YDM—1牙科电子麻醉仪诱发Vc内Fos表达

目的：探讨面部ＴＥＮＳ后,三叉神经脊束核尾侧亚核（Ｖｃ） 内兴奋细胞的分布。方法：利用免疫组织染色化学方法观察正常以及面部ＴＥＮＳ后１ 、２、４ｈ 大鼠Ｖｃ 内Ｆｏｓ 免疫阳性神经元的分布。结果：ＴＥＮＳ后１ｈ,Ｆｏｓ 免疫阳性神经元集中分布在Ｖｃ 浅层背侧区,ＴＥＮＳ后２ｈ ,内层也出现少量Ｆｏｓ 免疫阳性神经元,ＴＥＮＳ后４ｈ ,Ｖｃ 各层内可见Ｆｏｓ 免疫阳性神经元的分布。结论：Ｖｃ 浅层和内层的神经元均参与ＴＥＮＳ反应,早期主要是Ｖｃ 浅层背侧区神经元。     

Fos expression in gonadotropin-releasing hormone neurons by naloxone or bicuculline in intact male rats

Double immunocytochemistry for Fos and GnRH was performed after the intravenous infusion of naloxone or bicuculline. Either naloxone or bicuculline significantly increased serum LH concentrations. After the naloxone infusion, some Fos-positive GnRH neurons were found from the preoptic area to the basal hypothalamic area, whereas those were found from the diagonal band of Broca to the preoptic area after the bicuculline infusion. These results suggest the distribution of GnRH neurons activated by naloxone and bicuculline in intact male rats.     

Regional expressions of Fos-like immunoreactivity in rat cerebral cortex after stress; restraint and intraperitoneal lipopolysaccharide

To demonstrate regional activation in the rat cerebral cortex related to stress-evoked neuroendocrine response, Fos expression in both the cerebral cortex and hypothalamic paraventricular nucleus (PVN) was immunohistochemically examined in two experimental groups; a lipopolysaccharide (LPS) intraperitoneally injected group for inflammatory stress and a restraint group for emotional stress. The LPS injection (100 μg/100 g b.w.) and restraint (for 30 min) had similar effect on Fos-like immunoreactivity (Fos-LI) in PVN with regard to the number of immunoreactive nuclei and their distribution pattern, while the times to maximize Fos-LI were different. Numerical analysis of cortical Fos-LI in untreated rats showed a distinct region-specific pattern. Statistical analysis revealed no significant increase in Fos-LI density in any cortical regions in the LPS group, but restraint resulted in a dramatic and region-specific increase. A significant increase was detected in the prefrontal cortex (the cingulate, orbital and agranular insular cortex), the frontal area 2, the agranular retrosplenial cortex, the parietal cortex, and the medial and lateral occipital area 2. These results indicate that cortical activation relevant to specific functions may be involved in stress-specific neural circuitry.     

Convulsive effects of thiophene,a heterocyclic hydrocarbon: Behavioral,electrographic and c‐Fos immunocytochemical studies

The behavioral, electrographic and histopathological changes induced by the heterocyclic hydrocarbon thiophene were investigated in rats following intramuscular injection of 0.3 mL thiophene for 5 days. Generalized convulsions were noted in 29 out of 34 animals (85%) between 1 and 28 h after the final dose. Electroencephalography revealed that the discharges in the hippocampus and forebrain occurred simultaneously, although epileptic activity emerged more strongly from the hippocampus than from any other region. Neuron damage was detected histologically in the temporal and parietal neocortex, piriform gyrus, amygdaloid nucleus and cerebellar cortex, but not in the hippocampus. In contrast, c‐Fos was induced widely in the cerebral cortex and hippocampus, and was most marked in the dentate gyrus. These findings suggest that the hippocampus plays a crucial role in seizure onset following thiophene injection.     

行为训练诱导的大鼠背海马结构内c—Fos表达的老年相关性变化

采用避暗回避反应实验和免疫细胞化学相结合的方法,选用5个实验组（即：空白对照组、实验对照组、假训练组、训练组和记忆唤醒组）,对不同月龄大鼠背海马结构中的c-Fos表达进行了观察。结果发现：老年大鼠在避暗回避训练中,探索次数多于青年和成年大鼠,且滞留时间明显缩短;成年和老年大鼠在训练、假训练和记忆唤醒后,背海马内c-Fos的表达明显低于青年组大鼠,以训练组最为显著。该结果一方面表明随年龄的增长,海马神经元对应激和学习记忆尤其是后者的反应性降低;另一方面也提示成年和老年组大鼠背海马区神经元可能有丢失现象。     

大鼠肢体IRI后脊髓神经元Fos的表达

目的探讨脊髓神经元是否参与肢体缺血再灌注损伤（IRI）的发病过程以及有关神经元的分布特点。方法Wistar大鼠24只,随机分为4组,A：空白对照组;B：假手术对照组;C：单纯缺血组;D：缺血再灌注组。通过暂时阻断一侧髂总动脉和股动脉,建立肢体缺血再灌注损伤模型。采用免疫细胞化学ABC法,观察大鼠脊髓神经元原癌基因c—fos的表达和分布特点。结果大鼠肢体缺血4h,脊髓相应节段神经元Fos表达活跃。再灌注2h后,Fos表达更加活跃（P〈0．01）。并且Fos阳性神经元较集中分布于脊髓相应节段同侧后角及中央管周围。结论脊髓相应节段同侧神经元可能参与肢体IRI的发病过程,尤其是脊髓后角及中央管周围神经元可能具有更为重要的作用。     

Clozapine impact on c‐Fos expression in mild stress preconditioned male rats exposed to a novelty stressor

Clozapine (CLZ) stimulates several brain areas some of them being sensitive to stress. Aim of the present study was to reveal whether 7‐day CLZ administration may: (1) activate the selected forebrain areas; (2) modulate response of these structures to a single forced swimming episode (FSW); (3) modulate response of these structures to FSW after 13‐day preconditioning with mild unpredictable stress complex (CMS). Used groups of male Wistar rats: (a) vehicle or CLZ treated for 7 days; (b) vehicle or CLZ treated for 7 days and on the 7th day exposed to FSW; (c) CMS exposed for 13 days, from the 8th day injected with vehicle or CLZ and on the 14th day exposed to FSW. Vehicle or CLZ (10 mg kg^?1 day^?1 in 0.1% acetic acid) were administered intraperitoneally. c‐Fos quantification was performed 90 min after FSW in the medial prefrontal cortex (mPFC), dorsolateral (dLS) and ventrolateral (vLS) septum, dorsolateral (DLStr) and dorsomedial (DMStr) striatum, nucleus accumbens shell (NAc shell) and core (NAc core), and hypothalamic paraventricular nucleus (PVN). In unstressed animals CLZ increased c‐Fos expression in the mPFC, vLS, and PVN. After a single FSW, CLZ decreased the number of c‐Fos immunoreactive cells in the vLS, DMStr, NAc shell, and NAc core. In CMS rats, CLZ suppressed c‐Fos immunoreactivity in response to FSW in the PVN. Our data indicate that CLZ elicits different impact on neuronal activities in the brain areas studied and modifies the response of these structures to stress. CLZ effect seems to be affected by stress duration.     

Crocin improved amyloid beta induced long‐term potentiation and memory deficits in the hippocampal CA1 neurons in freely moving rats

Extracellular beta‐amyloid (Aβ) accumulation and deposition is the main factor, which causes synaptic loss and eventually cells death in Alzheimer's disease (AD). Memory loss and long‐term potentiation (LTP) dysfunction in the hippocampus are involved in the AD. The involvement of crocin, as the main and active constituent of saffron extract in learning and memory processes, has been proposed. Here we investigated the probable therapeutic effect of crocin on memory, LTP, and neuronal apoptosis using in vivo Aβ models of the AD. The Aβ peptide (1–42) was bilaterally administered into the frontal‐cortex using stereotaxic apparatus. Five hours after surgery, rats were given intraperitoneal crocin (30 mg/kg) daily, which repeated for 12 days. Barnes maze results showed that administration of crocin significantly improves spatial memory indicators such as latency time to achieving the target hole and the number of errors when compared to Aβ‐group. Passive avoidance test revealed that crocin significantly increased the step‐through‐latency compared to Aβ‐treated alone. These learning deficits in Aβ‐treated animals correlated with a reduction of LTP in hippocampal CA1 synapses in freely moving rats, which crocin improved population spike amplitude and mean field excitatory postsynaptic potentials (fEPSP) slope reduction induced by Aβ. Neuronal apoptosis was detected by TUNEL assay and the expression levels of c‐Fos proteins were examined by Western blotting. Crocin significantly reduced the number of TUNEL‐positive cells in the CA1 region and decreased c‐Fos in the hippocampus compared to Aβ‐group. In vivo Aβ treatment altered significantly the electrophysiological properties of CA1 neurons and crocin further confirmed a neuroprotective action against Aβ toxicity.     

Prelimbic cortex is a common brain area activated during cue‐induced reinstatement of cocaine and heroin seeking in a polydrug self‐administration rat model

Many preclinical studies examined cue‐induced relapse to heroin and cocaine seeking in animal models, but most of these studies examined only one drug at a time. In human addicts, however, polydrug use of cocaine and heroin is common. We used a polydrug self‐administration relapse model in rats to determine similarities and differences in brain areas activated during cue‐induced reinstatement of heroin and cocaine seeking. We trained rats to lever press for cocaine (1.0 mg/kg per infusion, 3‐hr/day, 18 day) or heroin (0.03 mg/kg per infusion) on alternating days (9 day for each drug); drug infusions were paired with either intermittent or continuous light cue. Next, the rats underwent extinction training followed by tests for cue‐induced reinstatement where they were exposed to either heroin‐ or cocaine‐associated cues. We observed cue‐selective reinstatement of drug seeking: the heroin cue selectively reinstated heroin seeking and the cocaine cue selectively reinstated cocaine seeking. We used Fos immunohistochemistry to assess cue‐induced neuronal activation in different subregions of the medial prefrontal cortex, dorsal striatum, nucleus accumbens, and amygdala. Fos expression results indicated that only the prelimbic cortex (PL) was activated by both heroin and cocaine cues; in contrast, no significant cue‐induced neuronal activation was observed in other brain areas. RNA in situ hybridization indicated that the proportion of glutamatergic and GABAergic markers in PL Fos‐expressing cells was similar for the heroin and cocaine cue‐activated neurons. Overall, the results indicate that PL may be a common brain area involved in both heroin and cocaine seeking during polydrug use.