冷束缚应激大鼠室旁核Fos表达的检测

目的：探讨应激对下丘脑室旁核中Fos表达的影响，以期揭示应激性溃疡发病的神经内分泌机制。方法：采用SD大鼠冷束缚应激模型，用免疫组织化学方法检测应激前后大鼠下丘脑室旁核Fos的表达。结果：应激后室旁核Fos阳性细胞数量显著增多（t=26.7,P＜0．001）。结论：室旁核可能参与了应激性溃疡的病理过程。     

Lignocaine–induced convulsion does not induce c–fos protein (c–Fos) in rat hippocampus

Recent studies have shown that proto–oncogene c–fos mRNA is induced in the central nervous system by a variety of stimuli including generalised convulsions. In this study, the expression of c–fos protein (c–Fos) following lignocaine–induced convulsions was examined and compared with that following convulsions induced by non–anesthetic convulsants, such as pentylenetetrazol, kainic acid and electroconvulsive shocks, in rat brain.
Administration of 120 mg kg^-1 lignocaine by the intraperitoneal route induced generalised convulsions in all rats examined within 10 min. C–Fos was markedly induced in the piriform cortex and amygdala, and slightly induced in the neocortex and thalamus, while no c–Fos expression was observed in the hippocampus. In contrast, c–Fos expression following generalised convulsions induced by non–anaesthetic convulsants was very marked in the hippocampal region, piriform cortex and amygdala, and extended to the thalamus and neocortex.
These results contradict those of previously reported local cerebral metabolic studies using 2–deoxyglucose as a metabolic marker, and suggest that lignocaine–induced convulsions, unlike those induced by non–anaesthetic convulsants, may not cause severe sequelae (plastic changes) in the hippocampus.     

Reversal of dexfenfluramine-induced anorexia and c-Fos/c-Jun expression by lesion in the lateral parabrachial nucleus

The external subdivision of the lateral parabrachial nucleus (LPBE) shows strong Fos-like immunoreactivity (FLI) following anorectic doses of the indirect serotonin agonist dexfenfluramine (DFEN). In an effort to determine the contribution of the LPBE to DFEN-induced anorexia, bilateral ibotenate lesions were made in the LPBE, and the effects of the lesion on DFEN-induced anorexia and FLI as well as c-June-like immunoreactivity (JLI) were examined. It was found that LPBE lesion significantly attenuated DFEN anorexia: in a 1-h food intake test following 24-h food deprivation, DFEN (2 mg/kg) suppressed food intake by 60% in intact rats but only 34% in rats with LPBE lesions. In addition to this behavioral change, LPBE lesion completely abolished DFEN-induced FLI and JLI in the lateral subdivision of the central nucleus of the amygdala (CeL) and laterodorsal subdivision of the bed nucleus of stria terminalis (BSTLD), both of which showed strong FLI and JLI in intact rats. DFEN-induced FLI and JLI in other brain regions were not affected by LPBE lesion, including the ventromedial and lateral hypothalamus, caudate-putamen, and the nucleus of the solitary tract (NST). The parallel loss of DFEN-induced anorexia and FLI/JLI following LPBE lesion raises the novel possibility that LPBE-CeL/BSTLD pathway may be involved in DFEN anorexia.     

Local muscimol disinhibits mesolimbic dopaminergic activity as examined by brain microdialysis and Fos immunohistochemistry

Infusion of muscimol (5×10⁻⁵ M, 60 min) into the nucleus accumbens (NAC) through a dialysis membrane caused a significant increase in extracellular dopamine (DA) and its metabolite, 3,4-dihydroxyphenylacetic acid (DOPAC). Fos-like immunoreactivity induced by intra-NAC infusion of muscimol was seen ipsilaterally in many accumbofugal target areas, but no Fos-positive neurons were seen in the vicinity of the dialysis membrane in the NAC. Sequential staining of Fos and tyrosine hydroxylase (TH) immunoreactivities revealed that a portion of A10 dopaminergic neurons were double-labelled. These results suggest that muscimol in the NAC disinhibits mesolimbic DA neuronal activity possibly through activity of the accumbofugal GABA neuron system.     

Expression of c-fos, fos B, and egr-1 in the medial preoptic area and bed nucleus of the stria terminalis during maternal behavior in rats

The spatial and temporal pattern of expression of the protein products of immediate early genes (IEGs) c-fos, fos B, and egr-1 were mapped in medial preoptic area (MPOA) and ventral bed nucleus of stria terminalis (VBST) during maternal behavior in rats. Immunocytochemical analysis indicated significant increases in the number of cells expressing c-Fos after 2 h of pup exposure, while Fos B levels showed a delayed response, reaching maximal levels after 6 h.     

Fos oncoprotein expression in the rat forebrain following muscimol-induced absence seizures

Fos oncoprotein expression is a marker of neuronal activation following seizures. Here, using this method we examined the anatomical locations of muscimol-induced absence seizures in the rat forebrain. Six hours after a systemic injection of muscimol a massive Fos immunoreactivity appeared in the olfactory system, retrosplenial cortex and paraventricular thalamic nucleus, whereas other cortical areas contained low level of Fos expression. These results provide the first functional morphological evidence suggesting that these forebrain structures with Fos expression may play an important role in the pathophysiology of muscimol-induced absence seizures.     

白细胞介素—1对大鼠下丘脑室旁核Fos癌蛋白和CRF的诱导作用

将白细胞介素-1(IL)注入大鼠侧脑室,用Fos癌蛋白抗体免疫组化法检测了下丘脑室旁核的激活神经元:大量位于含促肾上腺皮质激素释放因子(CRF)相应区域的室旁核小细胞部神经元呈Fos免疫强阳性。Fos和CRF的免疫双染色显示了许多Fos免疫阳性神经元也呈CRF免疫阳性。此外,在IL-1注射动物中,CRF的免疫阳性显著加强,提示CRF合成增加。     

在戊四氮致痫大鼠早期前脑中OX-42和Fos蛋白的表达变化

研究大鼠在戊四氮导致癫痫发作早期前脑内小胶质细胞的变化及其与神经元的关系,本研究应用免疫组织化学法分别显示前脑内OX-42和Fos蛋白表达的时程变化,并用双重标记显示OX-42和Fos阳性细胞的相互关系。结果发现:在戊四氮导致大鼠癫痫发作早期(从15min到360min),前脑的小胶质细胞OX-42表达阳性,随着存活时间的变化,OX-42的阳性反应经历逐渐升高又降低的过程;Fos蛋白在神经元和小胶质细胞中有表达,也呈现逐渐升高又降低的变化;Fos在小胶质细胞表达高峰的时间早于在神经元的表达;另外OX-42阳性小胶质细胞和Fos阳性神经元在前脑分布基本相同,主要分布在大脑皮层、海马、杏仁核等部位。以上结果表明,前脑的小胶质细胞和神经元一样在戊四氮所致癫痫发作的早期表现明显的反应,但小胶质细胞反应的意义有待进一步研究。     

Differential fos activation in virgin and lactating mice in response to an intruder

Lactating (L) mice display fierce aggression towards novel, male mice, while virgin (V) mice do not. This study compares patterns of brain activation in V and L mice in response to a novel intruder using immunohistochemical detection of Fos (Fos-IR). Animals were sampled 120 min after either a sham or real 10 min test with a male intruder. L mice were aggressive towards intruders, but V mice were not. In general, Fos-IR for both groups increased with exposure to an intruder, with L mice showing higher increases in Fos-IR than V mice. In only medial preoptic nucleus and ventral portion of bed nucleus of stria terminalis (BNST) was Fos-IR significantly increased in both groups with testing. In V mice, testing resulted in Fos-IR increases in an additional 10 regions examined that did not reach significance in L mice, including lateral septum, lateral and medial preoptic areas, and anterior hypothalamus. Fos-IR also increased with testing in nine regions unique to L mice, including the mitral and granular layers of accessory olfactory bulb, regions of the amygdala, dorsal BNST, and caudal portions of the hypothalamic attack area. These increases in Fos-IR with testing suggest alterations in the circuitry governing response to pheromonal cues and imply some commonalities between the circuitries governing maternal aggression and intermale aggression. These results support the hypothesis that pregnancy and lactation induce substantial changes in brain circuitry and function; changes that enable maternal defense of offspring by altering the neural response to an intruder male.