清醒大鼠海马内theta波的自适应波束形成定向计算

目的：利用波速形成算法研究大鼠海马中theta波的传播规律。方法 ：探讨了自适应波速形成算法在大鼠场电位中的应用。选取了5只大鼠,在大鼠的海马中植入8×2阵列的微丝电极阵列,训练大鼠做静止、跑动、攀爬等动作,利用视屏跟踪系统监视大鼠活动,神经信号记录仪记录大鼠的海马神经元放电和场电位,利用自适应波束形成算法分析theta波对记录电极的到达角。结果：在大鼠静止时无theta波,运动时存在明显的theta波,其传播角度保持稳定。本研究确认了theta波在海马中以行波的方式传播,传播的角度可以通过波束形成算法计算。结论：通过应用在雷达和声纳技术广泛使用的波束形成算法,能够简便的计算theta波相对于电极阵列的到达角,可能为手术电极定位提供辅助。     

海马区神经电信号相位同步化的初步研究

大脑各个区域的神经电活动存在各种不同频率的振荡,而theta节律振荡(5～10 Hz)是海马区神经活动具有代表性的特征.本文用海马区theta节律显著性检测和theta节律相位同步化的方法来分析多电极记录的神经元放电及其局部场电位信号,验证了theta节律成分的显著性和动物行为之间的关系,并首次研究了小鼠在不同行为状态下左右海马神经电活动之间的相位同步化的差异.     

Serotonin and histamine mediate gastroprotective effect of fluoxetine against experimentally-induced ulcers in rats

Research in the treatment of gastric ulcer has involved the investigation of new alternatives, such as anti-depressant drugs. The present study was designed to investigate the gastroprotective effects of fluoxetine against indomethacin and alcohol induced gastric ulcers in rats and the potential mechanisms of that effect. Fluoxetine (20?mg/kg) was administered IP for 14 days. For comparative purposes, other rats were treated with ranitidine (30?mg/kg). Thereafter, after 24?h of fasting, INDO (100?mg/kg) or absolute alcohol (5?ml/kg) was administered to all rats (saline was administered to naïve controls) and rats in each group were sacrificed 5?h (for INDO rats) or 1 h (for alcohol rats) later. Macroscopic examination revealed that both fluoxetine and ranitidine decreased ulcer scores in variable ratios, which was supported by microscopic histopathological examination. Biochemical analysis of fluoxetine- or ranitidine-pre-treated host tissues demonstrated reductions in tumor necrosis factor (TNF)-α and myeloperoxidase (MPO) levels and concomitant increases in gastric pH, nitric oxide (NO) and reduced glutathione (GSH) contents. Fluoxetine, more than ranitidine, also resulted in serotonin and histamine levels nearest to control values. Moreover, immuno-histochemical analysis showed that fluoxetine markedly enhanced expression of cyclo-oxygenases COX-1 and COX-2 in both models; in comparison, ranitidine did not affect COX-1 expression in either ulcer model but caused moderate increases in COX-2 expression in INDO-induced hosts and high expression in alcohol-induced hosts. The results here indicated fluoxetine exhibited better gastroprotective effects than ranitidine and this could be due to anti-secretory, anti-oxidant, anti-inflammatory and anti-histaminic effects of the drug, as well as a stabilization of gastric serotonin levels.     

Correlational Relationships Between the Hippocampus and Medial Septal Area and Their Changes During Epileptogenesis

EEG traces were recorded from the hippocampus and medial septal area of conscious guinea pigs in control conditions and on repeated stimulation of the perforant path. Changes in the correlations of activity in these structures during stimulation-evoked convulsions (a model of acute epilepsy) and during the process of epileptogenesis (a model of chronic epilepsy) were analyzed. A high correlation between baseline activity in the hippocampus and medial septal area seen in control conditions decreased sharply with the appearance of acute and chronic convulsions. Kindling led to hippocampus-independent generation of field convulsive discharges in the medial septal area. During kindling, there was a gradual disintegration of activity in the hippocampus and septum, which provides evidence for impairment of the operation of the septo-hippocampal network during epileptogenesis. Translated from Zhurnal Vysshei Nervnoi Deyatel’nosti imeni I. P. Pavlova, Vol. 58, No. 3, pp. 345–350, May–June, 2008.     

Serotonin Modulates Oscillations of the Membrane Potential in Isolated Spinal Neurons from Lampreys

Studies were performed on spinal neurons from lampreys isolated by an enzymatic/mechanical method using pronase. The effects of 100 M serotonin (5-HT) on membrane potential oscillations induced by a variety of excitatory amino acids were studied. 5-HT was found to depolarize branched cells (presumptive motoneurons and interneurons) by 2–6 mV without inducing membrane potential oscillations. However, when oscillations were already present because of an excitatory amino acid, 5-HT changed the parameters of these oscillations, increasing the amplitudes of all types of oscillations, increasing the frequency of irregular oscillations, and increasing the duration of the depolarization plateaus accompanied by action potentials. Serotonin modulation of the effects of excitatory amino acids and the electrical activity of cells in the neural locomotor network facilitates motor activity and leads to increases in the contraction of truncal muscles and more intense movements by the animal. The possible mechanisms of receptor coactivation are discussed, along with increases in action potential frequency and changes in the parameters of the locomotor rhythm.     

Role of serotonin transporter inhibition in the regulation of tryptophan hydroxylase in brainstem raphe nuclei: time course and regional specificity

Drugs that selectively inhibit the serotonin transporter (SERT) are widely prescribed for treatment of depression and a range of anxiety disorders. We studied the time course of changes in tryptophan hydroxylase (TPH) in four raphe nuclei after initiation of two different SERT inhibitors, citalopram and fluoxetine. In the first experiment, groups of Sprague–Dawley rats received daily meals of rice pudding either alone (n=9) or mixed with citalopram 5 mg/kg/day (n=27). Rats were sacrificed after 24 h, 7 days or 28 days of treatment. Sections of dorsal raphe nucleus (DRN), median raphe nucleus (MRN), raphe magnus nucleus (RMN) and caudal linear nucleus (CLN) were processed for TPH immunohistochemistry. Citalopram induced a significant reduction in DRN TPH-positive cell counts at 24 h (41%), 7 days (38%) and 28 days (52%). Similar reductions in TPH-positive cell counts were also observed at each timepoint in the MRN and in the RMN. In the MRN, citalopram resulted in significant reductions at 24 h (26%), 7 days (16%) and 28 days (23%). In the RMN, citalopram induced significant reductions of TPH-positive cell counts at 24 h (45%), 7 days (34%) and 28 days (43%). By contrast, no significant differences between control and treatment groups were observed in the CLN at any of the time points that we studied. To investigate whether these changes would occur with other SERT inhibitors, we conducted a second experiment, this time with a 28-day course of fluoxetine. As was observed with citalopram, fluoxetine induced significant reductions of TPH cell counts in the DRN (39%), MRN (38%) and RMN (41%), with no significant differences in the CLN. These results indicate that SERT inhibition can alter the regulation of TPH, the rate limiting enzyme for serotonin biosynthesis. This persistent and regionally specific downregulation of serotonin biosynthesis may account for some of the clinical withdrawal symptoms associated with drugs that inhibit SERT.     

Serotonin transporter in the temporal lobe,hippocampus and amygdala in SUDEP

Several lines of evidence link deficient serotonin function and SUDEP. Chronic treatment with serotonin reuptake inhibitors (SRIs) reduces ictal central apnoea, a risk factor for SUDEP. Reduced medullary serotonergic neurones, modulators of respiration in response to hypercapnia, were reported in a SUDEP post‐mortem series. The amygdala and hippocampus have high serotonergic innervation and are functionally implicated in seizure‐related respiratory dysregulation. We explored serotonergic networks in mesial temporal lobe structures in a surgical and post‐mortem epilepsy series in relation to SUDEP risk. We stratified 75 temporal lobe epilepsy patients with hippocampal sclerosis (TLE/HS) into high (N = 16), medium (N = 11) and low risk (N = 48) groups for SUDEP based on generalised seizure frequency. We also included the amygdala in 35 post‐mortem cases, including SUDEP (N = 17), epilepsy controls (N = 10) and non‐epilepsy controls (N = 8). The immunohistochemistry labelling index (LI) and axonal length (AL) of serotonin transporter (SERT)‐positive axons were quantified in 13 regions of interest with image analysis. SERT LI was highest in amygdala and subiculum regions. In the surgical series, higher SERT LI was observed in high risk than low risk cases in the dentate gyrus, CA1 and subiculum (p < 0.05). In the post‐mortem cases higher SERT LI and AL was observed in the basal and accessory basal nuclei of the amygdala and peri‐amygdala cortex in SUDEP compared to epilepsy controls (p < 0.05). Patients on SRI showed higher SERT in the dentate gyrus (p < 0.005) and CA4 (p < 0.05) but there was no difference in patients with or without a psychiatric history. Higher SERT in hippocampal subfields in TLE/HS cases with SUDEP risk factors and higher amygdala SERT in post‐mortem SUDEP cases than epilepsy controls supports a role for altered serotonergic networks involving limbic regions in SUDEP. This may be of functional relevance through reduced 5‐HT availability.     

Serotonergic pre-treatments block in vitro serotonergic phase shifts of the mouse suprachiasmatic nucleus circadian clock

The suprachiasmatic nucleus (SCN) contains a circadian clock that maintains its time-generating and phase-modulating capacities in vitro. Previous studies report clear differences in the ability of serotonergic stimuli to phase-shift the SCN clock when applied directly to the SCN either in vivo or in vitro: while mice and rat circadian clocks are readily phase-shifted by serotonin (5-HT) or 5-HT agonists applied in vitro, hamster and mice circadian clocks respond inconsistently to 5-HT agonists injected directly into the SCN in vivo. Here we have investigated one possible explanation for these differences: that the SCN isolated in vitro experiences reduced endogenous 5-HT signaling, which increases clock sensitivity to subsequent 5-HT stimulation. For these experiments we treated mouse SCN brain slices with low concentrations of compounds that increase serotonin signaling: 5-HT, a 5-HT agonist (8-OH-DPAT), the 5-HT precursor, l-tryptophan, or the 5-HT re-uptake inhibitor, fluoxetine. Pretreatment with each of these substances completely blocked subsequent phase-shifts induced by mid-subjective day treatment with either 5-HT or 8-OH-DPAT, while they did not block phase-shifts induced by the adenylate cyclase activator, forskolin. Time-course data on l-tryptophan-induced inhibition are consistent with this treatment inducing receptor internalization, while timing of the recovery from inhibition is consistent with receptor reinsertion. Together these data support the hypothesis that SCN clock sensitivity to serotonergic phase modulation is affected by the amount of prior serotonin signaling present in the SCN, and that this signaling alters the density of surface 5-HT receptors on SCN clock neurons.     

Respiratory Effects of Stimulation of the Limbic Cortex in Rats and Their Modulation with Serotonin

Acute experiments on rats showed that the anterior cingulate gyrus contains 2 efferent regions of the functional respiratory system (inhibitory supragenual and excitatory infragenual areas). Stimulation of these cortical areas produced a respiratory effect, which depended on activity of serotoninergic mechanisms in the solitary tract nucleus. __________ Translated from Byulleten' Eksperimental'noi Biologii i Meditsiny, Vol. 140, No. 9, pp. 244–246, September, 2005     

Sensory Responses of Neurons in the Medial Septal Area in Conditions of Modulation of Theta Activity Using the Alpha-2-Adrenoreceptor Agonist Clonidine

Our previous studies on conscious rabbits showed that administration of the alpha-2-adrenoreceptor agonist clonidine induces dose-dependent changes in theta oscillations in the septohippocampal system. Low doses of clonidine suppressed theta activity, while high doses produced significant potentiation. It was suggested that the different effects of clonidine might be associated with differences in the sensitivities of pre- and postsynaptic alpha-2-adrenoreceptors to clonidine, this agent being a pure agonist of noradrenaline when used at high doses. It was suggested that functional synergism occurs between the activatory reticular formation and the noradrenergic system of the locus ceruleus in controlling the theta rhythm. The present study was performed to identify the nature of the responses of sensory neurons in the medial septal region in conditions of alterations in the magnitude of the theta rhythm induced by different doses of clonidine. Low and high doses of the agonist given bilaterally into the lateral ventricles were found to have different effects on the sensory responses of neurons in the medial septal region. Injection of small clonidine doses (0.5 microg in 5 microl into each lateral ventricle), which decrease theta activity, was found to lead to weakening of activatory processes and enhancement of inhibitory processes in the medial septal region. The number of activatory responses decreased significantly and persisting responses were significantly weakened; inhibitory responses, conversely, were seen more frequently and were significantly more marked. Administration of high clonidine doses (5 microg in 5 microl), which produce sharp increases in theta oscillations, led to significant reductions in the reactivity of cells in the medial septal region to sensory stimuli (from 76.8% in controls to 45% after clonidine), regardless of the nature of the initial responses. Persisting activatory and inhibitory responses were in most cases less marked than the initial responses. These results suggest that alpha-2-adrenoreceptors are involved in controlling the sensory reactivity of neurons in the medial septal region. The impairment of the normal processing of sensory stimuli seen during the continuous generation of rhythmic activity provoked by injection of large clonidine doses supports the role of the theta rhythm in the septohippocampal system as an active filter during the processing and recording of information.     

Coexpression of Serotonin and Nitric Oxide in the Raphe Complex: Cortical Versus Subcortical Circuit

Several lines of evidence have implicated a direct reciprocal interaction between serotonin and nitric oxide (NO). The goal of this investigation was, therefore, to examine the coexpression of tryptophan hydroxylase (TPH; the rate limiting enzyme for the synthesis of serotonin) and neuronal NO synthase (nNOS) in the ascending cortical projecting raphe nuclei (B6–B9 subgroups), when compared with the descending spinal cord projecting raphe nuclei (B1–B3 subgroups). Our data demonstrated that: (1) a significant number of raphe‐cortical projecting neurons was identified not only in the midline subgroup of dorsal raphe (B6, 7) but also in the median raphe (B8), as well as in the supralemniscal nucleus (B9); (2) serotonergic cortical projecting neurons from these three raphe nuclei exhibited a high (>80%) percentage of coexpression with nNOS immunoreactivity; (3) similarly, serotonin transporter immunoreactive fibers in the medial prefrontal cortex were also double‐labeled with nNOS immunoreactivity; (4) in contrast, the descending spinal cord projecting raphe nuclei revealed only TPH but not nNOS immunoreactivity. Our present findings suggest the existence of a direct interaction between serotonin and NO in the ascending cortical projecting raphe system. In contrast, a different strategy appears to operate the descending spinal cord projecting raphe system. Anat Rec, 2010. © 2010 Wiley‐Liss, Inc.     

Anxious Behavior and Fenfluramine-Induced Prolactin Secretion in Young Rhesus Macaques with Different Alleles of the Serotonin Reuptake Transporter Polymorphism (5HTTLPR)

Anxiety is a normal aspect of human personality, which can manifest in a variety of disorders and other negative traits. The primary treatment for anxiety is the class of drugs known as the selective serotonin reuptake inhibitors (SSRIs), which bind to the serotonin reuptake transporter. The upstream region of the gene that codes for this transporter contains a polymorphism that is an insertion/deletion event that in turn, produces long (l) and short (s) alleles in the population. This particular polymorphism in the serotonin transporter, the 5HTTLPR (serotonin transporter linked polymorphic region), is thought to be involved in the genesis of anxious traits and disorders. Most studies with human subjects have examined adult behavior, which may derive from diverse experiential and environmental backgrounds, as well as genetic differences. To better isolate the effect of genetics, we genotyped 128 infant and juvenile monkeys for the 5HTTLPR and tested for behavioral response in four testing paradigms designed to elicit fearful-anxious behaviors: a free play, remote-controlled car, human intruder, and novel fruit test. The s/s monkeys were found to be behaviorally inhibited in the free play test, engaged in more fear behaviors in the remote-controlled car test, and threatened more in the stare portion of the human intruder test, even though a small number of monkeys were assessed. There was no difference between genotypes of either sex in the prolactin response to fenfluramine. These data indicate greater anxiety in the s/s monkeys for distinct facets of anxious behavior, which are independent of a global neurohormonal challenge test. These neurobehavioral data support recent neuroimaging findings in humans indicating the importance of the 5HTTLPR for amygdala-dependent anxious behavior.     

Differential effect of orexins (hypocretins) on serotonin release in the dorsal and median raphe nuclei of freely behaving rats

Orexin (hypocretin)-containing neurons in the perifornical hypothalamus project to widespread regions of the brain, including the dorsal and median raphe nuclei [Peyron C, Tighe DK, van den Pol AN, de Lecea L, Heller HC, Sutcliffe JG, Kilduff TS (1998) Neurons containing hypocretin (orexin) project to multiple neuronal systems. J Neurosci 18:9996-10015; Wang QP, Koyama Y, Guan JL, Takahashi K, Kayama Y, Shioda S (2005) The orexinergic synaptic innervation of serotonin- and orexin 1-receptor-containing neurons in the dorsal raphe nucleus. Regul Pept 126:35-42]. Orexin-A or orexin-B was infused by reverse microdialysis into the dorsal raphe nucleus or median raphe nucleus of freely behaving rats, and extracellular serotonin was simultaneously collected by microdialysis and analyzed by high-performance liquid chromatography. We have found that orexin-A produced a dose-dependent increase of serotonin in the dorsal raphe nucleus, but not in the median raphe nucleus. However, orexin-B elicited a small but significant effect in both the dorsal raphe nucleus and median raphe nucleus. Orexins may have regionally selective effects on serotonin release in the CNS, implying a unique interaction between orexins and serotonin in the regulation of activities including sleep-wakefulness.     

Brainstem sites for the carbachol elicitation of the hippocampal theta rhythm in the rat

The effects of brainstem microinjections of carbachol on the hippocampal theta rhythm were examined in urethane anesthetized rats. The two most effective theta-eliciting sites with carbachol were the nucleus pontis oralis (RPO) and the acetylcholine-containing pedunculopontine tegmental nucleus (PPT) of the dorsolateral pontine tegmentum. RPO injections generated theta at mean latencies of 38.5±70.8 s and for mean durations of 12.9±5.1 min. Five of seven RPO injections gave rise to theta virtually instantaneously, i.e., before the completion of the injection. PPT injections generated theta at mean latencies of 1.7±1.1 min and for mean durations of 11.9±6.0 min. Injections rostral or caudal to RPO in the caudal midbrain reticular formation (RF) or the caudal pontine RF (nucleus pontis caudalis) generated theta at considerably longer latencies (generally greater than 5 min) or were without effect. Medullary RF injections essentially failed to alter the hippocampal EEG. The finding that theta was produced at very short latencies at RPO suggests that RPO, the putative brainstem source for the generation of theta, is modulated by a cholinergic input. The further demonstration that theta was also very effectively elicited with PPT injections suggests this acetylcholine-containing nucleus of the dorsolateral pons may be a primary source of cholinergic input to RPO in the generation of theta. The hippocampal theta rhythm is a major event of REM sleep. The present results are consistent with earlier work showing that each of the other major events of REM sleep, as well as the REM state, are cholinergically activated at the level of the pontine tegmentum.     

Neonatal Exposure to Citalopram Selectively Alters the Expression of the Serotonin Transporter in the Hippocampus: Dose‐Dependent Effects

Infants born to mothers taking selective serotonin reuptake inhibitors (SSRIs) late in pregnancy have been reported to exhibit signs of antidepressant withdrawal. Such evidence suggests that these drugs access the fetal brain in utero at biologically significant levels. Recent studies in rodents have revealed that early exposure to antidepressants can lead to long lasting abnormalities in adult behaviors, and result in robust decreases in the expression of a major serotonin synthetic enzyme (tryptophan hydroxylase) along the raphe midline. In the present investigation, we injected rat pups with citalopram (CTM: 5 mg/kg, 10 mg/kg, and 20 mg/kg) from postnatal Days 8–21, and examined serotonin transporter (SERT) labeling in the hippocampus, ventrobasal thalamic complex, and caudate‐putamen when the subjects reached adulthood. Our data support the idea, that forebrain targets in receipt of innervation from the raphe midline are particularly vulnerable to the effects of CTM. SERT‐immunoreactive fiber density was preferentially decreased throughout all sectors of the hippocampal formation, whereas the subcortical structures, each supplied by more lateral and rostral aspects of the raphe complex, respectively, were not significantly affected. Reductions in SERT staining were also found to be dose‐dependent. These findings suggest that SSRIs may not only interfere with the establishment of chemically balanced circuits in the neonate but also impose selective impairment on higher cortical function and cognitive processes via more circumscribed (i.e., regionally specific) deficits in 5‐HT action. Anat Rec, 2010. © 2010 Wiley‐Liss, Inc.     

Circadian rhythm in metabolic activity of suprachiasmatic, supraoptic and raphe nuclei

Previous studies using 2-deoxyglucose (2-DG) autoradiography have demonstrated that the suprachiasmatic nucleus (SCN) of the hypothalamus, a putative neural circadian pacemaker, displays circadian rhythmicity in its metabolic activity. In the present study, we show that distinct circadian variations in 2-DG uptake occur not only in the suprachiasmatic, but also in the supraoptic and median raphe nuclei of the rat brain. On the other hand, several other brain areas failed to display systematic circadian variations in 2-DG uptake. These results indicate that circadian metabolic rhythms are not unique to the SCN. Further studies are required to precisely define the extent of such phenomena.     

Relaxin-3 in GABA projection neurons of nucleus incertus suggests widespread influence on forebrain circuits via G-protein-coupled receptor-135 in the rat

Relaxin-3 (RLX3) is a newly identified member of the relaxin/insulin peptide family that is highly conserved across a range of species from fish to mammals and is highly expressed in rat, mouse and human brain. Extensive pharmacological studies have demonstrated that RLX3 is a high affinity, selective ligand for G-protein-coupled receptor-135 (GPCR135, now classified as relaxin family peptide-3 receptor; RXFP3). In ongoing studies to understand the physiological functions of RLX3, the distribution of RLX3-containing neuronal elements in rat brain was determined by immunohistochemistry, using an affinity-purified polyclonal antiserum raised against a conserved segment of the RLX3 C-peptide (AS-R3(85-101)). Consistent with the distribution of RLX3 mRNA, neurons containing RLX3-like immunoreactivity (LI) were observed in the pontine nucleus incertus and the majority of these cells, which are known to express corticotropin-releasing factor receptor-1, were shown to express glutamic acid decarboxylase-65-immunoreactivity, suggesting a GABA phenotype. Nerve fibers and terminals containing RLX3-LI were observed adjacent to cells in the nucleus incertus and in various forebrain regions known to receive afferents from the nucleus incertus, including cortex, septum, hippocampus, thalamus, hypothalamus and midbrain. Regions that contained highest densities of RLX3-positive fibers included the medial septum, lateral preoptic area, lateral hypothalamus/medial forebrain bundle and ventral hippocampus; and additional fibers were observed in olfactory bulb and olfactory and frontal/cingulate cortices, bed nucleus of the stria terminalis, dorsal endopiriform, intergeniculate, and supramammillary nuclei, and the periaqueductal gray and dorsal raphe. The RLX3-positive network overlapped the regional distribution of GPCR135 mRNA and specific binding sites for an [125I]-GPCR135-selective, chimeric peptide. These anatomical findings further support the proposition that RLX3 is the endogenous ligand for GPCR135 in rat brain and provide evidence for broad modulatory activity of RLX3 in behavioral activation relating to autonomic and neuroendocrine control of metabolism and reproduction and higher-order processes such as stress and cognition.     

米氮平和氟西汀治疗伴抑郁的心血管神经症的临床观察

目的：评价米氮平治疗伴抑郁的心血管神经症的临床疗效和安全性。方法：将60例伴抑郁的心血管神经官能症患者随机分为米氮平组和氟西汀组，进行为期42天的治疗观察。采用汉密顿抑郁量表（HAMD）、心血管神经症积分评价临床疗效，采用TESS、体检及实验室检查评价安全性，分别在治疗前和治疗后第7、14、28、42天评定疗效和不良反应。结果：（1）两组治疗后HAM／）和心血管神经症积分均明显低于治疗前，差异有统计学意义（P〈0．01）。（2）治疗后第7天，米氮平组HAMD量表总分、焦虑评分、迟滞评分、睡眠紊乱评分、心血管神经症积分均较氟西汀组低，且有统计学意义（P〈0．01）；研究结束时，上述指标的组间差异没有统计学意义。（3）经过42天治疗，有效率和治愈率米氮平组分别为83．3％和66．7％，氟西汀组分别为80．0％和63．3％，差异没有统计学意义（P〉0．05）。（4）安全性评定：两组比较差异无统计学意义（P〉0．05）。结论：米氮平治疗伴抑郁的心血管神经症有效而安全，且起效时间早于氟西汀。     

糖尿病大鼠海马超微结构观察及胰岛素治疗作用

目的 观察实验性糖尿病大鼠海马超微结构改变。方法 将成年ＳＤ大鼠随机分为正常对照组（５只）、糖尿病组（１２只,经腹腔注射链脉佐菌素制备实验性糖尿病大鼠模型）、糖尿病治疗组门 只,给子部分成模大凤长效胰岛素２－３Ｕ／日治疗,使空腹血糖低于 １０ｍｍｏｌ／Ｌ）,于成模第３月末及第６月末灌注固定取脑,透射电镜下观察梅马起微结构。结果 电镜下可见糖尿病大鼠海马发生锥体细胞退变。６月组病变较三月组更显著,相应治疗组改变较轻傲。结论 糖尿病可导致大鼠海马锥体细胞退变,早期应用胰岛素治疗可延缓其发生。     

Serotonin immunoreactivity in the circumesophageal nervous system of Hermissenda crassicornis

Immunohistochemical techniques were used to examine the distribution of serotonin-immunoreactive (5-HT-IR) neurons and processes in the circumesophageal nervous system of Hermissenda. Both the pedal and the cerebropleural ganglia contained immunoreactive neuronal somata, with the majority occurring in the pedal ganglia. Immunoreactive fibers and varicosities were identified in portions of the central neuropil, where we noted a consistent and specific relationship between 5-HT-IR axons, the optic nerve and the synaptic region in the neuropil near the photoreceptor terminals.