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1.
The distribution of glutamate receptors in transverse hippocampal sections has been well investigated. However, in spite
of the known septotemporal gradients of hippocampal connectivity no systematic studies exist about the distribution of glutamate
receptors along the septotemporal (longitudinal) hippocampal axis. Therefore, in the present study this issue was investigated
using receptor autoradiography for the [3H]MK-801, [3H]AMPA and [3H]Kainate binding sites. Hippocampi from 30-day-old rats were sectioned perpendicularly to their longitudinal axis, yielding
a total of 25–30 equidistantly spaced autoradiographs for each hippocampus. For each section layer-specific concentrations
of binding sites were calculated by the aid of a computerized image analysing system. The dependency of concentrations of
binding sites on the septotemporal position was evaluated by regression analysis. Gradients of binding were confined to distinct
hippocampal layers. Significant septotemporal gradients of [3H]MK-801 binding were observed in selected layers of CA1 and the dentate gyrus, a septal to temporal decrease of binding in
the oriens and radiatum layers of CA1 being most prominent. For [3H]AMPA, significant septotemporal gradients of binding were restricted to layers of CA3, CA4 and the dentate gyrus, with values
generally increasing from septal to temporal levels. The observed septotemporal gradients possibly reflect functional segregations
along the longitudinal hippocampal axis and could be important for the comparability of ligand binding studies using transverse
hippocampal sections or hippocampal slice cultures.
Accepted: 2 April 1998 相似文献
2.
The effects of glycine on the release of [3H]noradrenaline ([3H]NA) have been investigated using rat hippocampus slices previously labeled with the radioactive catecholamine. Glycine (30-1000 microM) produced a potent and concentration-dependent increase of the release of [3H]NA evoked by 12 mM KCl. The effect of 1000 microM glycine was totally antagonized by 3 microM strychnine suggesting that, in rat hippocampus, glycine may regulate the release of NA by activating a receptor of the strychnine-sensitive subtype. 相似文献
3.
C. Albrecht H. G. Bloss R. Jackisch T. J. Feuerstein 《Experimental brain research. Experimentelle Hirnforschung. Expérimentation cérébrale》1999,128(3):383-389
In order to assess the autoinhibitory control of endogenous acetylcholine (ACh) in rat and human neocortex, slices of these
tissues were prelabelled with [3H]choline, superfused continuously and stimulated electrically using various frequencies in the presence or absence of drugs.
The autoinhibitory feedback control of [3H]ACh release was operative – despite the absence of blockers of ACh esterase – at stimulation frequencies ≥3 Hz in rat and
≥6 Hz in human neocortex tissue. At these frequencies the muscarinic antagonist atropine (0.1 μM) disinhibited the release
of [3H]ACh in both species. Estimation of the biophase concentration of ACh near the autoreceptor in the rat neocortex from concentration-response
curves of the muscarinic agonist oxotremorine revealed that at 3 Hz about 25% of the autoreceptors were activated by endogenously
released ACh. This estimation is consistent with an increase in [3H]ACh release to about 120% of control values by complete blockade of autoreceptors with atropine. The observation that in
human neocortical tissue presynaptic autoinhibition of [3H]ACh release is operative at stimulation frequencies ≥6 Hz suggests that selective blockade of autoinhibition may also increase
ACh release in the cortex of Alzheimer’s disease patients, without additional blockade of the enzyme acetylcholinesterase.
Received: 22 September 1998 / Accepted: 27 April 1999 相似文献
4.
N. J. H. Raat G. E. C. Wetzels J. G. R. De Mey 《Pflügers Archiv : European journal of physiology》1998,436(2):262-269
We evaluated the relationship between intracellular calcium concentration ([Ca2+]i) and vasoconstriction during the presence of exogenous noradrenaline (NA) and sympathetic nerve stimulation. An imaging technique
was used to determine calcium/tension relationships in isolated rat mesenteric resistance arteries that had been mounted for
recording of isometric tension development and loaded with Fura-2/AM. Experiments were performed after depletion of vasodilator
neuropeptides and in the continuous presence of 1 μM propranolol, 3 μM indomethacin, and 30 μM nitro-l-arginine. NA (10 μM) was shown first to induce a further increase in tension, but not [Ca2+]i, during the contraction induced by 125 mM K+. Subsequently, calcium/tension relationships were determined during stimulation with graded increases in extracellular [K+] (5.9–125 mM K+), cumulative administration of NA (0.2–10 μM) and electrical field stimulation of perivascular nerves (EFS, 1–16 Hz). A basal
calcium/tension relationship without the calcium-sensitizing property of NA was constructed using a cumulative concentration/response
curve of 5.9–125 mM K+ in arteries after prior exposure to the irreversible α-adrenoceptor antagonist phenoxybenzamine (POB). K+ series before and during α-blockade were also studied using the combination of the α1-antagonist prazosin and α2-antagonist yohimbine yielding comparable results as with POB. Calcium/tension curves obtained in the presence of NA, K+ and during EFS all were shifted to the left compared with the basal condition and all showed a similar slope indicating that
neurogenically released NA is equally capable of inducing calcium sensitization in smooth muscle of mesenteric resistance
arteries as exogenously applied NA. In the presence of exogenous and endogenous NA we not only observed an elevated contractile
response for a given increase in [Ca2+]i, but also an attenuated rise in [Ca2+]i for a given intensity of stimulation. This suggests that the agonist-induced calcium-sensitization is accompanied by a reduction
of the rise in [Ca2+]i.
Received: 24 October 1997 / Received after revision: 26 January 1998 / Accepted: 26 February 1998 相似文献
5.
The distribution of ionotropic glutamate receptors in transverse hippocampal sections and along the septotemporal hippocampal
axis can be correlated to hippocampal connectivity, in particular to area- and layer-specific termination zones of afferents.
However, in isolated organotypic hippocampal slice cultures developing without extrinsic afferent input no systematic studies
exist about the distribution of glutamate receptors. In the present study we used receptor autoradiography to examine [3H]MK-801, [3H]AMPA and [3H]Kainate binding sites in hippocampal slice cultures prepared from 6-day-old rats. After 24 days in vitro layer-specific
concentrations of [3H]MK-801, [3H]AMPA and [3H]Kainate binding sites were compared to age-matched hippocampi in situ (P30 rats). An obvious difference between hippocampal
slice cultures and hippocampi in situ was a changed distribution of binding sites among the hippocampal areas showing a relative
increase of [3H]MK-801 and [3H]AMPA binding sites in CA3 as compared to CA1 and to the dentate gyrus in the cultures. In CA1, however, the relative layer-specific
distributions of [3H]MK-801 and [3H]AMPA binding sites were identical in hippocampal slice cultures and in hippocampi in situ. Interestingly, layer-specific
binding of [3H]Kainate in the cultures exceeded that in the hippocampi in situ 3–5 times. Moreover, in the cultures the binding of the
three ligands varied systematically showing gradients along the ”superficiomembranal’’ axis. Cultures taken from different
positions along the hippocampal axis differed with respect to concentrations of [3H]MK-801 and [3H]Kainate binding sites, but not of [3H]AMPA binding sites. The results suggest a massive sprouting and reorganisation of intrinsic projections in long-term hippocampal
slice cultures.
Accepted: 6 February 2001 相似文献
6.
R. Jackisch Jeanne Stemmelin Brigitte Neufang Dorothee Lauth Bogdan Neughebauer Christian Kelche Jean-Christophe Cassel 《Experimental brain research. Experimentelle Hirnforschung. Expérimentation cérébrale》1999,124(1):17-24
Lesions of the septohippocampal pathways elicit sprouting of sympathetic fibers from the superior cervical ganglion, a phenomenon
which, within a few months, raises the hippocampal noradrenaline (NA) content above normal. In peripheral sympathetic fibers,
the release of NA is modulated via presynaptic muscarinic receptors. Such receptors have not been detected so far on terminals
of noradrenergic neurons originating in the locus coeruleus. Whether the release of NA could become sensitive to muscarinic
modulation in the hippocampus following sympathetic fiber ingrowth was the major question in this experiment. The contribution
of presynaptic nicotinic receptors was also studied. Slices from the ventral hippocampus (only dentate gyrus+CA3 region) of
sham-operated (SHAM) and fimbria-fornix lesioned (LES) Long-Evans rats (8–10 months after surgery) were preincubated with
[3H]NA and stimulated either once (S1) with 100 μM nicotine or (in parallel experiments) twice electrically (S1, S2), using conditions (six pulses 100 Hz, 2 ms, 28 mA, 4 V/chamber) that precluded autoinhibition. In experiments using electrical
stimulation, the superfusion medium contained desipramine (1 μM). In LES rats, the tissue NA content had almost doubled (171%
of SHAM levels), but the amount of [3H]NA taken up by the slices was unchanged, and the overflow evoked at S1 by both nicotinic and electrical stimulation was significantly reduced in comparison with SHAM rats. In both groups, the
addition of oxotremorine or oxotremorine+atropine (1 μM, each) before S2 failed to affect the electrically evoked overflow of 3H. Nicotine-induced NA release was inhibited by hexamethonium (100 μM) in both groups, although significantly less potently
in LES rats. Tissue activity of choline acetyltransferase was reduced in LES rats to 15% of SHAM levels and the 5-hydroxytryptamine
content was also strongly diminished (38% of SHAM values). It is concluded that lesion-induced sprouting of sympathetic fibers
into the hippocampus is not accompanied by the emergence of a muscarinic modulation of NA release in this tissue, and that
the sensitivity of the presynaptic stimulatory effect of nicotine was modified by the lesion.
Received: 22 April 1998 / Accepted: 23 July 1998 相似文献
7.
The distribution of glutamate receptors in transverse hippocampal sections has been well investigated. However, in spite of the known septotemporal gradients of hippocampal connectivity no systematic studies exist about the distribution of glutamate receptors along the septotemporal (longitudinal) hippocampal axis. Therefore, in the present study this issue was investigated using receptor autoradiography for the [3H]MK-801, [3H]AMPA and [3H]Kainate binding sites. Hippocampi from 30-day-old rats were sectioned perpendicularly to their longitudinal axis, yielding a total of 25–30 equidistantly spaced autoradiographs for each hippocampus. For each section layer-specific concentrations of binding sites were calculated by the aid of a computerized image analysing system. The dependency of concentrations of binding sites on the septotemporal position was evaluated by regression analysis. Gradients of binding were confined to distinct hippocampal layers. Significant septotemporal gradients of [3H]MK-801 binding were observed in selected layers of CA1 and the dentate gyrus, a septal to temporal decrease of binding in the oriens and radiatum layers of CA1 being most prominent. For [3H]AMPA, significant septotemporal gradients of binding were restricted to layers of CA3, CA4 and the dentate gyrus, with values generally increasing from septal to temporal levels. The observed septotemporal gradients possibly reflect functional segregations along the longitudinal hippocampal axis and could be important for the comparability of ligand binding studies using transverse hippocampal sections or hippocampal slice cultures. 相似文献
8.
Weanling rats were injected intraperitoneally with [3H]thymidine and sacrificed from 5 min to 20 days later. Their mandibular condylar cartilages were examined histologically, by thin-layer autoradiography, and by using liquid scintillation and microscopic counting methods. Labeled DNA appeared in some of the chondrocytes of the resting zone as early as 10 min postinjection, and reached the proliferative zone by 24 hr and the hypertrophic zone by 4 days. The labeling pattern in the last zone was more disperse, being oriented toward the periphery of the cells as they became hypertrophic. The maximum number of labeled chondrocytes was reached by 2 hr postinjection. These amounted to approximately 11% of the total chondrocyte population, the majority of which were located in the resting zone (73%). It is concluded that, over this period, the mitotic index for these cells is 50–60 per thousand resulting in approximately 100 labeled chondrocytes. In addition, some of the chondroclasts at the erosion front contained labeled DNA as early as 5 min after [3H]thymidine administration. By 10 min, 65% of these cells exhibited one or more labeled nuclei, and the ratio of labeled cells remained high through 20 days. Chondroclasts were seen to contain a diffuse label within their cytoplasm after 5 days. This label was similar to that seen in hypertrophic chondrocytes that had reached the erosion front by that time. Clearly, chondroclasts exhibit nuclear division and do not form from fusion of hypertrophic chondrocytes, although which specific mononuclear cells may act as chondroclast progenitors is not clear. In addition, these multinucleate resorbing cells are capable of ingesting or phagocytizing nuclear remnants from hypertrophic chondrocytes at the eroding face of cartilage. 相似文献
9.
David Gaffan 《Experimental brain research. Experimentelle Hirnforschung. Expérimentation cérébrale》1998,123(1-2):201-209
Memory for object-place configurations appears to be a common function of the hippocampus in the human and monkey brain. The
nature of the spatial information which enters into these object-configural memories in the primate, and the location of the
memories themselves, have remained obscure, however. In the rat, much evidence indicates that the hippocampus processes idiothetic
spatial information, an estimate of the animal’s current environmental location derived from path integration. I propose that
in primates the hippocampus provides idiothetic information about the environmental location of body parts, and that the main
function of this information in the primate brain is to become configured with object-identity information provided by temporal
lobe cortex outside the hippocampus. 相似文献
10.
Hiroyuki Cho K. Shimazaki Kosei Takeuchi Satoru Kobayashi Kazutada Watanabe Keiji Oguro Toshio Masuzawa Nobufumi Kawai 《Experimental brain research. Experimentelle Hirnforschung. Expérimentation cérébrale》1998,122(2):227-234
We studied changes in expression of F3/contactin (F3), a neuron-specific adhesion molecule, in the gerbil hippocampus after
transient forebrain ischemia for 5 min. By immunohistochemical techniques using F3 antibody, we found a biphasic change in
immunoreactivity for F3 in the CA1 area after ischemia. Western blotting of F3 protein showed a similar biphasic change. F3
immunoblots decreased to 67% of the control at 1 week, but then they increased and attained 159% at 3 weeks and 152% at 5
weeks after ischemia. Immunoreactivity of a neurofilament (NF145) showed a similar biphasic change to F3 but to a lesser extent.
In contrast, microtubule-associated protein 2 (MAP2) immunoreactivity uniformly decreased after ischemia. In situ hybridization
revealed that F3 messenger RNA (mRNA) hybridization signals in CA1 area were greatly reduced 1 week after ischemia, while
the signals in the CA3 area were unchanged and even increased 3 weeks after ischemia. Damage to CA3 neurons by hyperthermic
ischemia blocked the F3 increase in area CA1. Our results suggest that the initial decrease in F3 following ischemia reflects
loss of CA1 neurons and the late increase in F3, which shows that a similar time course with neurofilaments may be caused
by neurite sprouting.
Received: 25 August 1997 / Accepted: 1 April 1998 相似文献
11.
J. Folbergrová Ping-An Li H. Uchino Maj-Lis Smith B. K. Siesjö 《Experimental brain research. Experimentelle Hirnforschung. Expérimentation cérébrale》1997,114(1):44-50
A recent study from this laboratory has shown that brief transient ischemia (2 min 30 s) in normo- and hyperglycemic rats
leads to moderate neuronal necrosis in CA1 cells of the hippocampus, of equal density in the two groups. However, hyperglycemic
animals failed to depolarize during the ischemia, nor did they show a decrease in extracellular calcium concentration. The
present study was undertaken to study the metabolic correlates to these unexpected findings. Normoglycemic (plasma glucose
∼6 mM) and hyperglycemic (∼20 mM) rats were subjected to ischemic periods of 1 min and 2 min 15 s (2 min 30 s with freezing
delay considered), and their brains were frozen in situ. Samples of dorsal hippocampus were dissected at –22°C and extracted
for the measurement of phosphocreatine (PCr), creatine, ATP, ADP, AMP, glucose, glycogen, and lactate. Normoglycemic animals
showed rapid depletion of PCr, ATP, glucose, and glycogen, and a rise in lactate content to 10–12 mM·kg–1 during the ischemia. Hyperglycemic animals displayed a more moderate rate of fall of PCr and ATP, with ATP values exceeding
50% of control after 2 min 30 s. Glycogen stores were largely maintained, but degradation of glucose somewhat enhanced the
lactic acidosis. The results demonstrate that hyperglycemic rats maintained ATP at levels sufficient to prevent cell depolarization
and calcium influx during the ischemic period. However, the metabolic perturbation observed must have been responsible for
the delayed neuronal damage. We speculate that lowered ATP, increased inorganic P, and oxidative stress triggered a delayed
mitochondrial permeability transition (MPT), which led to delayed neuronal necrosis. This assumption was supported by a second
series of experiments in which CA1 damage in hyperglycemic rats was prevented by cyclosporin A, a virtually specific inhibitor
of the MPT.
Received: 24 May 1996 / Accepted: 30 September 1996 相似文献
12.
目的:观察黄芪注射液对脑缺血再灌注大鼠海马神经元凋亡及c-Jun N末端激酶3(JNK3)表达的影响。方法:四血管阻断法制备脑缺血再灌注大鼠模型。设假手术组、脑缺血再灌注模型组(模型组)、脑缺血再灌注模型+黄芪注射液组(黄芪注射液组)和脑缺血再灌注模型+黄芪注射液溶剂对照组(溶剂对照组)。除假手术组外其余3组根据再灌注时间不同又分为0 h、0.5 h、2 h、6 h、24 h、72 h和120 h 7个亚组。采用TUNEL法检测海马神经元凋亡,Western blotting法检测海马组织JNK3蛋白变化,real-time PCR法检测海马组织JNK3 mRNA 的表达变化。结果:与假手术组比,模型组大鼠各个时点凋亡细胞数均增多(P<0.05);与模型组比,黄芪注射液组各个时点的细胞凋亡数明显减少(P<0.05),而黄芪注射液溶剂对照组各个时点的细胞凋亡数无明显变化(P>0.05)。除120 h外,模型组各时点海马组织JNK3蛋白及mRNA表达均较假手术组增加(P<0.05);与模型组相比,黄芪注射液可减弱除120 h之外的各时点JNK3 蛋白及mRNA的表达(P<0.05),而黄芪注射液溶剂对照组则无明显变化(P>0.05)。结论:黄芪注射液可抑制脑缺血再灌注大鼠海马神经元凋亡,其抗凋亡机制可能与下调JNK3 mRNA及蛋白表达有关。 相似文献
13.
The influence of felodipine and diethyl-stilboestrol on [3H]noradrenaline release in the rat trachea
The fractional release of [3H]noradrenaline was measured in rings from the rat trachea. Transmitter release was induced either by isotonic KCl (124 mM) or by 2.5 mM Ca added to a Ca-free depolarizing solution. Felodipine, a Ca antagonist (10(-4)M), had no effect on the basal release of [3H]NA whereas it reduced the overflow of transmitter caused by KCl or Ca. Diethyl-stilboestrol (25 microM), which also inhibits Ca influx in smooth muscle, had a stronger inhibitory effect than felodipine on [3H]NA release induced by high K and addition of Ca. Basal efflux of [3H]NA was increased by diethyl-stilboestrol. This increase also occurred in the absence of extracellular Ca. 相似文献
14.
Stella E. Tsirka 《Journal of molecular medicine (Berlin, Germany)》1997,75(5):341-347
Tissue plasminogen activator (tPA), the serine protease that converts inactive plasminogen to the protease plasmin, was recently
shown to mediate neurodegeneration in the mouse hippocampus. Mice deficient in tissue plasminogen activator (tPA) display
a dramatic resistance to a paradigm of excitotoxic neuronal death that involves intrahippocampal injection of the excitotoxin.
This model is thought to reproduce the mechanism of neuronal death observed during acute (such as ischemic stroke) and degenerative
(such as amyotrophic lateral sclerosis) diseases of the nervous system. The requirement for the proteolytic activity of tPA
to mediate neuronal death is acute in the adult mouse. Serine protease inhibitors, specific for tPA or the tPA/plasmin proteolytic
cascade, are effective in conferring extensive neuroprotection following the excitotoxic injection. These findings suggest
possible new ways for interfering with the neuronal death observed in the hippocampus as a result of excitotoxicity. In addition,
tPA is produced in the hippocampus primarily by microglial cells, which become activated in response to the neuronal injury.
Blocking microglial activation has been shown in other injury paradigms to protect against neuronal death, therefore suggesting
another way to retard neurodegeneration in the CNS. Furthermore, after the insult has been inflicted and in the presence of
a compromised blood-brain barrier macrophages (cells deriving from the same lineage as microglia) migrate into the brain,
where they are thought to contribute to the neuronal cell loss by secreting neurotoxic molecules. If these macrophages/microglia
expressed, however, a tPA inhibitor, rather than the possibly neurotoxic tPA, they might be able to protect the neurons from
dying.
Received: 1 October 1996 / Accepted: 27 January 1997 相似文献
15.
T. Tömböl D. C. Davies A. Németh T. Sebestény A. Alpár 《Brain structure & function》2000,201(2):85-101
Neurons and fibres in the chick and homing pigeon hippocampus were described following Golgi impregnation. Two principal classes
of neurons were distinguished: projection neurons with distant projecting axons and spiny dendrites, and local circuit neurons.
In the homing pigeon and chicken hippocampus there are three types of projection neurons: pyramidal, pyramidal-like and multipolar.
The pyramidal and pyramidal-like neurons are only found in the central ’pyramidal’ layer of the hippocampus whereas multipolar
neurons are present in the suprapyramidal, pyramidal and infrapyramidal layers. The axon of projection neurons typically emits
several varicose collaterals from the initial section. Most of these collaterals extend along the infrapyramidal layer of
the hippocampus, while others ascend to the pyramidal and suprapyramidal layers where they branch. The number of impregnated
axon collaterals was higher in the homing pigeon than in the chick hippocampus. A variety of multiangular/ovoid local circuit
neurons ranging from small to large size are found in the homing pigeon and chick hippocampus. Their axons develop local arborisation
of varicose branches, the extent of which varies with the type of local circuit neurons. The density of GABA immunopositive
local circuit neurons was found to be greater in the homing pigeon than in the chick. The profuse arborisation of projection
neuron axon collaterals and the higher density of GABA-immunopositive local circuit neurons in the homing pigeon hippocampus
may underlie the differences in hippocampal function between the homing pigeon and chick, and this complex local connectivity
may contribute to the ability of spatial orientation and memory.
Accepted: 16 July 1999 相似文献
16.
J.-M. Ye J.T. Steen A. Matthias M.G. Clark E.Q. Colquhoun 《Acta physiologica (Oxford, England)》1998,163(1):49-57
Skeletal muscle can release or take up lactate depending on the lactate concentration gradient across the cell membrane. In the perfused rat hindlimb without arterial lactate, both noradrenaline (NA) infusion and increased flow promote lactate release and oxygen consumption (VO 2). However, it is unclear whether NA or increased flow rate have similar effects on lactate uptake. The present study compares these effects in the rat hindlimb perfused at a basal flow rate of 0.33 mL min?1 g?1 and 25 °C in the presence of added arterial lactate. When 10 mmol L?1 L-(+)-lactate was added to the arterial perfusate, lactate was taken up (16 ± 1.0 μmol g?1 h?1, n = 13) by the hindlimb with a 35% higher VO 2 than that without added lactate. Doubling perfusion flow rate enhanced lactate uptake and VO 2 by 120% and 40%, respectively. Glucose uptake was also increased (by 253%) with increased flow. Infusion of NA increased perfusion pressure, VO 2 and glucose uptake similarly to those induced by increased flow rate. However, lactate uptake was inhibited by NA. This inhibition was not altered by the β-adrenergic antagonist propranolol. Vasopressin also showed similar effects to NA to decrease lactate uptake associated with increased VO 2 and vasoconstriction. These data indicate that in the presence of a high arterial lactate concentration, NA has opposite effects from increased flow rate on skeletal muscle lactate uptake although both have similar effects on lactate release in the absence of arterial lactate. Inhibition of lactate uptake may relate to the vasoconstrictive action of NA. 相似文献
17.
目的:观察产前应激(PS)对子鼠海马神经元和神经元超微结构是否有损伤作用, 以及这种损伤是否与氧化物的过度生成有关。方法:采用束缚应激模型, 观察出生后1个月雄性子鼠的海马神经元数量、神经元超微结构及神经型一氧化氮合酶(nNOS)表达的变化。结果:晚期应激(LS)引起子鼠海马CA1和CA4区的细胞数量明显减少;电镜可见PS使子鼠海马CA1区神经元超微结构发生改变, 表现为线粒体肿大、边界不清、电子密度不均, 脂褐素增多, 偶见核变形;中期应激(MS)使子鼠海马CA1、CA2、CA3区和DG内nNOS阳性表达量显著升高, LS使子鼠海马CA1、CA2、CA3、CA4区和DG内nNOS阳性表达量也显著升高。结论:结果提示, PS对子鼠海马神经元及神经元超微结构有损伤作用, 这种损伤可能由氧化物过度生成引起。 相似文献
18.
A. Ameri T. Peters 《Experimental brain research. Experimentelle Hirnforschung. Expérimentation cérébrale》1997,114(3):518-524
Extracellular recording of the stimulus-evoked population spike was performed in the CA1 area of rat hippocampal slices in
order to investigate delayed effects of the plant alkaloids aconitine and veratridine. Veratridine (1 μM and 10 μM) suppressed
the orthodromic and antidromic population spike. After washout of the drug, only a partial recovery was obtained. Aconitine
(1 μM) exerted the same inhibitory action as veratridine. However, after washout, the spike amplitude was enhanced compared
with the control. This enhancement of the spike amplitude was dependent on the concentration of aconitine and was maintained
during the observation period of at least 2 h. Lowering the Ca2+ concentration of the bathing medium from 2.5 mM to 1.25 mM during application of aconitine attenuated recovery and prevented
the enhancement observed during washout of the drug. Application of aconitine in the presence of CdCl2 as well as in the presence of inhibitors of protein kinase C and Ca2+/calmodulin-dependent protein kinase II prevented the increase in spike amplitude during washout with standard artificial
cerebrospinal fluid. In contrast, the N-methyl-d-aspartate (NMDA) receptor antagonists D-AP5 and MK-801 as well as the non-NMDA receptor antagonist 6-cyano-7-nitroquinoxaline-2,3-dione
were ineffective in abolishing the aconitine-induced enhancement. These data support the conclusion that different modes of
action are involved in the effects of aconitine but not veratridine. It is concluded that the aconitine-induced increase in
neuronal activity is mediated by intracellular Ca2+-dependent mechanisms leading to an activation of Ca2+-dependent protein kinases. This effect is independent of Ca2+ entrance through NMDA and non-NMDA receptors.
Received: 3 July 1996 / Accepted: 14 November 1996 相似文献
19.
Effects of injury on [3H]putrescine uptake by types I and II cells in rat lung slices 总被引:1,自引:0,他引:1
The capacity of different lung parenchymal cells to accumulate putrescine was investigated by incubating slices of rat lung in a medium containing the tritiated compound. Quantitative examination of autoradiographs, by electron microscopy, indicated that accumulation of putrescine occurred in both the Type I and Type II cells of the alveolar epithelium. Putrescine uptake was abolished by the addition of spermidine to the medium or by incubating at 0 degrees C. Lung samples from rats dosed with the pneumotoxin O,S,S-trimethyl phosphorodithioate (OSSMeO), which selectively damages Type I pneumocytes, showed a large reduction in the uptake of label by both Type I and Type II cells. This treatment also resulted in an increase in the labeling of alveolar macrophages. Control samples, from undosed rats, were incubated in medium containing tritiated 5-hydroxytryptamine; this compound did not accumulate in epithelial cells but it was concentrated in the endothelium of the alveolar capillaries and in the blood cells within these vessels. The demonstration of putrescine uptake by both Type I and Type II pneumocytes, together with its reduction by dosing with OSSMeO, has vindicated the use of this activity, in lung slices, as an index of damage to the alveolar epithelium. 相似文献
20.
脑源性神经营养因子体外诱导神经干细胞向神经元分化 总被引:1,自引:1,他引:0
目的观察脑源性神经营养因子(BDNF)对新生SD大鼠海马神经干细胞在体外分化为神经元的作用。方法取新生SD大鼠海马组织,以无血清培养技术培养获得神经干细胞,在BDNF诱导下让其在体外分化,7d后,通过免疫荧光技术结合图像分析技术来观察分化所得神经丝(neurofilament,NF)抗原阳性神经元的比率及其最长突起的长度。结果BDNF组分化所得细胞NF阳性率为13.66%,神经元突起长度为(146.27±26.30)μm,对照组分化所得细胞NF阳性率为9.38%,神经元突起长度为(117.00±23.98)μm,两组结果有显著性差异。结论BDNF能提高新生SD大鼠海马神经干细胞体外定向分化为神经元的比率,并且能刺激新生神经元突起的生长。 相似文献