不同频率电针足三里对运动大鼠腓肠肌核因子-κB、血清肿瘤坏死因子-α和白细胞介素-1β的影响

目的研究不同频率电针对运动大鼠腓肠肌核因子(NF)-κB、血清肿瘤坏死因子(TNF)-α和白细胞介素(IL)-1β的影响。方法采用Bedford渐增负荷跑台跑运动模型,用韩式电针仪对运动性疲劳大鼠双侧足三里穴进行2/15 Hz、2/100 Hz两种不同频率的刺激,观察血清睾酮/皮质酮比值、腓肠肌NF-κB含量、血清TNF-α和IL-1β含量的变化。结果 1与安静对照组比较,运动组大鼠血清睾酮/皮质酮比值显著降低(P0.05,P0.01);2运动组大鼠腓肠肌NF-κB、血清TNF-α和IL-1β显著升高(P0.05,P0.01);3运动+2/15 Hz电针组和运动+2/100 Hz电针组两组大鼠腓肠肌NF-κB、血清TNF-α和IL-1β与运动后60 min组比较差异显著(P0.05,P0.01);4运动+2/15 Hz电针组大鼠腓肠肌NF-κB、血清TNF-α和IL-1β与运动+2/100 Hz电针组比较,差异显著(P0.05,P0.01)。结论 1急性运动后可显著增加大鼠腓肠肌NF-κB、血清TNF-α和IL-1β含量;2不同频率电针均可降低急性运动后大鼠腓肠肌NF-κB、血清TNF-α和IL-1β的含量;32/15 Hz可能是要筛选的电针消除运动性疲劳的最佳频率。     

帕金森病大鼠行为学评价体系的创建在电生理学中的应用

目的创建适宜Plexon信号采集系统的帕金森病(PD)大鼠行为学评价体系,对PD大鼠运动缺陷症状进行量化评测。方法选取成年雄性Wistar大鼠18只,随机分为对照组8只,实验组10只,实验组大鼠建立PD模型,有8只大鼠PD模型鉴定成功,2组大鼠手术置入脑内电极。2组大鼠使用自制跑步机、多通道在体记录系统分别进行最长运动时间、步频、失误次数和不连续运动频率量化评测,对9~30r/min旋转速度(转速)筛选,并组织学鉴定。结果与对照组大鼠比较,在20和30r/min转速评测中,实验组最长运动时间显著变短[(18.03±2.74)min vs(26.98±0.91)min;(3.33±1.45)min vs(26.67±0.71)min],失误次数显著增多[(7.50±0.76)次vs(1.50±0.43)次;(10.00±0.00)次vs(2.00±0.58)次],步频显著降低[(73.33±7.00)步/min vs(95.50±4.94)步/min;(76.33±7.41)步/min vs(110.33±7.58)步/min,P<0.05,P<0.01];在9和15r/min转速评测中,实验组最长运动时间、步频均无明显变化,差异无统计学意义(P>0.05);在9和30r/min转速评测中,实验组不连续运动频率显著降低,在15和20r/min转速评测中,实验组不连续运动频率显著升高[(2.00±0.31)次/min vs(0.70±0.21)次/min;(7.00±0.37)次/min vs(1.00±0.33)次/min,P<0.05,P<0.01]。结论行为学评价体系有效地评价了PD大鼠对高转速控制能力差,运动协调性差的运动缺陷症状,筛选出了12r/min为适宜的转速。     

颐脑解郁方对卒中后焦虑大鼠炎性因子及p38-MAPK信号蛋白表达的影响

目的探讨炎性因子及p38丝裂原活化蛋白激酶(p38-MAPK)信号蛋白与卒中后焦虑(PSA)的关系及颐脑解郁方的干预作用。方法采用不确定性空瓶饮水刺激复合脑缺血建立卒中后焦虑大鼠模型,随机分为模型组、治疗组,另设正常组、卒中组,每组15只。治疗组大鼠灌胃中药颐脑解郁方,正常组、卒中组、模型组大鼠常规饲养,灌胃生理盐水,连续灌胃4周。大鼠末次灌胃行旷场实验及高架十字迷宫相关检测后每组随机选择12只大鼠进行腹主动脉取血,采用放射免疫法检测血清肿瘤坏死因子-α(TNF-α)、白细胞介素-1α(IL-1α)、白细胞介素-6(IL-6)的含量;每组随机选择6只大鼠采用蛋白免疫印迹(Western Blot)法检测大鼠右侧(病侧)皮质及海马p38-MAPK蛋白的表达。结果旷场试验及高架十字迷宫结果显示,与正常组比较,卒中组水平及垂直运动次数减少(P<0.01),模型组、治疗组的水平及垂直运动次数、开放臂次数及时间均明显减少(P<0.05或P<0.01);与卒中组比较,模型组水平及垂直运动次数、开放臂次数及时间均减少(P<0.01);与模型组比较,治疗组水平及垂直运动次数、开放臂次数及时间均明显升高(P<0.05或P<0.01)。放射免疫法检测结果显示,与正常组比较,卒中组、模型组、治疗组大鼠血清TNF-α、IL-1α、IL-6含量升高(P<0.01);与卒中组比较,模型组大鼠血清TNF-α、IL-1α、IL-6含量明显升高(P<0.05或P<0.01);与模型组比较,治疗组大鼠血清TNF-α、IL-1α、IL-6含量降低(P<0.01)。Western Blot检测结果显示,与正常组比较,模型组大鼠海马及皮质p38-MAPK表达升高(P<0.01);与卒中组比较,模型组大鼠海马p38-MAPK表达明显升高(P<0.05);与模型组比较,治疗组大鼠海马及皮质p38-MAPK表达下降(P<0.01)。结论颐脑解郁方可改善脑卒中后引起的焦虑障碍,其机制可能与抑制下丘脑和皮质p38-MAPK磷酸化水平,减轻炎性因子应答相关。     

急性痛风性关节炎大鼠关节滑膜核因子-κB水通道蛋白4P物质基因表达和丘脑腹后外侧核痛敏神经元放电频率变化规律

目的 动态观察急性痛风性关节炎(AGA)大鼠关节滑膜核转录因子(NF-κB)、水通道蛋白-4(AQP4)、P物质(SP)基因表达和丘脑腹后外侧核(VPL)痛敏神经元(PSN)放电频率变化规律,探讨AGA的神经源性炎症机制.方法 48只雄性Wistar大鼠,随机分为对照组(6只)和实验组(共7组,42只).实验组又根据注射尿酸钠(MSU)后不同时间点分为0.5、2、6、12、24、48、72 h组,每组6只.于相应时间点记录各组大鼠VPL核PSN放电频率变化后,取大鼠关节滑膜组织,聚合酶链反应(PCR)检测其NF-κB、SP和AQP4基阒表达.结果 AGA大鼠VPL核PSN放电频率和关节滑膜SP基因表达于注射MSU后即刻增加,6 h达高峰(P＜0.05),12 h后逐渐减少,AGA大鼠关节滑膜NF-κB和AQP4基因表达于注射MSU后0.5 h开始增加,12 h达高峰(P＜0.05),24 h后逐渐减低.经统计学相关性分析,NF-κB、SP、AQP4基因表达和PSN放电频率之间存在正相关(r=0.8875,0.9445,0.8126,P＜0.05).结论 丘脑VPL核PSN放电频率和SP基因表达水平町作为反映AGA大鼠关节疼痛严莺程度的客观指标;NF-κB和SP基因表达可作为反映其组织炎症和神经源性反应严重程度的指标;AQP4基因表达可作为反映其组织水肿严重程度的指标;疼痛和神经源性炎症在AGA发病机制中发挥着重要作用;采用神经电生理学和分子生物学相结合的方法 ,可以从新角度研究痛风的发病机制,为开发新药和临床治疗痛风提供新思路.     

6-羟基多巴胺损伤黑质致密部对大鼠脚桥核神经元的影响

目的观察6-羟基多巴胺损伤黑质致密部对大鼠脚桥核神经元的影响。方法选择健康雄性Wistar大鼠22只,13只大鼠内侧前脑束位点注射6-羟基多巴胺损伤黑质致密部多巴胺能神经元建立帕金森病大鼠模型作为模型组,另9只大鼠作为正常组。分别记录分析正常组9只和模型组7只脚桥核神经元信号电生理特性的变化,同时利用尼氏染色法观察6只帕金森病大鼠脚桥核神经元形态学变化。结果模型组脚桥核神经元类型Ⅰ和神经元类型Ⅱ放电频率较正常组显著增加[(12.09±1.62)Hz vs(7.35±0.98)Hz,P0.05;(4.09±0.34)Hz vs(2.87±0.26)Hz,P0.01],放电变得不规则;脚桥核神经元数量减少,形态发生显著变化,损伤侧脚桥核大型神经元、中型神经元、小型神经元较正常侧分别减少了20.3%,19.4%和20.9%(P0.05)。结论 6-羟基多巴胺损伤黑质致密部多巴胺能神经元导致了脚桥核内神经元电生理特征和形态学特征的广泛变性及损伤。     

细胞外调节激酶抑制剂PD98059对大鼠心肺复苏后脑缺血再灌注损伤的改善作用及其机制

目的 通过观察细胞外调节激酶（ERK）抑制剂PD98059对大鼠心肺复苏（CPR）后脑缺血再灌注损伤的改善作用，探讨其机制是否与抑制ERK/Calpain-2/Caspase-12信号通路、降低内质网应激介导的细胞凋亡有关。方法 将36只SD大鼠随机分为对照组、PD98059组、假手术组各12只。除假手术组外，各组均经食道交流电刺激诱导建立心跳骤停/心肺复苏模型。电刺激诱导心跳骤停6 min后，PD98059组、对照组大鼠经静脉分别注射0.3mg/kg PD98059及等体积生理盐水，并启动常规心肺复苏；假手术组仅进行手术操作而不行电刺激诱导心跳骤停。记录大鼠CPR后自主循环恢复（ROSC）时间、ROSC后24 h神经功能评分（NDS）;Western blotting法检测ROSC后24 h大鼠脑皮质组织中内质网应激相关凋亡蛋白钙蛋白酶2(Calpain-2)、天冬氨酸蛋白水解酶12(Caspase-12)、cleaved Caspase-3表达。结果 PD98059组ROSC后24 h NDS高于对照组（P<0.05），两组ROSC时间比较差异无统计学意义。大鼠脑组织Calp...     

芬太尼对创伤性脑损伤后大鼠丘脑腹后内侧核电生理变化的影响

目的 观察芬太尼对大鼠创伤性脑损伤( TBI) 后丘脑腹后内侧核(VPM)痛觉敏感神经元放电频率和次数的变化.方法 Wistar大鼠45只,随机分为3组:对照组(假手术组)、芬太尼组、TBI组.使用Feeney 法自由落体致伤原理,制作TBI 模型,连续记录大鼠丘脑腹后内侧核痛觉敏感神经元的放电频率及次数,再将各组进行比较.结果 电生理纪录显示:与假手术组相比较,TBI 组的放电频率明显增加(P<0.01),芬太尼组腹腔注射芬太尼后VPM核的痛觉敏感神经元的放电被明显抑制,与TBI 组比较差别具有统计学意义(P<0.01).结论 芬太尼可抑制TBI后VPM的放电频率,阻断痛觉传导,减轻神经源性炎症,从而发挥脑保护作用.     

电刺激缰核对大鼠血压影响的实验研究

目的　探讨电刺激缰核不同部位对大鼠血压的影响。方法　观察电刺激大鼠内、外侧缰核引起血压的变化及同一部位不同电流强度刺激下血压的变化情况。结果　电刺激内、外侧缰核均引起血压升高 ,以内侧缰核和血压升高的幅度、斜率更为明显。结论　缰核参与对血压的调解 ,整体反应以内侧缰核为主。     

不同频率电针足三里对运动大鼠下丘脑单胺类神经递质的影响

目的 研究不同频率电针对运动大鼠下丘脑单胺类神经递质的影响,筛选出电针消除运动性疲劳的最佳频率.方法　选用SD大鼠,采用Bedford渐增负荷跑台跑运动模型,用韩氏电针仪对运动性疲劳大鼠双侧足三里穴进行2/15 Hz 、2/100 Hz两种不同频率的刺激,用高效液相电化学法检测各组下丘脑单胺类神经递质的含量.结果 (1)运动组大鼠下丘脑内5-羟色胺(5-HT)升高,而多巴胺(DA)水平则显著降低(P＜0.05,P＜0.01).(2)运动+电针(2/15 Hz)、运动+电针(2/100 Hz)两组下丘脑内 5-HT、DA含量与运动后60 min组比较,差异显著(P＜0.05).(3)运动+电针(2/15 Hz)组下丘脑DA含量与运动+电针(2/100 Hz)组比较,差异显著(P＜0.05).结论 (1)急性运动后可显著增加下丘脑内5-HT和NA含量,降低下丘脑DA含量.(2)不同频率电针均可降低急性运动后大鼠下丘脑5-HT含量,增加DA含量.(3)2/15 Hz可能是要筛选的电针消除运动性疲劳的最佳频率.     

电刺激老龄大鼠缰核引起的呼吸效应

目的探讨电刺激大鼠缰核(Hb)对呼吸运动的影响及阻塞性睡眠呼吸暂停综合征(OSAS)的可能机制.方法电刺激大鼠Hb相应部位,同一刺激位点调整刺激参数,分别给予70 μA或90 μA电流强度,对照组给予同样电流刺激,记录刺激前后呼吸频率、胸廓运动幅度的数值.结果电刺激Hb可以引起呼吸频率加快、呼吸幅度加大(P＜0.05),同一刺激位点刺激强度增加可引起呼吸频率增加更明显(P＜0.05),呼吸幅度变化不大(P＜0.05).电刺激内侧缰核(MHb)内侧部出现呼吸明显减慢甚至呼吸暂停,同时呼吸幅度变浅(P＜0.05).电刺激MHb外侧部(L:0.3)和外侧缰核(L:0.5)均出现刺激过程中呼吸加快,但电刺激时胸廓运动幅度可有幅度变大或变小两种改变.结论 Hb可能参与呼吸运动的调节及OSAS的发生.     

The spatial receptive field of thalamic inputs to single cortical simple cells revealed by the interaction of visual and electrical stimulation

Electrical stimulation of the thalamus has been widely used to test for the existence of monosynaptic input to cortical neurons, typically with stimulation currents that evoke cortical spikes with high probability. We stimulated the lateral geniculate nucleus (LGN) of the thalamus and recorded monosynaptically evoked spikes from layer 4 neurons in visual cortex. We found that with moderate currents, cortical spikes were evoked with low to moderate probability and their occurrence was modulated by ongoing sensory (visual) input. Furthermore, when repeated at 8-12 Hz, electrical stimulation of the thalamic afferents caused such profound inhibition that cortical spiking activity was suppressed, aside from electrically evoked monosynaptic spikes. Visual input to layer 4 cortical cells between electrical stimuli must therefore have derived exclusively from LGN afferents. We used white-noise visual stimuli to make a 2D map of the receptive field of each cortical simple cell during repetitive electrical stimulation in the LGN. The receptive field of electrically evoked monosynaptic spikes (and thus of the thalamic input alone) was significantly elongated. Its primary subfield was comparable to that of the control receptive field, but secondary (flanking) subfields were weaker. These findings extend previous results from intracellular recordings, but also demonstrate the effectiveness of an extracellular method of measuring subthreshold afferent input to cortex.     

大鼠大脑皮质梗死后同侧丘脑组织蛋白酶B表达的动态变化

目的 探讨大鼠大脑皮质梗死后同侧丘脑腹后外侧核(ventroposterior nucleus of the thalamus, VPN) 组织蛋白酶B(cathepsin B, CathB)的表达变化.方法 成年雄性Sprague-Dawley大鼠随机分为假手术组和模型组,后者进一步分为术后1周组、2周组、3周组、4周组和8周组.电凝法闭塞大脑中动脉皮质支制作大脑皮质梗死模型.采用免疫组织化学染色和免疫荧光检测各时间点丘脑VPN CathB蛋白表达和细胞定位.结果 大脑皮质梗死后丘脑VPN CathB表达水平逐渐增高,4周时达高峰,8周时下降,但仍然高于对照组(P均<0.05);可见CathB从溶酶体释放到细胞质.此外,在大脑皮质梗死后3周时,活化星形胶质细胞CathB表达水平也显著增高.结论 大脑皮质梗死后1~8周期间,丘脑VPN CathB维持较高的表达水平,提示其可能在大脑皮质梗死后继发丘脑变性中起着一定的作用.     

Brain-state-independent neural representation of peripheral stimulation in rat olfactory bulb

It is critical for normal brains to perceive the external world precisely and accurately under ever-changing operational conditions, yet the mechanisms underlying this fundamental brain function in the sensory systems are poorly understood. To address this issue in the olfactory system, we investigated the responses of olfactory bulbs to odor stimulations under different brain states manipulated by anesthesia levels. Our results revealed that in two brain states, where the spontaneous baseline activities differed about twofold based on the local field potential (LFP) signals, the levels of neural activities reached after the same odor stimulation had no significant difference. This phenomenon was independent of anesthetics (pentobarbital or chloral hydrate), stimulating odorants (ethyl propionate, ethyl butyrate, ethyl valerate, amyl acetate, n-heptanal, or 2-heptanone), odor concentrations, and recording sites (the mitral or granular cell layers) for LFPs in three frequency bands (12-32 Hz, 33-64 Hz, and 65-90 Hz) and for multiunit activities. Furthermore, the activity patterns of the same stimulation under these two brain states were highly similar at both LFP and multiunit levels. These converging results argue the existence of mechanisms in the olfactory bulbs that ensure the delivery of peripheral olfactory information to higher olfactory centers with high fidelity under different brain states.     

Changes in local cerebral glucose utilization during rewarding brain stimulation.

The quantitative 2-deoxy[14C]glucose method was used to determine local cerebral glucose utilization in unrestrained rats responding (lever-press) for rewarding electrical stimulation to area A10 (ventral tegmental area) and in similarly implanted inactive controls. Self-stimulation was associated with significant increases in metabolic activity, highly circumscribed in the ventral tegmental area, that continued rostrally within a rather compact zone of activity through the medial forebrain bundle, extending via the diagonal band of Broca to the level of the preoptic area. In the forebrain terminal areas bilateral increases in local cerebral glucose utilization were noted in the nucleus accumbens, lateral septum, hippocampus, and the mediodorsal nucleus of the thalamus. Ipsilateral (i.e., side of stimulation) increases in glucose utilization were noted in the bed nucleus of the stria terminalis, the basolateral and central amygdaloid nuclei, and the medial prefrontal cortex. Caudal to the stimulation site, increases in glucose utilization were found in the midline dorsal raphe, the ipsilateral pontine gray, medial parabrachial nucleus, and the locus coeruleus. Significant bilateral increases were noted in various sensory and motor areas. These results indicate that rather than a diffuse pattern of activity, rewarding brain stimulation is associated with discrete activation of specific neuronal projection fibers and selective terminal sites.     

Oscillations in local field potentials of the primate motor cortex during voluntary movement.

We investigated the occurrence and distribution of oscillatory activity in local field potentials (LFPs) recorded from the frontal motor cortex of behaving monkeys performing skilled voluntary movements. LFPs were recorded simultaneously from up to 12 sites distributed throughout motor cortex while monkeys performed a visually guided, instructed delay task using the wrist or digits. Oscillatory activity between 15 and 50 Hz was evident in the LFP recorded from both primary motor cortex and premotor areas. Oscillations occurred preferentially before the visual cue to initiate movement but were infrequent during movement. Oscillations typically stopped before movement initiation during the wrist task, although they often continued into the initial phases of movement during the digit task. The relationship of oscillations to task performance was consistent across trials over periods of many months, although the amplitude and duration of oscillations varied across trials and days. Interactions between pairs of LFP recordings, evaluated with cross-correlation analysis, revealed synchronous oscillations over long distances (> 7 mm) and across primary motor cortex and premotor recording sites. These studies demonstrate that oscillations recorded in the LFP in motor cortex during trained motor tasks are not related to the details of movement execution but may be related to aspects of movement preparation.     

Altered thalamic response to levodopa in Parkinson’s patients with dopa-induced dyskinesias

Parkinson’s disease (PD) is a progressive neurologic condition characterized by tremor, slowness, stiffness, and unstable posture. Degeneration of dopamine-producing neurons in the substantia nigra causes PD. Treatment with levodopa, a precursor of dopamine, initially ameliorates the clinical manifestations of PD. However, chronic levodopa treatment can produce severe involuntary movements (so-called dopa-induced dyskinesias or DID), limiting treatment. Pallidotomy, placement of a surgical lesion in the internal segment of the globus pallidus, reduces DID. Because this result is inconsistent with current theories of both basal ganglia function and DID, it prompted us to investigate the brain’s response to levodopa. We measured regional cerebral blood flow response to levodopa with positron-emission tomography in 6 PD patients with DID, 10 chronically treated PD patients without DID, 17 dopa-naïve PD patients, and 11 normals. The dose of levodopa was chosen to produce clinical benefit without inducing DID. This strategy allowed us to examine the brain response to levodopa across groups without the confounding effect of differences in motor behavior. We found that the DID group had a significantly greater response in ventrolateral thalamus than the other groups. This was associated with decreased activity in primary motor cortex. These findings are consistent with increased inhibitory output from the internal segment of the globus pallidus to thalamus after levodopa administration. They provide a physiological explanation for the clinical efficacy of pallidotomy and new insights into the physiology of the basal ganglia.     

Role of vasopressin in the cardiovascular response to stimulation of the locus coeruleus

Hypothalamic vasopressin synthesizing nuclei (paraventricular and supraoptic) send vasopressin-containing projections to a number of neural target areas thought to be involved in cardiovascular regulation. One area known to receive vasopressinergic projections from the paraventricular nucleus is the pontine nucleus locus coeruleus. To examine the possible functional participation of vasopressin in central cardiovascular regulation, we examined mean arterial pressure (millimeters of Hg) and heart rate (beats per min) responses to electrical stimulation of the locus coeruleus in conscious, unrestrained vasopressin-deficient Brattleboro rats homozygous for diabetes insipidus (DI rats) and long Evans (LE) rats. Rats received chronic arterial and venous catheters and bipolar stimulating electrodes 3-5 days before experiment. Stimulation of the locus coeruleus (100 microA, 10-40 Hz) produced frequency-dependent increases in mean arterial pressure and heart rate in LE and DI, but the responses were significantly less in the latter group. The deficiency in mean arterial pressure and heart rate responses to locus coeruleus stimulation in DI rats was found to be centrally mediated in that responses to peripherally administered phenylephrine were the same as those for LE rats. Ganglionic blockade significantly attenuated responses to locus coeruleus stimulation in LE rats but had little effect in DI rats. Pretreatment of DI rats with chronic intracerebroventricular infusion of vasopressin (osmotic minipump) at a dose that had no effect peripherally increased the mean arterial pressure and heart rate responses to locus coeruleus stimulation. Our results suggest that vasopressin acts in the region of the locus coeruleus to exert a central action on sympathetic outflow.     

高频电刺激丘脑底核治疗帕金森病的实验研究

目的验证高频电刺激丘脑底核治疗帕金森病的疗效及探讨其作用机理。方法应用６－羟基多巴胺（６－ＯＨＤＡ）制备偏侧帕金森病（ＰＤ）大鼠模型，丘脑底核区插入刺激电极进行高频刺激，观察ＰＤ大鼠旋转行为改善程度，检测纹状体多巴胺（ＤＡ）、兴奋性氨基酸即谷氨酸（Ｇｌｕ）和天门冬氨酸（Ａｓｐ）含量，并记录皮质和丘脑底核区脑电图改变情况。结果高频电刺激丘脑底核可使ＰＤ模型鼠旋转行为明显下降；刺激同侧纹状体，ＤＡ含量增加，Ｇｌｕ含量减少，Ａｓｐ含量无变化；脑电图示皮质兴奋性增强，丘脑底核区兴奋性却下降。结论本实验从理论上验证了丘脑底核在帕金森病运动症状调节中的重要作用，提示高频电刺激丘脑底核可能成为治疗帕金森病的最有效方法，并且其作用机理与刺激后ＤＡ、Ｇｌｕ、Ａｓｐ之间的相互作用有关     

过敏性哮喘大鼠大脑和肺组织c-fos蛋白的表达

目的：探讨哮喘大鼠肺脏和大脑中c-fos表达的分布及其意义。方法：制作卵蛋白致敏大鼠哮喘模型,采用免疫组织化学ABC方法和图像分析等技术观察Fos蛋白在肺脏和大脑内的分布情况。结果：哮喘组大鼠（10只）肺脏和大脑中c-fos表达与正常对照组大鼠比较,差异有显著性（P＜0．05）;Fos阳性产物在脑内主要集中分布在额顶皮质、边缘前脑（扣带皮质、梨状皮质和中央杏仁核等）、丘脑室旁核、下丘脑室旁核、视上核、下丘脑外侧区、下丘脑室周核、孤束核、最后区和延髓腹外侧区内;小脑内无明显Fos分布密集区。结论：哮喘的发病机制中可能存在神经免疫调节的参与;Fos蛋白可能参与了哮喘的神经免疫调节。     

Rapid reorganization of adult rat motor cortex somatic representation patterns after motor nerve injury.

The potential for peripheral nerve injury to reorganize motor cortical representations was investigated in adult rats. Maps reflecting functional connections between the motor cortex and somatic musculature were generated with intracortical electrical stimulation techniques. Comparison of cortical somatotopic maps obtained in normal rats with maps generated from rats with a facial nerve lesion indicated that the forelimb and eye/eyelid representations expanded into the normal vibrissa area. Repeated testing from an electrode placed chronically in the motor cortex showed a shift from vibrissa to forelimb within hours after facial nerve transection. These comparatively quick changes in motor cortex representation pattern suggest that synaptic relations between motor cortex and somatic musculature are continually reshaped in adult mammals.