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At least 793 records · Page 44Linked to original sources
PubMed2000

Effects of NaCN and ionomycin on neuronal viability and on the abundance of microtubule-associated proteins MAP1, MAP2, and tau in isolated chick cortical neurons.

The effects of two toxins, sodium cyanide (NaCN) and ionomycin (IM), on neuronal viability and on the expression of the microtubule-associated proteins MAP1, MAP2, and tau were studied in isolated chick cortical neurons. Cytotoxic hypoxia due to NaCN treatment was performed to mimic acute neuronal damage, whereas long-term IM treatment was used as a model for chronic neuronal impairment. After 5 days in vitro, a cytotoxic lesion was induced either by addition of NaCN (0.01-10 mM) or IM (0.01-10 microM). The NaCN solution was aspirated after 30 min and cells were allowed to regenerate for 6 h, 24 h, 48 h, or 72 h; whereas the permanent IM lesions were left undisturbed during the same periods of time. Neuronal viability was assessed by MTT assay. The abundance of MAP1, MAP2, and tau was evaluated by immunoblotting and, for MAP2, by immunohistochemistry also. Results showed that NaCN and IM lesions dose-dependently decreased viability. Irreversible cell damage occurred after impairment with 10 mM NaCN and 1 microm or 10 microm IM, while neurons lesioned with lower concentrations regenerated partially or adapted to the toxic environment. However, the same level of viability as of untreated cells was never reached. Furthermore abundance of MAPs was changed after both lesions. But while after extended recovery from NaCN lesion protein expression was normalizing (MAP2) or at least still detectable (MAP1A, tau), the consequences of a permanent IM lesion were more severe, since neurons were not able to maintain or even restore their MAP expression. Immunohistochemical experiments for MAP2 revealed that, compared with controls, NaCN and, to a much higher extent, IM treatment resulted in a loss of immunoreactivity in neurites due to progressing cell death.

Animals↗
PubMed2004

Distribution of neuronal nitric oxide synthase-immunoreactive neurons in the cerebral cortex and hippocampus during postnatal development.

Although many reports have argued a role for nitric oxide (NO) during postnatal development, there has been no combined demonstration in the cerebral cortex and hippocampus. We have investigated the distribution and morphology of neurons and fibers expressing neuronal NO synthase (nNOS) in the cerebral cortex and hippocampal formation of rats during the postnatal development, and correlated these findings with developmental events taking place in these regions. In the cerebral cortex, the nNOS-immunoreactive cells could be divided into two classes : heavily stained neurons and lightly stained neurons. For the lightly stained nNOS-positive neurons, only the cell bodies were observed, whereas for the heavily stained neurons, the cell bodies and their dendrites were visible. During the postnatal days, heavily stained neurons reached their typical morphology in the second week and appeared in all layers except for layer I. In the hippocampus, there was a transient expression of nNOS in the pyramidal cell layer at P3-P7, and this expression disappeared during following days. The adult pattern of staining developed gradually during the postnatal period. This study suggested that these alterations might reflect a region-specific role of NO and a potential developmental role in the postnatal cerebral cortex and hippocampus.

Animals↗
PubMed2006

Neuronal nitric oxide synthase immunopositive neurons in cat vestibular complex: a light and electron microscopic study.

Nitric oxide is a unique neurotransmitter, which participates in many physiological and pathological processes in the organism. Nevertheless, there are little data about the neuronal nitric oxide synthase immunoreactivity (nNOS-ir) in the vestibular complex of a cat. In this respect, the aims of this study were to: (1) demonstrate nNOS-ir in the neurons and fibers, from all major and accessory vestibular nuclei; (2) describe their light microscopic morphology and distribution; (3) investigate and analyze the ultrastructure of the NOS I-immunopositive neurons, fibers, and synaptic boutons. For demonstration of the nNOS-ir, the peroxidase-antiperoxidase-diaminobenzidin method was applied. Immunopositive for nNOS neurons and fibers were present in all major and accessory vestibular nuclei. On the light microscope level, the immunopositive neurons were different in shape and size. According to the latter, they were divided into four groups--small (with diameter less than 15 microm), medium-sized (with diameter from 15 to 30 microm), large type I (with diameter from 30 to 40 microm), and large type II (with diameter greater than 40 microm). On the electron microscope level, the immunoproduct was observed in neurons, dendrites, and terminal boutons. According to the ultrastructural features, the neurons were divided into three groups--small (with diameter less than 15 microm), medium-sized (with diameter from 15 to 30 microm), and large (with diameter greater than 30 microm). At least two types of nNOS-ir synaptic boutons were easily distinguished. As a conclusion, we hope that this study will contribute to a better understanding of the functioning of the vestibular complex in cat and that some of the data presented could be extrapolated to other mammals, including human.

Animals↗
PubMed2006

Neuroprotective effect of a chuk-me-sun-dan on neurons from ischemic damage and neuronal cell toxicity.

Chukmesundan (CMSD), composed of the following 8 medicinal herbs including Panex ginseng C.A. MEYER, Atractylodes macrocephala KOID, Poria cocos WOLF, Pinellia ternata BREIT, Brassica alba BOISS, Aconitum carmichaeli DEBX, Cynanchum atratum BGE and Cuscuta chinensis LAM. CMSD is being used in Korea for the treatment of various symptoms accompanying hypertension and cerebrovascular disorders. This study was carried out to examine the effects of CMSD on cultured primary neuron cell, cell cytotoxicity and lipid peroxidation in Abeta-treated cells. Cell death was enhanced by addition of Abeta. Pretreatment of CMSD attenuated in cell killing induced by Abeta. The protective effect of the CMSD water extracts on Abeta-induced neuronal death was also observed by lactate dehydrogenase assay using cultured astrocyte cells. Abeta-induced cell death was protected by the water extract of CMSD in a dose-dependent manner, and 25-50 microg/ml was the most effective concentration. CMSD has been also shown to protect primary cultured neurons from N-methyl-D: -aspartate receptor-mediated glutamate toxicity. It was in vivo evidenced that CMSD protects neurons against ischemia-induced cell death. Moreover, oral administration of CMSD into mice prevented ischemia-induced learning disability and rescued hippocampal CA1 neurons from lethal ischemic damage. The neuroprotective action of exogenous CMSD was also confirmed by counting synapses in the hippocampal CA1 region. The presence of CMSD in neuron cultures rescued the neurons from nitrogen oxide (NO)-induced death. From these, it was suggested that CMSD may exert its neuroprotective effect by reducing the NO-mediated formation of free radicals or antagonizing their toxicity.

Amyloid beta-Peptides↗
PubMed1978

Changes in the distribution of non-neuronal elements in rat median eminence and in anterior pituitary hormone secretion after activation of tuberoinfundibular dopamine neurones by brain stimulation or nicotine.

In order to investigate the posssibility of acute functional changes in non-neuronal elements (mainly tanycytes) of the median eminence, the proportion of portal capillary surface covered by such elements was measured by quantitative electron microscopy in ovariectomized, oestrogen-progesterone-pretreated rats. In some of these animals, the functional state of the tuberoinfundibular dopamine (DA) neurones was assessed by histochemical microfluorimetry. Serum concentrations of luteinizing hormone (LH), growth hormone (GH) and prolactin were determined by radioimmunoassay. Two different types of treatment, i.e. systemic administration of nicotine (1 mg/kg, s.c.) or electrical stimulation in the medial amygdaloid nucleus, markedly reduced the percentage of capillary surface covered by non-neuronal profiles within 20 and 15 min, respectively. At the same time, the tuberoinfundibular DA system responded by an increase in cellular fluorescence intensity, reflecting neuronal activation. Medial preoptic stimulation had basically the same effect but with more variability in the change in capillary coverage by tanycytes. The action of nicotine was prevented by pretreatment with the DA receptor blocking agent, pimozide (5 mg/kg), which indicates (1) that a dopaminergic mechanism was involved in the nicotine effect and (2) that the tanycyte response was elicited by DA released from nerve terminals acting at some receptor site. Nicotine also lowered serum levels of GH and prolactin. Pimozide antagonized only the effect on prolactin. While the reaction of DA neurones and capillary coverage by tanycytes were correlated with each other in individual rats, no statistically significant correlation was observed between tanycyte response and hormone levels, so that no conclusions can as yet be drawn as to the neuroendocrine significance of the tanycyte reaction. These results indicate that rapid changes in the proportion or portal capillary surface covered by non-neuronal profiles can be elicited by stimulation of extrahypothalamic brain areas or by activation of cholinergic mechanisms. The tanycyte response appears to be mediated at least in part by the tuberoinfundibular DA neurones.

Animals↗
PubMed1981

Are CNS neurons polyploid? A critical analysis based upon cytophotometric study of the DNA content of cerebellar and olfactory bulbar neurons of the bat.

A cytophotometric study of the nuclear DNA content of bat cerebellar and olfactory bulbar neurons was performed with particular attention to corrections for distributional error and non-specific light loss and to selection of appropriate control nuclei for the establishment of reliable haploid and diploid DNA values. Feulgen stained sections were measured with an integrating, scanning microdensitometer for correction of distributional error. The values thus obtained were further corrected in 3 different ways to subtract the contribution of background absorbance at 546 nm. Bat haploid (1c) DNA values were derived from spermatozoa, and diploid (2c) values from pancreatic acinar cells, hepatocytes and non-hepatocyte liver cells. Microglia of olfactory bulb also had 2c values. After correction, all neurons measured, except Purkinje cells, had DNA values more closely approximating the tetraploid (4c) than the diploid (2c) level. Purkinje neurons had mean DNA values closer to 2c than to 4c, but inherent technical difficulties in measuring these very large, light staining nuclei has created less confidence in the values obtained than for those of the other neurons. This uncertainty, plus the apparent existence of two populations of Purkinje neurons, one 2c and the other hyperdiploid, suggested by the DNA distribution curves, make it difficult to eliminate the possibility of polyploidization of Purkinje neurons. A critical analysis of various cytophotometric, radioautographic and biochemical approaches to the problem of CNS neuron polyploidization has revealed potentially serious flaws in many of them, rendering virtually impossible interpretation of the numerous contradictory results in the literature. Standardization of the cytophotometric technique and improvement of the radioautographic approach seem to be prerequisite to the resolution of the existing dilemma.

Animals↗
PubMed1983

Uptake of [3H]taurine into medium-size neurons and into identified striatonigral neurons in the rat neostriatum.

Injection of [3H]taurine into the neostriatum of the rat led to accumulation of radioactivity in a distinct population of neurons. Taurine-accumulating neurons had a medium-size cell body, a smooth nucleus and relatively little cytoplasm. Other neuron types, e.g. large neurons with indented nuclei, did not accumulate taurine. Striatonigral neurons, identified by retrograde transport of horseradish peroxidase, were found to take up [3H]taurine. It is suggested that taurine-accumulating neurons in the neostriatum are projection neurons.

Animals↗
PubMed1983

Excitation by dopamine of putative oxytocinergic neurones in the rat supraoptic nucleus in vitro: evidence for two classes of continuously firing neurones.

Neurones from the supraoptic nucleus in the rat hypothalamic slice preparation in vitro have been recorded from using conventional extracellular techniques. Neurones which fired in a slow continuous manner (putative oxytocinergic cells) increased their firing pattern in response to dopamine applied in the perfusate or pressure ejected onto the slice. Of these neurones, 85% were inhibited by spiperone, haloperidol or cis-flupenthixol applied in the bath. A small proportion (approximately 15%) of neurones excited by dopamine (DA) were not affected by these DA antagonists but were inhibited strongly by (+/-)-sulpiride. Similar results were also obtained on a small number of cells recorded from an 'island-slice' preparation, utilized to isolate the observed responses to an area immediately adjacent to the supraoptic nucleus. These results may be relevant to earlier work on in vivo anaesthetized preparations using intracerebroventricular injections of DA and antagonists, and indicate that such substances may act directly on a synapse(s) within the magnocellular nucleus in addition to other possible actions within the neurohypophyseal tract. The differential response to the dopamine antagonists indicate that the majority of continuously firing neurones in the supraoptic nucleus are of the DI receptor class, but the presence of possible D2 receptors on a small proportion of these neurones suggests that a second type of continuously firing neurone may exist in this nucleus.

Animals↗
PubMed1986

Localization of aromatase and 5 alpha-reductase to neuronal and non-neuronal cells in the fetal rat hypothalamus.

Experiments were designed to identify the neural cell type(s) responsible for the aromatization and 5 alpha-reduction of androgens in the rat hypothalamus. Primary cultures of fetal rat hypothalamic cells, which had enhanced neuronal morphology, were treated at various times after plating with kainic acid (KA), a neurotoxic agent which selectively destroys neuronal cells. Neuronal morphology was disrupted in a time (0-6 days)- and dose (10(-4)-10(-2) M)-dependent fashion after KA treatment, with no apparent change in the appearance of the flattened, underlying non-neuronal cells. KA treatment for 4 days decreased aromatization by 94% in a dose-dependent fashion (10(-4)-10(-2) M KA), while 5 alpha-reduction declined by no more than 25%. A 6-day time course with 10(-3) M KA showed a dramatic decline in aromatization and no alteration in 5 alpha-reduction. In control experiments, substance P, a neuronal peptide, declined after KA treatment while the activity of glutamine synthetase, a glial enzyme, did not change. We conclude from these results that aromatase is localized primarily to neuronal cells in the hypothalamus while 5 alpha-reductase is confined primarily to non-neuronal cells.

3-Oxo-5-alpha-Steroid 4-Dehydrogenase↗
PubMed1989

Characterization of superficial T13-L2 dorsal horn neurons encoding for colorectal distension in the rat: comparison with neurons in deep laminae.

Fifty-five neurons responsive to colorectal distension located in the superficial spinal dorsal horn (0.0-0.3 mm ventral to the cord dorsum) of the T13-L2 spinal segments of pentobarbital-anesthetized, physiologically intact or spinalized (C1 transection), decerebrate rats were characterized. These neurons could be separated into three groups based upon their response to an 80 mm Hg, 20 s colorectal distension: (1) short latency-abrupt (SL-A) neurons (n = 22) that were excited by colorectal distension at a short latency (less than 1 s) and abruptly terminated responses following the termination of the distending stimulus; (2) short latency-sustained (SL-S) neurons (n = 26) that were excited by colorectal distension at a short latency (less than 1 s) and demonstrated sustained responses (greater than 4 s) following termination of the distending stimulus; and (3) INHIB neurons (n = 7) that were spontaneously active and were inhibited by colorectal distension. All 55 neurons had convergent cutaneous receptive fields (i.e. were 'viscerosomatic'), exhibiting excitatory responses to noxious (pinch/heat) and/or non-noxious (brush) stimuli. Neurons excited by colorectal distension also demonstrated monotonic, accelerating responses to graded colorectal distension, were excited by the intraarterial administration of bradykinin, could be antidromically activated by electrical stimulation in the caudal ventrolateral medulla and were subject to tonic descending inhibitory modulation as evidenced by more vigorous responses to distension when rats were reversibly spinalized using a cold block.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1989

Immunocytochemical characterization of neuron-rich rat brain primary cultures: calbindin D28K as marker of a neuronal subpopulation.

The function in neurons of the vitamin D-dependent calcium ion-binding-protein of 28 kDa mol. wt., calbindin D28K, is unknown. In order to find a simple system for studying the function of this protein, neuron-rich primary cultures derived from brains of 16-day-old rat embryos were analyzed for the presence of calbindin D28K by immunocytochemical mono- and double-labelling techniques. The studies were carried out between the 5th and 23rd day after seeding. In contrast to the neuronal marker neuron-specific enolase which was found in nearly all cells in the culture, calbindin D28K was expressed only in a subpopulation of neurons. Calbindin D28K-positive cells were intensely stained in their cell bodies and were also stained in their processes. Astroglial cells identified by the presence of the processes. Astroglial cells identified by the presence of the specific marker glial fibrillary acidic protein did not express calbindin D28K. Therefore, calbindin D28K is a useful marker for defining a neuronal subpopulation in neuron-rich primary cultures. Such cultures may be employed as a tool in searching for function(s) of calbindin D28K.

Animals↗
PubMed1990

High oxygen atmosphere for neuronal cell culture with nerve growth factor. I. Primary culture of basal forebrain cholinergic neurons from fetal and postnatal rats.

Cholinergic neurons cultured from postnatal days 11-13 (P11-P13) rat basal forebrain showed better survival in the culture condition using a 50% O2 atmosphere with and without nerve growth factor (NGF) than in a low (10 or 20%) O2 atmosphere. Except for the culture at a low cell density, the beneficial effect of the highly oxidized culture condition was found in the culture from P3 neurons, but not from embryonic day 18 neurons. The survival of microtubule-associated protein 2 (MAP2)-positive neurons in culture from P3 basal forebrain regions was more enhanced in a 50% O2 atmosphere than in 20% and also 10% O2 atmosphere. The viable number of the MAP2-positive neurons in a 10% O2 condition was about half of that in a 20% condition. These results suggest that the response of the cultured neurons to an incubator O2 concentration changes during the neuronal development in CNS from fetal to postnatal stages.

Acetylcholine↗
PubMed1990

Thoracic expiratory motor neurons of the rat: localization and sites of origin of their premotor neurons.

The expiratory motor neurons of the representative thoracic segment of the rat were examined as to their localization and sites of origin of their premotor neurons in the lower brainstem. Either T6 or T7 was selected as a representative target segment for horseradish peroxidase (HRP) injection. The intercostal motor neurons in the T6 or T7 were doubly labeled by HRP placed in the cut end of the internal intercostal nerve and True blue placed in the cut end of the external intercostal nerve. The thoracic expiratory motor neurons labeled by HRP were concentrated in the oblique zone running along the dorsal to ventrolateral direction in both the T6 and T7 segments. By contrast, the thoracic inspiratory motor neurons labeled by True blue were concentrated in the horizontal zone running along the bottom of the ventral horn in both the T6 and T7 segments. A small amount of HRP was iontophoretically injected through a double-barrel coaxial electrode to sites of the expiratory motor neurons which had been identified electrophysiologically. In 5 successful experiments, the HRP-labeled cells were bilaterally distributed in the para-ambiguus nucleus (59.0%), ventral subnucleus of the paramedian reticular nucleus (13.6%), and raphe nuclei (10.8%). In another experiment, it was found that the expiratory premotor neurons in the para-ambiguus nucleus were present in a narrow column over the entire length of the nucleus at a level between 1.0 mm rostral and 1.4 mm caudal to the obex.

Animals↗
PubMed1993

Substance P receptor-immunoreactive neurons in the rat neostriatum are segregated into somatostatinergic and cholinergic aspiny neurons.

Immunochemical characteristics of neostriatal neurons producing substance P receptor (SPR) were examined in adult rats by double- and triple-immunofluorescence methods. In the neostriatum, SPR immunoreactivity was detected in large and medium-sized aspiny neurons. Virtually all SPR-immunoreactive neurons in the neostriatum contained somatostatin (SS) or choline acetyltransferase (ChAT), but not parvalbumin. All SS- and ChAT-immunoreactive neurons in the neostriatum showed SPR immunoreactivity. The co-existence of SS and ChAT was, however, not found in single neurons expressing SPR immunoreactivity. The present results indicate that neostriatal neurons immunoreactive for SPR are segregated into 2 groups: (1) medium-sized, spiny somatostatinergic, and (2) large, aspiny cholinergic neurons.

Animals↗
PubMed1994

Effect of anoxia on glutamate formation from glutamine in cultured neurons: dependence on neuronal subtype.

Synthesis and release of glutamate formed from labeled glutamine were studied in primary cultures of the glutamatergic cerebellar granule cells and of the mainly GABAergic cerebral cortical neurons under anoxic conditions and under normoxic control conditions. Under both control and anoxic conditions cerebellar granule cells synthesized and released glutamate more intensely than cerebral cortical neurons, but this difference was enhanced under anoxic conditions. Thus, under normoxic conditions synthesis of intracellular labeled glutamate from glutamine was twice as high in cerebellar granule cell neurons as in cerebral cortical neurons during 30 min of incubation, but the release of newly synthesized labeled glutamate to the extracellular medium from cerebellar granule cell neurons was more than 4 times higher than the release from cerebral cortical neurons during 30 min of incubation. Based on these observations it is suggested that a major reason for the increase in extracellular glutamate concentration during brain ischemia may be enhanced production and release of glutamate, especially in glutamatergic neurons.

Animals↗
PubMed1994

Monosynaptic excitation of preganglionic vasomotor neurons by subretrofacial neurons of the rostral ventrolateral medulla.

Extracellular single unit recordings were made from barosensitive neurons in the subretrofacial nucleus (SRF) of the rostral ventrolateral medulla in chloralose-anaesthetised cats. At the same time, single preganglionic neuron activity was recorded from filaments of the cervical sympathetic trunk (CST); barosensitive units were selected for study. Evidence for monosynaptic connections between the two neuron groups was sought by cross-correlation analysis of their ongoing activity. Cross-correlograms of 16/16 SRF/CST neuron pairs showed a broad peak (100-200ms wide), reflecting the synchronizing action of arterial baroreceptors on both neurons' activity. Two of the 16 cross-correlograms additionally showed a robust, statistically significant, narrow peak of a single 2 ms bin width, providing the first physiological demonstration that ventrolateral medullary neurons monosynaptically excite preganglionic sympathetic neurons. Deductions are made about the strength, convergence and divergence of the connection.

Animals↗
PubMed1978

Morphine: effects on serotonergic neurons and neurons in areas with a serotonergic input.

The hypothesis that morphine acts on the serotonergic system to produce analgesia is based on the previous observations that (1) lesions and stimulation of midbrain raphe nuclei after the threshold to nociceptive stimuli; (2) morphine alters the turnover of serotonin (5-hydroxytryptamine; 5-HT). Microiontophoretic experiments were carried out to determine if morphine affected the firing rate of cells in five areas of the serotonergic system consisting of 5-HT containing neurons in the midbrain raphe nuclei (dorsal raphe and median raphe) or neurons in three areas (amygdala, optic tectum and subiculum) which are thought to receive a 5-HT input from the raphe nuclei. Morphine administered microiontophoretically slowed or inhibited the spontaneous neuronal firing in 34% of the cells studied in both the pre- and post-synaptic areas; systemically administered morphine gave similar results. However, the inhibition of neuronal firing by morphine in the five areas of the serotonergic system studied was not a specific narcotic effect because (1) it was not stereospecific; and (2) it was rarely blocked by naloxone. The inhibitory effect of morphine does not appear to be related to the analgesic effects of morphine because neuronal firing in the midbrain raphe nuclei and three possible postsynaptic areas was rarely altered by a nociceptive stimulus. It is concluded that (1) the analgesic effect of morphine is not related to an effect on neurons in the midbrain raphe nuclei and three areas which receive an identified 5-HT input; and (2) the effect of morphine on neurons in these five areas of the serotonergic system is not a specific narcotic effect.

Animals↗
PubMed1990

Different populations of dorsal lateral geniculate nucleus neurons have concentration-specific requirements for a cortically derived neuron survival factor.

A macromolecular fraction of conditioned culture medium (CM) derived from explant cocultures of embryonic rat posterior cortex and caudal thalamus is able to support the survival of neurons in the dorsal lateral geniculate nucleus (dLGN) of newborn rats following ablation of dLGN cortical target areas. In the present study we tested whether the survival-promoting activity of this target-derived neurotrophic agent was concentration dependent and whether different subpopulations of dLGN neurons were equally responsive. With the starting concentration of the CM fraction designated X, increasing concentration results in a progressive falloff in trophic activity so that at 200X overall dLGN survival is similar to that seen in unconditioned medium (UM) controls. In contrast, diluting the fraction produces an increase in activity until maximal survival is achieved at 0.2X. Further dilutions result in a decline in trophic activity until control values are reached at 0.001X. Two populations of neurons within the dLGN, defined by their time of origin, respond in a specific manner to the different concentrations. Neurons generated during the early stages of neurogenesis (E14) have maximal survival (25.8%) at 0.05X, whereas those neurons generated later (E15/16) are maximally supported (30.7% survival) at 10X, a 200-fold difference in concentration. While it is possible that separate neurotrophic and neurotoxic molecules exist for each of these populations of dLGN neurons, the most parsimonious interpretation of the data is that a single cortically derived neurotrophic factor exists whose production is strictly controlled during development to achieve maximal effect on different populations of thalamic neurons that may be functionally distinct.

Animals↗