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At least 1,261 records · Page 70Linked to original sources
PubMed1982

Limbic status epilepticus: behaviour and sleep alterations after intra-amygdaloid kainic acid microinjections in Papio Papio baboons.

Limbic status epilepticus was produced with single microinjections of kainic acid in the amygdala of baboons (Papio papio). Long-term studies of the behavioural, electrographic and sleep alterations were performed. During status epilepticus the animals did not display aggressive behaviour. Feeding behaviour was diminished. Sleep was also deeply disturbed. Wakefulness was greatly increased, light slow wave sleep was diminished and deep slow wave sleep and paradoxical sleep was abolished. Sleep alterations persisted throughout the duration of status epilepticus (48-72 h). A modulation of paroxysmal discharges was observed depending on the degree of epileptogenicity of the limbic focus. Increased wakefulness cannot be attributed to convulsions since limbic status epilepticus in baboons is not accompanied by positive motor signs. It is proposed that increased wakefulness, of, a particular type as revealed by the alterations of different accompanying behaviours, during this type of status epilepticus, depends on an internal arousing mechanism.

Aggression↗
PubMed1990

Chronic focal epilepsy induced by microinjection of tetanus toxin into the cat motor cortex.

The tetanus toxin model of epilepsy, involving direct microinjection of toxin into the mammalian brain, has a number of advantages relative to other chronic models. However, chronic seizure foci have been confined primarily to the hippocampus. In the present study, 5 cats received total doses of 7.5-22.5 ng of tetanus toxin applied to the left primary motor cortex through an epidural cannula. After 2-18 days, all 5 cats exhibited similar persistent epileptiform syndromes. Three distinct types of spontaneous seizures were noted: focal motor seizures of variable complexity, focal motor seizures with secondary generalization, and epilepsia partialis continua. All cats required anticonvulsant therapy. Simple focal motor seizures, which predominated, were electrographically characterized by 3-5 Hz spike-sharp wave activity, originating in the left motor cortex, associated with contralateral shoulder and forepaw clonus and jacksonian spread. Electrographic activity quickly spread to ipsilateral neocortical structures, and in longer episodes to the cingulate gyri. Seizure foci were still active as long as 37 days after toxin injection. Light microscopic damage attributable to the toxin was absent. These experiments further generalized the tetanus toxin model and confirmed its advantages.

Animals↗
PubMed1982

Cardiovascular effects of beta-endorphin after microinjection into the nucleus tractus solitarii of the anaesthetised rat.

The cardiovascular effects of beta-endorphin after administration directly into the nucleus tractus solitari (NTS) of urethane-anaesthetised rats were investigated. Unilateral injection resulted in a U-shaped dose-response relationship with a fall in mean arterial pressure and heart rate occurring at low doses (less than 10 ng). No change in respiratory frequency was observed at any of the doses examined. The hypotensive effects of beta-endorphin were anatomically specific and restricted to the NTS. The depressor response was prevented and bradycardia reduced by naloxone (1 mg/kg s.c. or 10 ng injected into the NTS) and also by beta-endorphin antiserum (1:50 dilution) but not by antiserum to [Met5]enkephalin (1:50 dilution) applied locally into the NTS. The beta-endorphin antiserum caused a rise in blood pressure when administered alone. Conversely microinjection of antiserum to [Met 5]enkephalin resulted in a brief depressor response. Doses of beta-endorphin larger than 10 ng induced a rise in blood pressure accompanied by variable effects on heart rate. Similarly unilateral administration of Des-tyr-endorphin (100 pg) resulted in a blood pressure increase and [D-Ala2,Met5]enkephalin produced a dose-related pressor response and tachycardia. The results indicate that at least two separate endorphin systems are involved in cardiovascular control at the level of NTS, one being depressor in nature (beta-endorphin-like) and the other pressor ([met5]enkephalin-like).

Anesthesia↗
PubMed1983

Picrotoxin microinjections into the brain: a model of abrupt withdrawal 'jumping' behaviour in rats not exposed to any opiate?

Picrotoxin microinjections (0.5 microliter per side) given into the locus coeruleus, superior colliculus and central grey of freely moving Wistar rats produced an accelerating galloping locomotion, most often forwards but also upwards. Systemic administration of apomorphine (0.7-2.0 mg/kg s.c.) given 20 min earlier increased the number of rats that displayed the so-called 'running and jumping' behaviour after picrotoxin (0.1-0.2 microgram). The dose-effect curve, however, varied according to the brain structure selected. Systemic administration of morphine (1.0-10.0 mg/kg i.p.) was found to reduce the occurrence of running and jumping behaviour when it was elicited via the locus coeruleus, but not the superior colliculus and central grey. It is suggested that the running and jumping behaviour which is elicited via the locus coeruleus might be a suitable model of a partial morphine abstinence syndrome, i.e. withdrawal jumping, in experimental animals not exposed to any opiate. The superior colliculus and central grey appear to be involved in mediating an opiate-unrelated phenomenon of 'withdrawal' jumping in rats not exposed to any opiate.

Animals↗
PubMed1990

Dorsal raphe microinjection of 5-HT and indirect 5-HT agonists induces feeding in rats.

Previous work has shown that 5-hydroxytryptamine (5-HT) receptor agonists such as 8-hydroxy-2-(di-n-propylamino)tetralin (8-OH-DPAT) reduce 5-HT neurotransmission and induce feeding in rats. The effects of 8-OH-DPAT appear to be mediated in part in the dorsal raphe nucleus by serotonergic somatodendritic autoreceptors which normally regulate impulse flow in 5-HT dorsal raphe neurons. The present experiments sought to examine whether suppression of dorsal raphe serotonergic neural activity induced by exogenously applied, or endogenously released 5-HT would increase feeding. Free-feeding rats were microinjected in the dorsal raphe with 5-HT, the 5-HT releasing compound d-fenfluramine, the 5-HT re-uptake inhibitor zimelidine, or the type-A monoamine oxidase inhibitor brofaromine. Dose dependent increases in food intake over a 1 h period were found following treatment with 5-HT and the three indirectly acting compounds. Thus, increased serotonergic activity within the dorsal raphe increases feeding, presumably by inhibiting the activity of dorsal raphe 5-HT neurons. In addition the effects of 5-HT were blocked by pretreatment with haloperidol, indicating the involvement of a dopaminergic mechanism in mediating the effects of feeding of a suppression in dorsal raphe 5-HT neural activity. The results are discussed in terms of the general role which serotonergic neurons arising from the dorsal raphe may play in behavioural inhibition.

Animals↗
PubMed1992

Hippocampal lesions induced by microinjection of the nitric oxide donor nitroprusside.

Unilateral intrahippocampal microinjection of the nitric oxide (NO) donor, sodium nitroprusside (33 nmol in 1 microliter), in the rat resulted in a marked degeneration of the ipsilateral hippocampal formation characterised by a virtual absence of pyramidal cells and dentate granule cells. Damage was not observed contralateral to the injection site. Quinolinic acid (100 nmol in 1 microliter) also produced neuronal damage within the ipsilateral hippocampus although the lesion was considerably smaller and more discrete than that caused by sodium nitroprusside. Injection of equimolar amounts of potassium ferricyanide failed to mimic the neurotoxic effects of sodium nitroprusside suggesting that NO is responsible specifically for the neuronal damage observed.

Animals↗
PubMed1993

Opposite effects of mesencephalic microinjections of cholecystokinin octapeptide and neurotensin-(1-13) on brain stimulation reward.

Changes in operant responding for brain stimulation reward were studied before and after a microinjection of 1 nmol of sulphated cholecystokinin octapeptide, neurotensin or saline into the ventral tegmental area. Neurotensin produced a significant and long lasting decrease in the stimulation frequency required to produce a half-maximal rate of responding; cholecystokinin had the opposite effect, attenuating the rewarding efficacy the stimulation during the first 30 min post-injection. It is suggested that the opposite effects of the peptides on reward are due to their differential modulatory effects on a subpopulation of mesencephalic dopamine neurones.

Animals↗
PubMed1995

Systemic administration of the NMDA receptor antagonist MK-801 potentiates circling induced by intrastriatal microinjection of dopamine.

Systemic administration of the non-competitive antagonist of NMDA receptors MK-801 ((+)-5-methyl-10,11-dihydro-5H-dibenzo[a,d]cyclohepten-5,10-imine) potentiates the circling response induced by direct stimulation of the striatal dopaminergic receptors through intracerebral application of dopamine. Microinjection of dopamine (1, 5, 25 or 50 micrograms/1.0 microliters) induced a dose-dependent contralateral circling response, when injected directly into the lesioned side of unilaterally 6-hydroxydopamine-lesioned rats. Interestingly, intrastriatal application of dopamine (1, 5, 25 or 50 micrograms/1.0 microliters) followed by a systemic administration of MK-801 (100 micrograms/kg i.p.) produced a potentiated contralateral circling response in unilaterally 6-hydroxydopamine (6-OHDA)-lesioned rats. This motor effect is reversed compared to the marked ipsilateral circling response produced by MK-801 when given alone. Moreover, the potentiated responses persist 4-fold longer compared to the circling induced by dopamine alone. The results suggest that the potentiation by NMDA receptor antagonists of motor activity induced by dopaminergic agonists in animal models of Parkinson's disease cannot be ascribed simply to increased release of dopamine. Other mechanisms including increased sensitivity of dopamine D1 receptors or blockade or glutamatergic transmission in output structures must be considered.

Animals↗
PubMed1984

Microinjection in the chick blastoderm. An improved method to study the extracellular matrix in the living organism.

A microinjection technique for the chick blastoderm is described. With a micropipette attached to a de Fonbrune micromanipulator, 25-45 nl of a reagent was injected into the entophyllic crescent of a chick blastoderm explanted in vitro according to New [7]. This procedure offers the advantage of eliminating the concentration variability which was observed after subblastodisc injection, and in contrast to the in ovo techniques, it allows one to stage the blastoderms properly. To check its applicability, testicular hyaluronidase was injected. On the basis of morphological and histochemical observations we ascertained that the experimental procedure itself did not interfere with the results. This method may provide a reliable experimental procedure with which to study the interactions between several macromolecules and the tissues during morphogenesis.

Animals↗
PubMed1988

Degradation of horseradish peroxidase after microinjection into mammalian cells.

Horseradish peroxidase (HRP) has been microinjected into mammalian cells in tissue culture by the erythrocyte ghost-mediated technique. This protein was selected because it can be localized and quantified after injection by cytochemical and spectrophotometric methods. HRP labeled by reductive methylation retained full catalytic activity, was efficiently loaded into erythrocyte ghosts, and did not associate to a significant degree with ghost membranes. A combination of cytochemical staining and autoradiography established that HRP injected into rat L6 myoblasts, HE(39)L human diploid fibroblasts, or HeLa cells was intracellular and uniformly distributed throughout the cell, while cell lysis techniques showed that the catalytically active HRP was not membrane bound. Inactivation of labeled HRP after injection paralleled the disappearance of the 40-kDa polypeptide, and was always more rapid than its overall degradation. This difference was associated with a pool of water-insoluble radioactivity in the injected cells. This material was of smaller molecular size than the native protein: many labeled peptides were detected in the range of 10 to 38 kDa. By the use of inhibitors of autophagic proteolysis or lysosomal function it was established that HRP degradation was not subjected quantitatively to the same regulatory processes as the average endogenous protein labeled in the same cultures.

Animals↗
PubMed1988

Inhibition of nuclear accumulation of karyophilic proteins in living cells by microinjection of the lectin wheat germ agglutinin.

The lectin wheat germ agglutinin (WGA), which has been reported to inhibit nuclear protein uptake in vitro by isolated nuclei (Finlay et al. (1987) J. Cell Biol. 104, 189), also blocks, on microinjection into living cells, the migration of proteins into the cell nucleus. Radioactively labeled nuclear proteins were injected into the cytoplasm of Xenopus oocytes and their reentry into the nucleus was analyzed in the presence or absence of WGA by two-dimensional gel electrophoresis. In another set of experiments, fluorescently labeled nucleoplasmin was injected, alone or together with WGA, into the cytoplasm of rat hepatoma cells, and its nucleocytoplasmic distribution was studied by quantitative laser fluorescence microscopy. The results indicate that WGA inhibits the uptake of karyophilic proteins in general, independent of their sizes. Since the nucleocytoplasmic flux of a dextran with Mr 10,000 was not affected it can be excluded that WGA acts by a general blockade or constriction of the functional pore channel. At reduced WGA concentrations, the rate but not the final extent of nuclear protein accumulation was decreased. These findings support the concept that the O-glycosidically bound carbohydrates of certain nuclear pore complex proteins are exposed to the pore interior and that these regions are probably involved in nucleocytoplasmic translocation processes.

Animals↗
PubMed1991

The effects of microinjection of rhodamine-phalloidin on mitosis and cytokinesis in early stage Drosophila embryos.

Rhodamine-phalloidin was microinjected into early stage Drosophila embryos, which were then allowed to develop for various times, fixed, and examined by fluorescence microscopy. A gradient of effects was seen. Close to the site of injection an area of diffuse bright fluorescence was found which included lumps and long strands of fluorescent material. Around this region particular cytoplasmic domains showed a denser F-actin distribution. These domains included the nuclear islands of the preblastoderm, the cortical caps of the syncytial blastoderm, and the contractile ring network which forms during cellularization of the blastoderm. It is proposed that these domains are regions of preferential actin polymerization under the appropriate cellular conditions and that the injected phalloidin causes incorporation of additional polymer into existing structures. Further away the pattern of phalloidin staining corresponded to that found with fixed material. In contrast to the domains of apparent additional F-actin polymerization a reduction of actin incorporated into small aggregates was found, both in syncytial blastoderm stages and during cellularization. This occurred in regions where additional actin had been incorporated into adjacent actin-rich structures. A storage role for the aggregates, which are depleted when F-actin is polymerized, is proposed. Both mitosis and cytokinesis were found to be slowed but the inhibition was only transient. However, most embryos died without differentiating. Rarely, differentiated tissues formed and the musculature was strongly stained by rh-phalloidin. When embryos were injected immediately prior to the start of cellularization cytokinesis was inhibited only locally and continued normally elsewhere. This finding argues against the hypothesis that contraction of an actomyosin network over the whole surface is the only force involved in the cellularization of the blastoderm and that local factors, e.g., plasmalemma extension, must be involved.

Animals↗
PubMed1991

Induction of M-phase entry of prophase-blocked mouse oocytes through microinjection of okadaic acid, a specific phosphatase inhibitor.

We report that a specific inhibitor of types 1 and 2A phosphatases, okadaic acid (OA), induces germinal vesicle break down (GVBD) and chromosome condensation when microinjected into denuded mouse oocytes maintained in prophase block by analogs of cAMP, inhibitors of phosphodiesterase, or a tumor-promoting phorbol ester. GVBD and chromosome condensation are also observed when incompetent oocytes are similarly injected with OA, this effect being dependent on the oocyte diameter. Marked changes in cell shape, cytoskeletal organization, and chromosome condensation with abnormal or abortive spindle formation are associated with such injections. The polar body is not formed. These results led to the conclusions that in mouse oocytes, OA acts distal to both the cAMP-modulated pathway involved in meiotic arrest and the inhibitory action exerted by tumor-promoting phorbol esters.

1-Methyl-3-isobutylxanthine↗
PubMed1989

Microinjections of D-Ala2-Met5-enkephalinamide placed into nucleus accumbens suppress hypothalamically elicited hissing in the cat.

The effects of D-Ala2-Met5-enkephalinamide (DAME) upon the hissing component of hypothalamically elicited affective defense behavior in the cat were examined in this study. Microinjections of DAME placed into the nucleus accumbens significantly suppressed this response in a dose and time dependent manner. This dose dependent suppression of affective defense decreased toward baseline levels at 60 and 90 min following delivery of 1 and 10 micrograms/0.5 microliters of DAME, respectively. Similar injections placed into the caudate nucleus had no effects upon this response. Neither vehicle control nor naloxone placed into nucleus accumbens was found to significantly alter latencies for hissing. Naloxone injected into nucleus accumbens prior to administration of either a 1-microgram or a 10-micrograms dose of DAME blocked the suppressive effects of DAME that were observed when this drug was administered alone. These findings suggest that opioid receptors in the nucleus accumbens play an important role in the regulation of the hissing component of hypothalamically elicited affective defense behavior in the cat.

Aggression↗
PubMed1985

Inositol 1,4,5-triphosphate microinjection triggers activation, but not meiotic maturation in amphibian and starfish oocytes.

Inositol 3,4,5-triphosphate (InsP3) brought about cortical granule exocytosis and elevation of a fertilization membrane, due to a rapid increase of free calcium in cytoplasm, when injected into oocytes of the amphibian Xenopus laevis arrested at second meiotic metaphase. The same result was observed when injection was performed into oocytes of the starfish Marthasterias glacialis arrested either at the first meiotic prophase or after completion of meiosis. Although meiotic maturation was induced in both animals by specific hormones which have been previously shown to release Ca2+ within cytoplasm, InsP3 microinjection into prophase-arrested oocytes did not release them from prophase block.

Adenine↗
PubMed1987

Electrophysiological responses to bradykinin and microinjected inositol polyphosphates in neuroblastoma cells. Possible role of inositol 1,3,4-trisphosphate in altering membrane potential.

Addition of bradykinin to mouse N1E-115 neuroblastoma cells evokes a rapid but transient rise in cytoplasmic free Ca2+ concentration ([Ca2+]i). The [Ca2+]i rise is accompanied by a transient membrane hyperpolarization, due to a several-fold increase in K+ conductance, followed by a prolonged depolarizing phase. Pretreatment of the cells with a Ca2+-ionophore abolishes the hormone-induced hyperpolarization but leaves the depolarizing phase intact. The transient hyperpolarization can be mimicked by iontophoretic injection of IP3(1,4,5) or Ca2+, but not by injection of IP3(1,3,4), IP4(1,3,4,5) or Mg2+ into the cells. Instead, IP3(1,3,4) evokes a small but significant membrane depolarization in about 50% of the cells tested. Microinjected IP4(1,3,4,5) has no detectable effect, nor has treatment of the cells with phorbol esters. These results suggest that, while IP3(1,4,5) triggers the release of stored Ca2+ to hyperpolarize the membrane, IP3(1,3,4) may initiate a membrane depolarization.

Animals↗
PubMed1988

Microinjection of catalytic subunit of cyclic AMP-dependent protein kinase triggers acute morphological changes in thyroid epithelial cells.

In dog thyroid epithelial cells in primary culture, thyrotropin acting through cyclic AMP induced rapid morphological changes associated with complete disruption of actin containing stress fibers. This modification preceded cell retraction and rounding up. These morphological effects were also induced by glass capillary microinjection of purified catalytic subunit of cAMP-dependent protein kinase. This provides the first direct evidence in intact cells that catalytic subunit, which is released upon activation of cAMP-dependent protein kinases, is responsible for cAMP-dependent morphological transformation.

Actins↗