thoracic level (Sed-Hx), or (3) exercised, hemisected (Ex-Hx). One week after surgery, the Ex-Hx rats were exposed to voluntary running wheels for 3, 7, or 28 days. BDNF mRNA levels on the lesioned side of the spinal cord lumbar region of Sed-Hx rats were approximately 80% of Con values at all time points and BDNF protein levels were approximately 40% of Con at 28 days. Exercise compensated for the reductions in BDNF after hemisection, such that BDNF mRNA levels in the Ex-Hx rats were similar to Con after 3 days and higher than Con after 7 (17%) and 28 (27%) days of exercise. After 28 days of exercise, BDNF protein levels were 33% higher in Ex-Hx than Con rats and were highly correlated (r=0.86) to running distance. The levels of the downstream effectors for the action of BDNF on synaptic plasticity synapsin I and CREB were lower in Sed-Hx than Con rats at all time points. Synapsin I mRNA and protein levels were higher in Ex-Hx rats than Sed-Hx rats and similar to Con rats at 28 days. CREB mRNA values were higher in Ex-Hx than Sed-Hx rats at all time points. Hemisection had no significant effects on the levels of NT-3 mRNA or protein; however, voluntary exercise resulted in an increase in NT-3 mRNA levels after 28 days (145%). These results are consistent with the concept that synaptic pathways under the regulatory role of BDNF induced by exercise can play a role in facilitating recovery of locomotion following spinal cord injury.     

Region-specific response of the hippocampus to chronic unpredictable stress

The objective of the present study was to determine whether chronic unpredictable stress (CUS) would induce hippocampal neuroplasticity in a region-specific manner. Recent evidence suggests that the hippocampus has two functionally distinct subsections. The dorsal (septal) portion appears to be primarily associated with spatial navigation, while the ventral (temporal) region has been linked to affect-related functions, such as anxiety. Chronic stress has previously been shown to negatively affect the hippocampus by decreasing survival of progenitor cells, although it has also been shown to increase adaptive responses, such as increased expression of neuropeptide Y (NPY) and ΔFosB. Whether such events occur in a region-specific manner has not been investigated. We hypothesized that CUS would selectively impact cell survival, NPY, and ΔFosB expression in the more affect-related ventral subregion. Individually housed Long-Evans rats (n = 31) were divided into two groups: stressed and control. Stressed animals were exposed daily to an unpredictable schedule of ethologically relevant stressors, such as predator odors, forced swim, and open field exposure. All rats were injected with bromodeoxyuridine (BrdU) daily during the first 5 days of CUS in order to label dividing progenitor cells. Unbiased stereology was used to quantify BrdU+, NPY+, and ΔFosB+ cells in dorsal and ventral hippocampal subregions. In support of our hypothesis, we found that CUS selectively decreased cell survival in the ventral subregion. However, both NPY and ΔFosB were significantly increased only in the dorsal hippocampus. These results suggest that stress-induced adaptive neuroplasticity occurs primarily in the dorsal subregion, which may coincide with behavioral aspects of the stress response, such as avoidance or amelioration of the stressor.