Quantitative distribution of AChE-positive neurons in the hippocampus of young and aged rats

Summary Acetylcholinesterase (AChE)-positive neurons were counted in the different layers of the rostral (septal) third, the middle third and the caudal (temporal) third of the hippocampus from 3 month (young) and 27 month old rats (aged) using AChE stained cryostat sections. The rats were treated with 3 and 2.5 mg of diisopropylphosphofluoridate/kg body weight, respectively 3 h before sacrifice. The study showed — 1) a high numerical density of AChE-positive neurons (10.9 to 18.9 perikarya/mm²) in the hilus (fascia dentata), the str. oriens/pyramidale of CA1 and the subiculum, a particularly low density (< 0.1 perikarya/mm²) in the str. granulosum and moleculare of the dentate area; — 2) a significant (p < 0.05) linear increase of the numerical density in most of the hippocampal layers from the rostral to the caudal pole; — 3) no significant differences between young and aged animals; — and 4) a higher sensitivity to DFP-treatment in aged than in young animals. The distribution of AChE-positive neurons corresponds with the distribution of somatostatin-immunoreactive neurons described in the literature. A modulatory effect on neurotransmission is discussed as a possible function of the AChE in peptidergic neurons.     

GTP-binding proteins mediate acetylcholine inhibition of voltage dependent calcium channels in hippocampal neurons

Acetylcholine (Ach) was tested for its effect on calcium currents in primary cultures of embryonic rat hippocampal neurones. 10 M Ach reversibly depressed the high voltage activated (HVA) Ca current and the effect was blocked by atropine. When GTP binding proteins (G-proteins) were irreversibly activated by intracellularly perfusing the neurons with GTP[ S], one short-lasting application of Ach permanently inhibited Ca currents. Alternatively, the transmitter was inactive when the cells were preincubated with pertussis toxin, which inactivates some G-proteins by catalyzing ADP ribosylation. Our results suggest that a G-protein mediates the inhibitory modulation of the HVA Ca current by muscarinic agonists.     

Electrical stimulation of the lateral habenula increases hippocampal noradrenaline release as monitored by in vivo microdialysis

Summary Hippocampal extracellular levels of noradrenaline (NA) were monitored with the microdialysis technique during electrical stimulation of the lateral habenula (LHb) in halothane anaesthetized rats. The steady state NA level was 20.8±4.6 fmole/15 min of perfusion (mean ± SEM). Electrical stimulation of the LHb for 15 min (15 Hz, 0.5 mA) induced an immediate 228±48% increase in hippocampal NA release, compared to the pre-stimulation baseline (p<0.05). A second stimulation 90 min later induced a similar increase. The effect of LHb stimulation was completely abolished by a knife cut transecting the dorsal NA bundle either immediately rostral to the locus coeruleus or at the level of the parafascicular nucleus. This suggests that the effect was dependent on nerve impulses flow in the coeruleo-hippocampal NA neurons, and was not mediated, e.g., by a local spread of electricity into the hippocampus. Since the LHb has previously been shown to be a powerful activator of the mesencephalic raphe nuclei we tested whether the effect was mediated via the serotonergic system. However, the effect of LHb stimulation on hippocampal NA release persisted after 5,7-di-hydroxytryptamine treatment and after complete radiofrequency lesions of the dorsal and central superior raphe nuclei. The present data suggest that electrical stimulation of the LHb can increase hippocampal NA release through an activation of the locus coeruleus, and that this effect is not dependent on the mesencephalic raphe nuclei. The results support the role of the LHb as a link for limbic and striatal forebrain activation of brain stem monoaminergic systems.     

Intrahippocampal cholinergic grafts in aged rats compensate impairments in a radial maze and in a place learning task

Summary Age-related cognitive impairments were studied in rats kept in semi-enriched conditions during their whole life, and tested during ontogeny and adult life in various classical spatial tasks. In addition, the effect of intrahippocampal grafts of fetal septal-diagonal band tissue, rich in cholinergic neurons, was studied in some of these subjects. The rats received bilateral cell suspensions when aged 23–24 months. Starting 4 weeks after grafting, they were trained during 5 weeks in an 8-arm maze made of connected plexiglass tunnels. No age-related impairment was detected during the first eight trials, when the maze shape was that of a classical radial maze in which the rats had already been trained when young. The older rats were impaired when the task was made more difficult by rendering two arms parallel to each other. They developed an important neglect of one of the parallel tunnels resulting in a high amount of errors before completion of the task. In addition, the old rats developed a systematic response pattern of visits to adjacent arms in a sequence, which was not observed in the younger subjects. None of these behaviours were observed in the old rats with a septal transplant. Sixteen weeks after grafting, another experiment was conducted in a homing hole board task. Rats were allowed to escape from a large circular arena through one hole out of many, and to reach home via a flexible tube under the table. The escape hole was at a fixed position according to distant room cues, and olfactory cues were made irrelevant by rotating the table between the trials. An additional cue was placed on the escape position. No age-related difference in escape was observed during training. During a probe trial with no hole connected and no proximal cue present, the old untreated rats were less clearly focussed on the training sector than were either the younger or the grafted old subjects. Taken together, these experiments indicate that enriched housing conditions and spatial training during adult life do not protect against all age-related deterioration in spatial ability. However, it might be that the considerable improvement observed in the grafted subjects results from an interaction between the graft treatment and the housing conditions.     

老年记忆减退大鼠海马CA1区锥体细胞和神经毡线粒体的体视学研究

目的 应用电镜观察老年记忆损害大鼠海马线粒体的形态学改变.方法 青年(3月龄)和老年(26月龄)SD大鼠经Morris水迷宫测试后,以青年鼠平均逃避潜伏期正常值上限的95%和99%上限值为界将老年鼠分为老年记忆正常组和老年记忆减退组.用透射电镜观察海马CA1锥体细胞和神经毡内线粒体的体视学参数.结果 1.与青年大鼠相比,老年记忆正常大鼠海马线粒体数密度(Nv)、比膜面(Sm)、比表面(Ss)下降显著,但体密度(Vv)与青年大鼠相比无显著差异;老年记忆减退大鼠海马线粒体Nv、Ss、Sm、Vv均下降显著,且Vv、Nv的下降与老年记忆正常大鼠间有显著差异;2.老年记忆减退大鼠和老年记忆正常大鼠线粒体平均体积(V)均较青年组明显增加,但两老年组间无差异.讨论 线粒体的形态学参数体现了老年期海马线粒的代偿改变,而线粒体的功能失调可能在老年记忆损害中起重要作用.     

Traumatic brain injury reduces hippocampal high-affinity [H]choline uptake but not extracellular choline levels in rats

Hippocampal cholinergic hypofunction may contribute to memory deficits following experimental traumatic brain injury. These studies examined two important factors in acetylcholine synthesis: choline availability and neuronal uptake. No reductions in basal extracellular choline levels, using microdialysis, were observed 2 weeks after cortical impact injury. However, studies of high affinity [³H]choline uptake in the hippocampus, measured in a synaptosomal preparation, found a reduction in the maximum velocity of choline uptake (V_max), while no differences in affinity constants (K_m) were found. The results suggest that post-traumatic cholinergic deficits are not attributable to decreased availability of choline, but may be associated with either a decreased ability of cholinergic neurons to take up choline and/or a loss of cholinergic neurons.     

Effect of bite-raised condition on the hippocampal cholinergic system of aged SAMP8 mice

Occlusal disharmony induces chronic stress, which results in learning deficits in association with the morphologic changes in the hippocampus, e.g., neuronal degeneration and increased hypertrophied glial fibrillary acidic protein-positive cells. To investigate the mechanisms underlying impaired hippocampal function resulting from occlusal disharmony, we examined the effects of the bite-raised condition on the septohippocampal cholinergic system by assessing acetylcholine release in the hippocampus and choline acetyltransferase immunoreactivity in the medial septal nucleus in aged SAMP8 mice that underwent the bite raising procedure. Aged bite-raised mice showed decreased acetylcholine release in the hippocampus and a reduced number of choline acetyltransferase-immunopositive neurons in the medial septal nucleus compared to age-matched control mice. These findings suggest that the bite-raised condition in aged SAMP8 mice enhances the age-related decline in the septohippocampal cholinergic system, leading to impaired learning.     

Time-dependent effects of intrahippocampal grafts in rats with fimbria-fornix lesions

Summary Based on three experiments, this study examined whether behavioral and histological effects of fetal septal or hippocampal grafts placed in the denervated hippocampus depend on the duration of post-grafting delays. Each experiment included four groups of rats: sham-operated rats (Sham), rats with aspirative lesions of the fimbria-fornix (Fifo) and rats given both Fifo lesions and intrahippocampal fetal suspension grafts of either septal (Fifo.ST) or hippocampal (Fifo.HT) origin. All rats were tested (i) for home cage activity, (ii) for activity and reactivity in an open field and (iii) for learning ability in a 8-arm radial maze. Except for home cage activity which was also monitored preoperatively, behavioral tests were conducted between 1–2 months postgrafting in Experiment 1 (EXP1), 5–6 months post-grafting in Experiment 2 (EXP2) and 10–11 months postgrafting in Experiment 3 (EXP3). Each test period lasted 3 weeks. Histological controls consisted of acetylcholinesterase (AChE) and cresyl violet staining. Graft size was estimated by computerized image analysis. Normal rats performed well in each experiment. In all experiments, rats with fimbria-fornix lesions showed increased activity in both their familiar (home cage) and unfamiliar (open field) environments, and their performances in the radial maze task were impaired. In no experiment did grafts, whether hippocampal or septal, affect noncognitive behavioral variables. However, maze performance was improved by hippocampal grafts in EXP1 (short delay) and by septal grafts in EXP2 (intermediate delay). No graft-induced effect was found in EXP3 (long delay). Concerning AChE-positivity in the dorsal hippocampus, fimbria-fornix lesions reduced staining densities by at least 60%. Both types of grafts were undiscernably AChE-positive, but only septal grafts provided the denervated hippocampus with a significant AChE-positive fiber ingrowth. Differences among groups in density of hippocampal AChE staining were comparable in all three experiments and no correlation between hippocampal AChE-positivity and maze performance was found. Our results suggest that graft-induced recovery from behavioral effects of fimbria-fornix lesions may depend on both the type of tissue implanted (hippocampal vs septal) and the post-grafting delay (1–2, 5–6 and 10–11 months). The recovery observed at a short post-grafting delay with hippocampal grafts and at a longer post-grafting delay with septal grafts was not persistent and concerned only cognitive function as assessed by radial maze performance. Regarding (i) the absence of any correlation between AChE staining and radial maze performance, and (ii) the lack of graft-derived AChE-positive fiber ingrowth in Fifo.HT rats with improved radial maze performance in EXP1, our results also suggest that factors other than graft-derived cholinergic fiber ingrowth might be involved in the graft-induced recovery observed in the radial maze.     

Comparison of the neuroprotective effects and recovery profiles of isoflurane,sevoflurane and desflurane as neurosurgical pre-conditioning on ischemia/reperfusion cerebral injury

Background: There are a few reports regarding the comparison of these anesthetic agents, but previous studies mainly focus on the veterinary anesthesiology. Less attention has been focused comparing the effectiveness of these inhalational anesthetic agents in neurosurgery. This lack of interest is regretful particularly considering the fact that anesthetics during neurosurgery are an issue of extreme sensitivity and subtlety, where the cerebral oxygenation process plays a significant role in the neuroprotective mechanisms. Objective: The purpose of this retrospective study is to contribute to the existing knowledge of the comparative studies of the volatile anesthetic agents such as isoflurane, sevoflurane and desflurane by evaluating the maintenance and emergence characteristics after volatile anesthetics-induced preconditioning with isoflurane, sevoflurane or desflurane for inpatient ischemia/reperfusion cerebral injury during cerebral or neural surgeries. Methods: The aim was to investigate their neuroprotective mechanisms and effects by analyzing and comparing the superiority of each agent in a Chinese patient population, in terms of faster emergence, and early and intermediate recovery. The intraoperative haemodynamic profiles and postoperative adverse effects of these three agents were also systematically analyzed. Results: We found that sevoflurane, when compared with isoflurane and desflurane, provided anesthesia with similar hemodynamic stability but allowed for a smoother, more rapid emergence and better quality of induction and recovery to surgical patients under clinical conditions, particularly to those who were experiencing substantial cerebral vasodilation. Conclusion: Sevoflurane offers several advantages, including a relative lack of airway irritation, a more rapid onset and recovery, and greater hemodynamic stability than other potent inhaled agents. These properties would appear to afford sevoflurane significant clinical potential.     

吡格列酮对异氟醚麻醉引起的老年小鼠认知功能损伤的影响*

 目的：研究高选择性的过氧化物酶体增殖物激活受体γ（PPARγ）激动剂吡格列酮（Pi）对异氟醚引起的老年小鼠认知功能障碍和脑内炎症细胞因子的影响。方法：136只11个月大的雄性C57BL/6J 小鼠随机分成5组：对照组（Con）、异氟醚组（Iso）、吡格列酮（10 mg/kg）+异氟醚组（Pi10+Iso）、吡格列酮（20 mg/kg）+异氟醚组（Pi20+Iso）和单纯吡格列酮（20 mg/kg）组（Pi20）。各异氟醚处理组的小鼠吸入混合1.4%异氟醚的氧气2 h;Con和Pi20组的小鼠仅吸入氧气2 h。吡格列酮溶于1%的羧甲基纤维素钠（CMC）,在小鼠吸入异氟醚或单纯氧气前2 h,按10 mg/kg或20 mg/kg灌胃,Con组和Iso组小鼠仅给予相同容量的1% CMC。在异氟醚处理结束后48 h行恐惧记忆实验以检测小鼠的学习记忆功能;6 h时取部分小鼠分离皮质和海马行Western blotting检测PPARγ蛋白及ELISA法检测脑组织IL-1β和TNF-α水平。结果：与Con组比较,Iso组的僵住行为减少（P<0.05）,海马IL-1β水平增加 （P<0.05）;与Iso组比较,Pi10+Iso组的僵住行为和PPARγ蛋白表达无明显变化（P>0.05）,而Pi20+Iso组的僵住行为和PPARγ蛋白表达均明显增加（P<0.05）且海马中IL-1β水平降低（P<0.05）。各组海马和皮质TNF-α水平以及皮质中IL-1β水平无明显差异（P>0.05）。结论：吡格列酮可以减轻异氟醚引起的老年小鼠的认知功能障碍,并可以缓解异氟醚引起的小鼠海马IL-1β含量的增加。     

Partial hippocampal inactivation: effects on spatial memory performance in aged and young rats

Changes in anatomical or functional connectivity during normal aging are thought to contribute to cognitive alterations over the lifespan. Neural network theories predict that synaptic loss in an aging brain could place the organism near the point of dysfunction in the nonlinear curve defining neural compromise versus performance. The present experiments examined whether aged rats are closer to this point of behavioral dysfunction by reversibly inactivating one or both hippocampal hemispheres. As expected, bilateral tetracaine inactivation of the hippocampus disrupted spatial memory in both age groups. Unilateral left hippocampal inactivation significantly increased errors only in aged rats; however, unilateral inactivation of the right hippocampus had no effect. The present outcome could reflect more extensive synaptic dysfunction in the aged right hippocampus or a greater involvement of the left hippocampus in spatial working memory problems.     

Behavioral correlates of theta-on and theta-off cells recorded from hippocampal formation of mature young and aged rats

Summary Most hippocampal formation single units in freely behaving rats fall into one of two categories (Ranck 1973). The most obvious behavioral correlate of complex-spike (CS) cells is spatially selective discharge (O'Keefe and Dostrovsky 1971), while theta cells show increased firing in phase with the EEG rhythm associated with Vanderwolf's Type I behaviors (e.g. walking, exploration). Recently, Colom and Bland (1987) described, in urethane anesthetized animals, a class of non-CS cell which was inactive in the presence of EEG and discharged continuously during LIA. They called these theta-off cells and used the term theta-on to refer to the classical theta cell. We describe the behavioral correlates of 14 theta-off cells encountered in CA1 (n = 1), hilus fascia dentata (FD; n = 4), subiculum (n = 6), and entorhinal cortex (n = 3). These cells were encountered very infrequently in the course of several experimental investigations of mature young and old rats involving 885 hippocampal neurons recorded from 33 rats during radial maze performance. Fourteen theta-on cells encountered within a few hundred microns of the sites where theta-off cells were recorded were included for comparison. Both theta-on and theta-off cells discharged single spikes and did not show CS bursting characteristic of pyramidal cells. Theta-off cells, however, exhibited significantly greater spike durations than theta-on cells. Mean rates for theta-on and theta-off cells were 8.7 Hz and 6.5 Hz, respectively. Maximum rates were 114 Hz and 104 Hz, respectively. Some cells of both types showed 6–8 Hz modulation while animals traversed the maze. Whereas firing rate for theta-on cells increased smoothly with running velocity, it decreased smoothly for theta-off cells. While no theta-on cells exhibited clear spatial selectivity, two hilar theta-off cells did. When EEG rhythm was temporarily abolished by local injection of tetracaine into the medial septum, two theta-off cells were observed to fire continuously at high rates irrespective of behavior, with a pronounced 18–20 Hz rhythmic modulation. Under these circumstances, theta-on cells decrease their rates. Within the 7 theta-off cells recorded in each of the two age groups, there were no statistically significant differences in firing characteristics. Possible anatomical candidates for theta-off cells are considered.     

Amyloid β peptide levels and its effects on hippocampal acetylcholine release in aged, cognitively-impaired and -unimpaired rats

Excessive extracellular deposition of amyloid β (Aβ) peptide in neuritic plaques and degeneration of forebrain cholinergic neurones, which innervate the hippocampus and the neocortex, are the invariant characteristic features of Alzheimer's disease (AD). Studies of the pathological changes that characterize AD, together with several other lines of evidence, indicate that Aβ accumulation in vivo may initiate and/or contribute to the process of neurodegeneration observed in the AD brain. However, the underlying mechanisms by which Aβ peptide influences/causes degeneration of the basal forebrain cholinergic neurones in AD brains remain obscure. We reported earlier that nM concentrations of Aβ-related peptides, under acute conditions, can potently inhibit K⁺-evoked endogenous acetylcholine (ACh) release from the hippocampus and the cortex but not from striatum in young adult rats (J. Neurosci. 16 (1996) 1034). In the present study, to determine whether the effects of Aβ peptides alter with normal aging and/or cognitive state, we have measured Aβ_1–40 levels and the effects of exogenous Aβ_1–40 on hippocampal ACh release in young adult as well as aged cognitively-unimpaired (AU) and -impaired (AI) rats. Endogenous levels of Aβ_1–40 in the hippocampus are significantly increased in aged rats. Additionally, 10 nM Aβ_1–40 potently inhibited endogenous ACh release from the hippocampus of the three groups of rats, but the time-course of the effects clearly indicate that the cholinergic neurones of AI rats are more sensitive to Aβ peptides than either AU or young adult rats. These results, together with earlier reports, suggest that the processing of the precursor protein of Aβ peptide alters with normal aging and the response of the cholinergic neurones to the peptide possibly varies with the cognitive status of the animals.     

Strain comparison of synaptic density in hippocampal CA1 of aged rats

Synaptic density in hippocampal CA1 stratum radiatum was studied in two different strains of rat at 3 and 24-28 months of age. Neither Fischer 344 nor Sprague-Dawley rodents showed any age-related loss of synapses. These data support the contention that synapse loss with age is not a generalized phenomenon in the mammalian CNS.     

Modification of adenosine modulation of acetylcholine release in the hippocampus of aged rats

Adenosine is a neuromodulator acting through inhibitory A₁ receptors (A₁Rs) and facilitatory A_2ARs. Since A_2AR antagonists attenuate memory deficits in aged animals and memory deficits might involve a decreased cholinergic function, we investigated how aging affects the density and function of adenosine receptors in rat hippocampal cholinergic terminals. In young adult (2 months) rats, 64 and 36% of cholinergic terminals (immunopositive for vesicular ACh transporters) possessed A₁Rs and A_2ARs, respectively. In aged (24 months) rats, the percentage of cholinergic terminals with A₁Rs was preserved, whereas that with A_2ARs was larger (49%). In young adults adenosine only tonically inhibited ACh release through A₁Rs, whereas in aged rats there was a greater A₁R-mediated inhibition and a simultaneous A_2AR-mediated facilitation of ACh release. Thus, the enhanced A_2AR density and facilitation compensates for the greater tonic A₁R modulation, preserving the global adenosine modulation of ACh release in aged rats. Furthermore, since A_2AR antagonists inhibit ACh release, the beneficial effects of A_2AR antagonists on memory in aged rats might not result from ACh release modulation.     

Long term effects of septohippocampal lesions and intrahippocampal grafts on acetylcholine concentration,muscarinic stimulated formation of inositol phospholipids and electrically evoked release of neurotransmitters in the rat hippocampus

Summary Long Evans female rats sustained aspirative lesions of the septohippocampal pathways; subsequently, they received intrahippocampal suspension grafts of fetal septal-diagonal band or hippocampal tissue. The long term (8–10 months post-surgery) effects of these treatments were examined in the hippocampus for the following variables: concentration of hippocampal acetylcholine (ACh), muscarinic-stimulated (carbachol) formation of inositol monophosphate, accumulation of tritiated choline, noradrenaline (³H-NA) and serotonin (³H-5-HT), electrically evoked release of ³H-acetylcholine (³H-ACh), ³H-NA and ³H-5-HT, and choline acetyltransferase (ChAT) activity. The lesions decreased the levels of endogeneous ACh, the accumulation of ³H-choline and ³H-5-HT and the evoked release of both ³H-ACh and ³H-5-HT as well as the ChAT activity, but they failed to significantly affect the muscarinic-stimulated formation of inositol monophosphate and the accumulation and release of ³H-NA. Grafts of hippocampal cells were found to be ineffective on all lesion-induced effects. In contrast, grafts of septal-diagonal band origin attenuated the deficit of hippocampal concentrations of ACh and accumulation of ³H-choline without, however, improving release of ³H-ACh, accumulation and release of ³H-5-HT, and ChAT activity. These observations suggest that: (i) denervation-induced hippocampal muscarinic supersensitivity might not be long-lasting or the lesions, which in some cases spared the lateral edges of the fimbria, failed to induce any muscarinic supersensitivity, (ii) intrahippocampal grafts rich in cholinergic neurons do not foster recovery from the lesion-induced noncholinergic deficits we assessed, (iii) recovery of function may be expressed by some but not all biochemical or pharmacological cholinergic variables and (iv) graft-derived hippocampal reinnervation may be less efficient than the endogenous innervation of intact rats as indicated by the restoration of only some of the variables related to cholinergic function by intrahippocampal septal-diagonal band grafts.     

Nicotinic effects on excitatory field potentials recorded from the immature CA3 area of rat hippocampal slices

We investigated the nicotinic modulation of the excitatory field potentials recorded from the immature (postnatal day 10–20) hippocampal CA3 area, in the presence of the GABA_A antagonist bicuculline methiodide (BMI, 10 M). Nicotine (50 M) enhanced the evoked field potentials; its effects were also observed in the presence of the GABA_B antagonist 2-hydroxy-saclofen (250 M; added to BMI) and were blocked by pre-perfusion with the nicotinic antagonist hexamethonium (HXM, 50 M). The potentiating effects of nicotine in BMI persisted during prolonged perfusion (more than 20 min), while those in control perfusion medium were transient. The nicotinic antagonists HXM (50 M), methyllycaconitine (MLA, 0.01 M) and dihydro--erythroidine (DHE, 50 M) potentiated CA3-evoked field potentials. Perfusion of HXM in the presence of the anticholinesterase eserine (1 M) or the muscarinic antagonist atropine (1 M) did not alter its effects. None of the nicotinic agents tested changed the frequency of spontaneous BMI-induced epileptiform discharges (nicotine, HXM, MLA, DhE), suggesting that nicotinic receptors do not drive spontaneous epileptiform discharges in this in vitro model. These experiments demonstrate that nicotinic receptors are activated tonically during disinhibition and modulate the activity of excitatory synapses in the immature CA3 hippocampal area. The persistent nicotinic facilitatory effects during disinhibition versus the transient in control conditions indicate that nicotinic modulation depends on environmental conditions and also that nicotinic receptors may be a contributing factor in early-life seizures.     

手术结束前应用地氟醚替换异氟醚对麻醉苏醒及花费的影响

目的 探讨手术结束前30 min应用地氟醚替换异氟醚对患者麻醉苏醒的影响。方法 选取2016年4月~2017年4月择期妇科腹腔镜手术患者90例,ASAⅠ~Ⅱ级,随机分为D组（地氟醚）、I组（异氟醚）和I+D组（异氟醚+地氟醚）三组,每组30例。全麻诱导均为咪达唑仑0.03 mg/kg,舒芬太尼0.3 μg/kg,异丙酚2 mg/kg,顺式阿曲库铵0.15 mg/kg。麻醉维持:D组开启地氟醚挥发罐至6%;I组开启异氟醚挥发罐至1.6%;I+D组开启异氟醚挥发罐至1.6%,手术结束前30 min关闭异氟醚,同时开启地氟醚挥发罐至6%,三组均复合瑞芬太尼0.1~1 μg/（kg·min）维持麻醉。手术结束停用所有麻醉药,观察呼吸恢复时间、苏醒时间、拔除喉罩时间、苏醒期躁动评分和术中知晓,计算三组用药量及花费。结果 D组和I+D组的呼吸恢复时间、苏醒时间、拔除喉罩时间均比I组缩短,差异有统计学意义（P＜0.05）;两两比较:D组和I+D组间差异无统计学意义（P＞0.05）,其余两两比较结果均有统计学意义（P＜0.05）。三组间苏醒期躁动评分差异无统计学意义（P＞0.05）。I+D组麻醉药花费较D组减少,差异有统计学意义（P＜0.05）。结论 手术结束前应用地氟醚替换异氟醚可加快患者麻醉苏醒且花费相对较低。     

Aging increases basal but not stress-induced levels of corticosterone in the brain of the awake rat

The main purpose of this study was to evaluate the effect of aging on plasma and free corticosterone (CORT) levels in the brain in basal conditions and in response to an acute stressor. Microdialysis experiments were performed in the hippocampus (HC) and the prefrontal cortex (PFC) of young adult (6 months) and aged (24 months) male Wistar rats. Basal free levels of CORT in the HC and the PFC were higher in aged animals. Restraint stress increased plasma CORT and free CORT levels in the HC and the PFC both in young and aged animals. However, while the increase of plasma CORT was higher in aged rats compared with young rats, the increases of free CORT in the HC and the PFC were not different between these two groups of rats. These results suggest that the changes produced by aging in the brain may be related to the enhanced basal levels of free CORT and not to the CORT increases in response to stress.     

大鼠海马多巴胺递质活动与类P300关系的探讨

目的：探讨海马多巴胺递活动与事件相关电位类P300的关系。方法：应用立体定位技术将绝缘电极植入大鼠海马腹侧记录类P300,观察局部给予多巴胺D2受体拮抗剂sulpiride对类P300的影响。结果：海马腹侧局部注射Sulpiride30min后类P300潜伏期明显延长,2h后基本恢复正常。结论：海马腹侧多巴胺递质活动在类P300形成中起重要作用。