PubMed Health⌕ Search

SEARCH · PubMed Health

Results for “Microinjection”

Explore indexed PubMed citations for clinical trials, systematic reviews and public health research. Read source abstracts and follow each citation to its original PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 1,171 records · Page 65Linked to original sources
PubMed1988

Induction of oral stereotypy following amphetamine microinjection into a discrete subregion of the striatum.

Amphetamine and other psychostimulant drugs induce perseverative motor behavior in rodents, such as compulsive sniffing, licking and biting. Although it is known that this behavior, termed stereotypy, is a consequence of dopaminergic stimulation of the striatum, the precise localization of the site of activation is unclear. It is reported here that microinjection of amphetamine (20 micrograms/0.5 microliter) into a circumscribed subregion of the striatum specifically produces intense oral stereotypy. It is proposed that this region, which corresponds to a small area within the ventrolateral striatum, contains motor circuitry critical to oral behavior, including feeding. The behavior elicited by amphetamine-induced stimulation of this area may represent a simple animal model in which to study certain orofacial dyskinesias.

Amphetamine↗
PubMed1994

A hypotensive and bradycardic action of gamma 2-melanocyte-stimulating hormone (gamma 2-MSH) microinjected into the nucleus tractus solitarii of the rat.

In conscious and urethane-anesthetized rats intravenously (i.v.) administered gamma 2-melanocyte-stimulating hormone (gamma 2-MSH), a melanotropin derived from the precursor peptide pro-opiomelanocortin (POMC), has been shown to induce a pressor response combined with a tachycardia. A site of action within the hindbrain, e.g. the nucleus tractus solitarii (NTS) or the area postrema (AP), has been suggested. In order to test the postulate that gamma 2-MSH acts within these hindbrain regions, the peptide was microinjected into various parts of the NTS and into the AP of urethane-anesthetized rats and blood pressure (BP) and heart rate (HR) were measured. Injection of gamma 2-MSH (100-500 pmol) into the NTS resulted in a dose-dependent decrease in BP and HR rather than in the expected pressor and tachycardiac response which is generally found in conscious and urethane-anesthetized rats following i.v. administration of the peptide. With respect to the depressor and bradycardiac effect the melanotropin was far more potent when injected into the pars commissuralis than into the medial part of the NTS. The responses were maximal after 3-4 min and lasted for about 15 min. gamma 2-MSH had no effect when injected into the AP. It is noteworthy that also a hypotensive and bradycardic effect for gamma 2-MSH is found in pentobarbital-anesthetized rats following i.v. administration. Therefore, we conclude that in addition to a pressor and tachycardic response gamma 2-MSH can elicit an opposite effect by interaction with structures within a discrete region in the NTS, the pars commissuralis.(ABSTRACT TRUNCATED AT 250 WORDS)

Anesthesia↗
PubMed1982

Correlation of mitochondrial form and function in vivo: microinjection of substrate and nucleotides.

Microinjection of adenine nucleotides and substrates into the cytoplasm of Amoeba proteus followed by EM examination has been used in an attempt to relate alterations in mitochondrial morphology with functional changes. Contracted mitochondria with dark matrix and wide cristae (Type I), and expanded mitochondria with light matrix and narrower cristae (Type II) coexist in normal active amoebae, but their numbers can be varied according to different cell activity states. Following injection of ATP, the mitochondria of the amoebae showed a time-dependent movement towards a predominately Type II form, whilst injections of ADP produced predominately the Type I form. Injection of succinate or deionised water, even in large amounts, had little effect on the numbers of Type I and Type II forms. The change induced by ATP was of long duration; that induced by ADP was influenced by both concentration injected and the cell's substrate levels. With 3 mM solutions of ADP the mitochondrial population was primarily of Type I organelles; higher ADP concentrations or the simultaneous injection of succinate, however, resulted in a switch with time to increased proportions of Type II mitochondria. The results extend the findings of previous in vivo and in vitro mitochondrial studies and are discussed in the light of these.

Adenosine Diphosphate↗
PubMed1983

Microinjection of Lucifer yellow CH into sea urchin eggs and embryos.

Eggs and embryos of Arbacia punctulata were microinjected with the fluorescent dye, Lucifer yellow CH, using a simple pressure injection system. When injected into eggs that were subsequently fertilized, the dye was distributed throughout all cells of the developing embryo. If one cell of a two-cell embryo was injected, dye did not diffuse into the uninjected blastomere. During subsequent development, all progeny of the injected cell contained dye resulting in an embryo that was half-fluorescent. Blue light irradiation of a two-cell embryo, one cell of which had been injected with Lucifer yellow, caused the injected blastomere to stop further divisions while the uninjected blastomere developed normally and was free of dye. These results indicate that the first two blastomeres of Arbacia embryos are not electrically coupled, nor up to the time of hatching, is there any coupling between cells in one half of the first cleavage plane and cells in the other half.

Animals↗
PubMed1984

Microinjection of RNA polymerase II corrects the temperature-sensitive defect of tsAF8 cells.

tsAF8 cells are a temperature-sensitive (ts) mutant of BHK cells that arrest in the G1 phase of the cell cycle at the non-permissive temperature of 40.6 degrees C. Previous reports had suggested that the temperature-sensitivity of these cells was based on a defect in either the synthesis, assembly or turnover of RNA polymerase II. We now show that the direct microinjection of purified RNA polymerase II into nuclei of tsAF8 cells corrects the ts defect and allows these cells to enter the S phase of the cell cycle.

Animals↗
PubMed1996

Desynchronized (REM) sleep inhibition induced by carbachol microinjections into the nucleus basalis of Meynert is mediated by the glutamatergic system.

The aim of this paper was to study the effects of microinjections of carbachol, a mixed cholinergic agonist, into the nucleus basalis of Meynert (NBM) of rats on the wake-sleep cycle. Carbachol (2.74 nmol) was able to increase wakefulness (W) and decrease desynchronized sleep (DS). To verify the hypothesis that the effects of carbachol are at least partially mediated by the glutamatergic system, the NMDA antagonist 2-amino-5-phosphonopentanoic acid and the non-NMDA antagonist D-gamma-glutamylaminomethanesulfonic acid were injected into the NBM before carbachol. Pretreatment with these glutamate receptor antagonists counteracted the effect of carbachol on DS. The effect of carbachol on W was not modified by the pretreatment with the glutamate receptor antagonists. This is the first study showing that carbachol injected into the NBM increases W and decreases spontaneous DS in the rat. Moreover, our results tend to indicate that the decrease in DS following the injection of carbachol into the NBM is related to the release of endogenous glutamate.

Animals↗
PubMed1991

Differential effects of bicuculline and muscimol microinjections into the vestibular nuclei on simian eye movements.

1.) Eye movements were recorded in four Java monkeys (M. fascicularis) after unilateral microinjections (1 microliter, concentration 1 micrograms/microliter) of the GABA antagonist, bicuculline, and the GABA agonist, muscimol, into oculomotor related regions of the vestibular nuclei. Eye movements were investigated in the dark and light during spontaneous eye movements, vestibular stimulation (sinusoidal: 0.2 Hz, +/- 40 deg/s, and velocity trapezoid: 40 deg/s2 acceleration, 120 deg/s constant velocity), and visual-vestibular conflict stimulation. 2.) Bicuculline and muscimol injections consistently led to specific eye movement changes, which were maximal 5-10 min after bicuculline injection (muscimol 10-30 min), and lasted 90-120 min (muscimol 2-4 h). Control injections with NaCl (0.9%) into the responsive area and with bicuculline 2-3 mm more lateral showed no effect. 3.) Bicuculline induced a spontaneous nystagmus of 40.9 deg/s (average, range 10.5-93 deg/s), beating in 60% of the cases to the contralateral and in 40% to the ipsilateral side. The analysis of the slope of the slow phase gave no evidence for an additional gaze holding deficit. The VOR gain in the dark showed a slight decrease (pre: 0.96; post: 0.86) on average. The time constant of decay for slow phase nystagmus velocity after vestibular ramp stimulation was reduced, reflecting a 'velocity storage' deficit. After bicuculline injections nystagmus suppression in the light and during visual-vestibular conflict stimulation was generally well preserved. 4.) After muscimol injections horizontal gaze holding was severely affected. Each saccade was followed by an exponentially decreasing postsaccadic drift with a time constant as short as 250 ms (average 414 ms). The eyes always drifted towards a null-position, which generally did not coincide with the midposition of the eye. The null-position could move up to 35 deg to the contralateral or ipsilateral side. The highly distorted eye movements after muscimol injections prevented VOR-measurements based on eye velocity. Instead vestibular stimulation led to a shift of the null-position with an amplitude corresponding to a gain (eye position/stimulus position) of 0.17 (average) at 0.2 Hz (+/- 40 deg/s). Vertical eye movements did not show a major gaze holding deficit. 5.) From the experiments it can be concluded that the inhibitory transmitter GABA plays an important role for eye movement generation within the vestibular nuclei. Bicuculline induces mainly a vestibular imbalance with little evidence for a neural integrator deficit. In contrast unilateral muscimol injections lead to a complete, reversible loss of function for the common horizontal neural integrator, which converts eye velocity into eye position signals. The accompanying shift of the null-position reflects an additional vestibular imbalance.

Animals↗
PubMed1980

Organization and spatial arrangement of fluorescein-labeled native actin microinjected into normal locomoting and experimentally influenced Amoeba proteus.

Fully polymerization-competent fluorescein-labeled actin from skeletal muscle was microinjected into both normal moving and experimentally treated Amoeba proteus. Its intracellular distribution was followed by integral image intensification of the fluorescence on a television screen and compared with controls injected with rhodamine-labeled serum albumin. The labeled actin was incorporated into the endogenous actin pool and exhibited a characteristic redistribution depending on the cellular morphology. Increased amounts of labeled actin could be detected within a thin layer separating the hyalo- and granuloplasm or running immediately beneath the plasma membrane when hyaloplasmic regions were absent. The topography of the fluorescent layer demonstrated in living cells is in agreement with the cortical microfilament layer described ultrastructurally recently in corresponding cells. The combined results emphasize the important role of the cortical filament layer in both morphogenetic processes (e.g., hyalo-granuloplasm separation or changes in cell shape) and motive force generation for cytoplasmic streaming and amoeboid movement.

Actins↗
PubMed1988

Catalepsy after microinjection of haloperidol into the rat medial prefrontal cortex.

To investigate the behavioural role of mesocortical dopamine innervation we performed bilateral microinjections of haloperidol into various parts of the rat frontal cortex and into adjacent subcortical forebrain structures. Haloperidol (2.5 micrograms/0.5 microliter) locally injected into the medial prefrontal cortex or into the rostral part of the neostriatum resulted in the development of catalepsy as measured in the bar test. In contrast, injections of haloperidol into the nucleus accumbens, more caudal parts of the neostriatum, anterior cingulate cortex, rostral and lateral parts of the prefrontal cortex and into the lateral ventricles failed to induce catalepsy. It is concluded that blockade of dopamine receptors located in the rostral neostriatum and in the medial prefrontal cortex contributes to the development of haloperidol induced catalepsy.

Animals↗
PubMed1987

The use of local anaesthetic microinjections to identify central pathways: a quantitative evaluation of the time course and extent of the neuronal block.

The time course and extent of local anaesthetic blocks within the spinal cord of cats were evaluated. A monopolar stimulation electrode with the tip lowered into the dorsal columns (DC) 1000 microns below cord surface was used to activate antidromically DC fibers at the T13 level and evoke cord dorsum potentials at the level of the lumbar spinal cord. The amplitude of the negative deflection, the N-wave, was determined for various stimulation intensities (stimulation-response-function, SRF). Lidocaine (1%) was microinjected in volumes of 0.5 or 1.0 microliter into the DC from a glass micropipette 1 mm caudal to the stimulation site. Conduction block was characterized by a reversible shift of the SRFs to higher stimulation intensities. The diameter of the blocked area in the transverse plane was evaluated from threshold intensities and was found to be 0.9 +/- 0.1 mm 4 to 30 min after the injection of 0.5 microliter lidocaine and 1.6 +/- 0.36 mm 10 to 45 min after the injection of 1.0 microliter lidocaine. In the sagittal plane, the diameter of the blocked area following 1.0 microliter lidocaine was found to be up to 2.8 mm. The DC-block was reversible within 92 min following injection of 1.0 microliter and 69 min after the injection of 0.5 microliter lidocaine. The application of the present findings for blocks in other CNS structures is discussed.

Anesthetics, Local↗
PubMed1987

Microinjection of normal cell extracts into Fanconi anemia fibroblasts corrects defective scheduled DNA synthesis recovery after 8-methoxypsoralen plus UVa treatment.

Fanconi anemia (FA) cells show an increased sensitivity to 8-methoxypsoralen (8-MOP) plus UVa treatment; after an initial reduction of their semiconservative DNA synthesis rate, they do not recover like normal cells. We microinjected extracts from normal cells into FA fibroblasts from complementation group A and determined semiconservative DNA synthesis rates by autoradiography; the hampered recovery phase was completely restored.

Anemia, Aplastic↗
PubMed1986

Rearrangements of microinjected recombinant DNA in the genome of transgenic mice.

Previously, mouse zygotes were microinjected with the recombinant plasmid pMA3, which contains the Herpes simplex virus thymidine kinase gene attached to the promoter region of the Rous sarcoma virus (Gazaryan et al. 1984a). In the present work the pMA3 fragment with the flanking genomic sequences was isolated from the DNA of one transgenic Fo mouse by the "plasmid rescue" technique. The rescued plasmid (pMAR1) lacked all virus-specific sequences and retained only some pBR322 sequences. The flanking region at one end of the integrated pBR322-specific fragment contained a highly conserved mouse repetitive sequence. The possible mechanisms of rearrangement of foreign DNA in germ line cells are discussed.

Animals↗
PubMed1992

Microinjections of vasopressin in the locus coeruleus complex affect posture and vestibulospinal reflexes in decerebrate cats.

Vasopressin (VP) acts as a neurotransmitter or a neuromodulator on noradrenergic locus coeruleus (LC) neurons by exciting them. Experiments were performed in precollicular decerebrate cats to investigate whether direct infusion of VP into the LC complex of one side produced changes in posture as well as in the gain of vestibulospinal reflexes acting on forelimb extensors. Unilateral microinjection of 0.25 microliters VP solution (10(-11) micrograms/microliters saline) into the LC complex increased the extensor rigidity in the ipsilateral limbs, while that of the contralateral limbs either remained unmodified or slightly decreased. The amplitude of modulation and thus the response gain of both the ipsilateral and the contralateral triceps brachii to roll tilt of the animal leading to stimulation of labyrinth receptors decreased (t-test, P less than 0.001 for both the ipsilateral and the contralateral responses). Moreover, a slight decrease in phase lead of the responses was observed. These findings occurred 5-10 min after the injection, were fully developed within 30 min and disappeared in about 2 h. The changes in posture as well as in the gain of vestibulospinal reflexes described above were site specific and depended upon the injected neuropeptide. They were attributed to tonic activation of presumptive noradrenergic neurons, which exert a facilitatory influence on limb extensor motoneurons either directly, by utilizing the coeruleospinal pathway, or indirectly by inhibiting the dorsal pontine reticular formation and the related medullary inhibitory reticulospinal neurons.

Animals↗
PubMed1992

Modulation of desynchronized sleep through microinjection of alpha 1-adrenergic agonists and antagonists in the dorsal pontine tegmentum of the cat.

Noradrenaline is involved in the regulation of the sleep/waking cycle by acting through various receptor types. In previous studies we investigated the role of beta- and alpha 2-adrenergic receptors through local microinjections of various drugs into the dorsal pontine tegmentum (DPT) of the cat. This region is known to be crucially involved in desynchronized sleep execution. In this study we examined the role of alpha 1-adrenergic receptors. The alpha 1-agonist methoxamine and the alpha 1-antagonist prazosin were injected into the DPT of freely moving, unanaesthetized cats. We found that methoxamine notably reduced desynchronized sleep, and that this effect was both dose-dependent and site-specific. These effects were prevented by the subsequent injection of prazosin. On the other hand, the injection into the DPT of prazosin alone produced scarce or inconsistent effects on the sleep/waking cycle.

Animals↗
PubMed1991

Suppression of desynchronized sleep through microinjection of the alpha 2-adrenergic agonist clonidine in the dorsal pontine tegmentum of the cat.

The relationships between sleep-waking states and the activity of the noradrenergic system are controversial. In particular, according to an influential model of desynchronized sleep (DS) generation, the arrest of firing of noradrenergic neurons in the locus coeruleus should enhance DS, due to the release from inhibition of executive neurons located in the nearby pontine tegmentum. Since locus coeruleus neurons are strongly inhibited by alpha 2-adrenergic agonists like clonidine, this agent would be expected to increase DS. Yet clonidine powerfully decreases DS when injected systemically in several species. In this study, clonidine was microinjected locally into the dorsal pontine tegmentum of the cat, a region which comprises anatomically the whole locus coeruleus complex and which plays a key role in the generation of DS. In accord with the results of systemic experiments, bilateral injections of clonidine almost suppressed DS and unilateral injections consistently reduced it. The effects were dose dependent and site specific. It is suggested that clonidine may suppress DS by acting additionally on non-noradrenergic cell groups located in the dorsal pontine tegmentum.

Adrenergic alpha-Agonists↗
PubMed1989

Tissue-specific processing and polarized compartmentalization of clone-produced cholinesterase in microinjected Xenopus oocytes.

1. To approach the involvement of tissue-specific elements in the compartmentalization of ubiquitous polymorphic proteins, immunohistochemical methods were used to analyze the localization of butyrylcholinesterase (BuChE) in Xenopus oocytes microinjected with synthetic BuChEmRNA alone and in combination with tissue-extracted mRNAs. 2. When injected alone BuChEmRNA efficiently directed the synthesis of small membrane-associated accumulations localized principally on the external surface of the oocyte's animal pole. Tunicamycin blocked the appearance of such accumulations, suggesting that glycosylation is involved in the transport of nascent BuChE molecules to the oocyte's surface. Coinjection with brain or muscle mRNA, but not liver mRNA, facilitated the formation of pronounced, tissue-characteristic BuChE aggregates. 3. These findings implicate tissue-specific mRNAs in the assembly of the clone-produced protein and in its nonuniform distribution in the oocyte membrane or extracellular material.

Animals↗
PubMed1991

Glutamate decarboxylase activity in the substantia nigra and the hippocampus of rats microinjected with inhibitors of the enzyme.

Three inhibitors of glutamate decarboxylase (GAD), acting through different mechanisms, as well as pyridoxal phosphate (PLP), were microinjected unilaterally by stereotaxic procedures into the substantia nigra reticulata or the CA1 area of the hippocampus of the rat. The inhibitors used were thiosemicarbazide (TSC), gamma-glutamyl hydrazide and the PLP-glutamyl-hydrazone (PLPGH) formed by the combination of the latter with PLP. No behavioral alterations were observed after the administration of any of the drugs used, in any of the two brain regions studied. When measured in the absence of exogenous PLP, GAD activity in the substantia nigra injected with TSC was diminished by about 35%, and no changes were observed with the other drugs. In the CA1 hippocampal area both TSC and PLPGH inhibited GAD by more than 50%, and this inhibition was not reversed by PLP added in vitro. The results are discussed in terms of the possible explanation for the differences between the drugs used and for the lack of effects of GAD inhibition on the behavior of the animals.

Animals↗